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Problems With Sulphur
- Thread starter chrismturner89
- Start date
Amazoniac
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- Hydrogen Sulfide in Physiology and Diseases of the Digestive Tract
- Ray Peat - Menopause & Estrogen; Thyroid; Coronavirus; Glaucoma; Food Combining and More (55:45) | Patrick Timpone (thanks to whoever is behind 'Ray Peat Archives')
If blood vessels is dilated and this toxin is capable of doing it, it must be possible to test which gas is responsible by boosting one while suppressing the others. Regulated, should be drugs as dangerous.
Official note: 'sulfur' in prolactinese is 'foulium' from now on.
"Experimental evidence generally supports an inhibitory role of H2S on gastrointestinal motility [156–161]. The negative effect of H2S in some cases is mediated through K[ATP] channels [159,162] but in others, blocking of K[ATP] channels did not affect H2S-induced inhibition [158,163]. The relaxant effect of H2S on colonic motility has also been explained, in part, by its direct inhibition of L-type calcium channel. H2S inhibits both L-type calcium channels and BK[Ca] channels in smooth muscle cells of rat colon [164]. In vascular smooth muscle cells, opening of K[ATP] channels hyperpolarizes cell membrane and inactivates voltage-dependent L-type Ca2+ channels, leading to relaxation of smooth muscle cell and dilation of blood vessel. Recently, it was demonstrated that H2S exerted suppressive effects on colonic contractility by decreasing neurally mediated cholinergic and tachykinergic excitatory pathways [165]. It has been previously shown that H2S significantly reduced cholinergic mediated contractions [158,160]. In another study, NaHS inhibited the contractile activity of smooth muscle cells in rat stomach and jejunum [165]. L-cysteine, a precursor of H2S, inhibited the electrical stimulation (ES) induced contraction of mouse ileum. Contractions increased following the administration of aminooxyacetic acid, an inhibitor of CBS and CSE. The treatment with glibenclamide, a KATP channel blocker, reduced both the L-cysteine response and NaHS-induced inhibition of contractions [166]. The same group later identified that inhibition of electrical field stimulation-induced contractions in ileum by L-cysteine and D,L-homocysteine was decreased by the treatment with 2-aminobicyclo [2.2.1]heptane-2-carboxylate (BCH), an inhibitor of L type and B[o,+] transporter systems, thus highlighting the role of the amino acid transport system in L-cysteine regulation (via H2S) of motility [167]."
"A dual excitatory and inhibitory role of H2S was demonstrated in smooth muscle contractility, which was dependent on the dose of NaHS. Typically at lower concentrations, NaHS stimulated the contraction while at higher doses caused relaxation. NaHS also caused a biphasic effect, early transient excitation and late long-lasting inhibition on the motility of rat duodenum jejunum, ileum and colon [168]. The excitatory effects of NaHS were mediated by TRPV1 channels since capsazepine, a TRPV1 antagonist, inhibited this effect. TRPV1 channels are known to be activated by NaHS [169,170] Glibenclamide, on the other hand, did not affect NaHS induced excitatory effect but rather inhibited NaHS-induced long-lasting inhibition on the contraction of muscle strips, indicating the role of KATP channels."
"A dual excitatory and inhibitory role of H2S was demonstrated in smooth muscle contractility, which was dependent on the dose of NaHS. Typically at lower concentrations, NaHS stimulated the contraction while at higher doses caused relaxation. NaHS also caused a biphasic effect, early transient excitation and late long-lasting inhibition on the motility of rat duodenum jejunum, ileum and colon [168]. The excitatory effects of NaHS were mediated by TRPV1 channels since capsazepine, a TRPV1 antagonist, inhibited this effect. TRPV1 channels are known to be activated by NaHS [169,170] Glibenclamide, on the other hand, did not affect NaHS induced excitatory effect but rather inhibited NaHS-induced long-lasting inhibition on the contraction of muscle strips, indicating the role of KATP channels."
- Ray Peat - Menopause & Estrogen; Thyroid; Coronavirus; Glaucoma; Food Combining and More (55:45) | Patrick Timpone (thanks to whoever is behind 'Ray Peat Archives')
If blood vessels is dilated and this toxin is capable of doing it, it must be possible to test which gas is responsible by boosting one while suppressing the others. Regulated, should be drugs as dangerous.
Official note: 'sulfur' in prolactinese is 'foulium' from now on.
Amazoniac
Member
It's addressing severe intoxication, but it hints at how useful methylene blue should be for milder cases.
↳ Hydrogen sulfide intoxication induced brain injury and methylene blue
"H2S, which is much more soluble than CO2 or O2 (Carroll and Mather, 1989; Furne et al., 2008; Goodwin et al., 1989), diffuses almost instantaneously into the blood as soon as it is inhaled. In the blood and tissues, only a very small portion of sulfide remains in a “free/soluble” or diffusible form (Fig. 1), comprising the gaseous form H2S (Barrett et al., 1988; Carroll and Mather, 1989; De Bruyn et al., 1995; Douabul and Riley, 1979) and the sulfhydryl anion HS− (Almgren et al., 1976; Millero, 1986). A larger pool of sulfide will combine with metalloproteins such as the ferrous iron of hemoglobin or will react with cysteine residues present in large number of proteins (Haggard, 1921; Smith, 1967; Smith and Gosselin, 1966; Wintner et al., 2010), creating a large sink for H2S (Haouzi et al., 2014b; Klingerman et al., 2013). The most remarkable feature of H2S metabolism is that H2S disappears spontaneously from the blood and the tissue (Haggard, 1921; Klingerman et al., 2013; Toombs et al., 2010) at a very rapid rate (Fig. 1). Indeed H2S is oxidized into suflite, sulfate and thiosulfate (Olson, 2012; Olson, 2011; Olson et al., 2018), a reaction catalyzed by various mitochondrial enzymes such as the sulfide quinone oxido-reductase (Bouillaud and Blachier, 2011; Lagoutte et al., 2010; Leschelle et al., 2005; Modis et al., 2014). We found that soluble H2S completely disappears from the blood and tissues within 1 min in large and small mammals exposed to very high levels of H2S (Haouzi et al., 2014b; Klingerman et al., 2013). In contrast, the forms “hidden” in disulfide bonds for instance persist for a much longer period of time (Klingerman et al., 2013) in the brain tissues (Warenycia et al., 1990). This notion has however been challenged for the heart, supporting the view that some of the persisting consequences of H2S intoxication are not directly related to the persistence of a pool of measurable sulfide (Sonobe and Haouzi, 2016a). Regardless, the toxic effects of H2S can persist beyond the phase of exposure, without being accessible to antidotes that would be mostly acting on the soluble form (Haouzi et al., 2014a; Haouzi and Klingerman, 2013; Haouzi et al., 2014b; Klingerman et al., 2013) []."
"H2S is considered as a mitochondrial poison, and its toxicity is usually assumed to result from its combination with the ferric iron of the mitochondrial cytochrome C oxidase (CCO) (Khan et al., 1990), inhibiting its activity (Cooper and Brown, 2008; Dorman et al., 2002), preventing in turn ATP formation and promoting the production of reactive O2 species (ROS) (Eghbal et al., 2004). As a consequence, the mitochondrial complexes upstream to CCO are all maintained in a reduced state and become unable to transfer protons across the inner mitochondrial membrane leading to a rapid depression of the mitochondrial membrane potential, preventing mitochondrial ATP synthesis (Kim et al., 2012). The resulting production of mitochondrial reactive O2 species also contributes to H2S toxicity. In addition, since NADH cannot be oxidized anymore by an already reduced mitochondrial complex I, the NADH/NAD ratio increases and virtually stops the TCA cycle (LaNoue et al., 1972; Liu et al., 2018). This, in turn, also suppresses synthesis of ATP via mitochondrial substrate-level phosphorylation (TCA cycle). The rise in the NADH/NAD ratio also increases the transformation of pyruvate into lactate in the cytoplasm (Burgner and Ray, 1984)."
"However, some manifestations produced by an intoxication by H2S compatible with survival are probably not related to a decrease in intracellular ATP concentration: Recent works on the interaction between H2S and proteins (Paul and Snyder, 2012), including ion channels (Zhang et al., 2012), have revealed much more complex sets of mechanisms potentially leading to an acute neuronal depression (apnea and coma). Such mechanisms include the effects of H2S on cysteine residues of proteins, by direct “sulfhydration” (S-SH bonds) (Mustafa et al., 2009). This mechanism has been put forward to account for the extreme and early toxicity of H2S on Ca2+ channels for instance (Sun et al., 2008; Zhang et al., 2012), including sarcoplasmic reticulum ryanodine receptors (RyR) rich in free cysteine residues. Various ion channels, including K+-ATP (Chen et al., 2012), Ca2+ (Sun et al., 2008; Telezhkin et al., 2010; Zhang et al., 2012), are affected by hydrogen sulfide in the heart and in the central nervous system. Not all the mechanisms of sulfide toxicity require the mitochondrial activity to be critically altered, as shown for the medullary neurons for instance (Greer et al., 1995)."
"H2S has been proposed to contribute to the phosphorylation of NMDA receptor subunits resulting in their activation (Abe and Kimura, 1996; Kimura, 2000) as well as an increase in glutamate production (Garcia-Bereguiain et al., 2008). Perhaps more interestingly, the inhibitory effect of H2S on GABAergic system (Han et al., 2005) may well represent the substratum for many of the clinical symptoms related to neural depression (coma, apnea) observed in sulfide intoxication. The very rapid production of neural inhibition including the brainstem respiratory neurons could be seen as a protective mechanism, which by a reduction in ATP demand could certainly anticipate and limit the consequences of a reduction in ATP production."
"[..]one of the first measurable symptoms of toxicity to an exposure to H2S is a stimulation of breathing, long identified as a result of a stimulation of the arterial chemoreceptors by H2S (Haouzi, 2012; Heymans et al., 1931). As the intoxication progresses this stimulation of breathing is replaced by a depression of breathing always associated with a coma (Beauchamp Jr, et al., 1984; Guidotti, 2010). This coma may be associated with seizures, although generalized seizures appears, at least in un-sedated rats, much less frequent than during cyanide intoxication (Haouzi et al., 2017)."
"The specific approach proposed to treat H2S poisoning has traditionally focused on trapping free H2S using metallo-compounds, e.g. ferric iron contained in methemoglobin (Chenuel et al., 2015; Haouzi and Klingerman, 2013; Van de Louw and Haouzi, 2013) or cobalt compounds such as in hydroxycobalamin (HyCo) (Haouzi, 2011; Smith, 1969; Smith and Gosselin, 1976; Truong et al., 2007; Van de Louw and Haouzi, 2013). Other antidotes are based on empirical observations, such as sodium bicarbonate (Almeida and Guidotti, 1999; Guidotti, 2010) and hyperoxia (Bitterman et al., 1986; Haouzi et al., 2011; Smilkstein et al., 1985; Smith et al., 1976). Vitamin B12 analogues or Nitrite-induced methemoglobinemia (Kohn et al., 2002; Smith, 1967, 1969, 1977; Smith and Gosselin, 1966; Van de Louw and Haouzi, 2013) can however only allow the rapid trapping of H2S outside the cells but have little or no effects on the combined forms after exposure (Haouzi et al., 2014a). In addition, sodium nitrite further decreases arterial blood pressure in subjects already in shock (Hall and Rumack, 1997; Hall et al., 2009) and affects oxygen transport (Ash-Bernal et al., 2004; Smith and Gosselin, 1979, 1966). Cobalt contained in HyCo (Van de Louw and Haouzi, 2013) has several theoretical advantages over methemoglobinemia (Mihajlovic, 1999; Truong et al., 2007), but whether this very large molecule can penetrate cells at sufficient concentrations and rapidly enough (Astier and Baud, 1996) to neutralize the effects of H2S remains to be demonstrated. We found that HyCo reduces the immediate mortality of sulfide in the sheep but only when used within one or 2 min following exposure (Haouzi et al., 2015). In our experience, no clear beneficial effects are demonstrable if administered later on, and more importantly HyCo did not prevent the development of a severe metabolic acidosis or lactate production in the surviving animals (Haouzi et al., 2015). As HyCo has no interaction with the sulfides “fixed” on proteins, new paradigms must be proposed using agents counteracting the deleterious consequences of H2S toxicity, rather than trying to trap soluble H2S. Of interest, recent works on cobinamide, a very soluble modified B12 analog (Brenner et al., 2010), have shown a clear efficacy in animal models receiving this antidotes when a continuous exposure to sulfide a low dose was maintained following a very toxic bout (Brenner et al., 2014; Ng et al., 2018). The effects of this promising agent administered at various timing after the end of a unique bout of H2S remain therefore to be characterized."
"Methylene blue (MB), a dye that was synthetized at the end of the 19th century (Clifton and Leikin, 2003; Ginimuge and Jyothi, 2010), appears to exert interesting antidotal properties against severe intoxications by H2S with very relevant neurological benefits in animal models. MB appears to act through a unique modality of action, resulting from its very distinctive cyclic redox properties. These properties are currently used to treat methemoglobinemia, restoring the ability of hemoglobin to carry O2 (Clifton and Leikin, 2003; Ginimuge and Jyothi, 2010; Mayer et al., 1993; Wright et al., 1999)."
"MB diffuses extremely rapidly and accumulates in all tissues including in the brain (Peter et al., 2000)."
"As soon as it enters the blood, MB, with a redox potential around zero, is reduced into leucomethylene blue (LMB)(Fig. 3) by NADH (Fig. 6) or other reducing agents present in cells (Buchholz et al., 2008). LMB is then re-oxidized into MB by molecules such as O2 and oxidized metallo-compounds and a new cycle of reduction can be initiated (Buchholz et al., 2008). Diffusing rapidly into the cytoplasm and in the mitochondria of any cells, including neurons (Peter et al., 2000), MB/LMB can therefore restore the TCA cycle and the glycolytic activity by oxidizing NADH and decreasing the NADH/ NAD ratio (Komlodi and Tretter, 2017). When the electron chain is immobilized in a reduced state, like during H2S intoxication, the reestablishment of the TCA cycle can, in turn, lead to the production of ATP via succinyl-CoA synthase – mitochondrial substrate-level phosphorylation (Komlodi and Tretter, 2017) – independently of the integrity of the mitochondrial ATPase activity."
"[..]MB appears to increase the pool of “trapped” H2S in red cells through a mechanism very similar to the mechanisms involved in the restoration of electron chain(Fig. 7)." "One could propose that molecules of hydrogen peroxide produced during the re-oxidation of LMB by O2 before being “transformed” into H2O by the catalase presents in red cells, could change the redox state of iron into a ferryl state, “fossilizing” H2S and in turn impeding sulfide diffusion to the tissues (see (Haouzi et al., 2019a; Haouzi et al., 2019b) for more discussion). This could certainly account for the lessening of H2S toxicity without creating a permanent methemoglobinemia."
"H2S is considered as a mitochondrial poison, and its toxicity is usually assumed to result from its combination with the ferric iron of the mitochondrial cytochrome C oxidase (CCO) (Khan et al., 1990), inhibiting its activity (Cooper and Brown, 2008; Dorman et al., 2002), preventing in turn ATP formation and promoting the production of reactive O2 species (ROS) (Eghbal et al., 2004). As a consequence, the mitochondrial complexes upstream to CCO are all maintained in a reduced state and become unable to transfer protons across the inner mitochondrial membrane leading to a rapid depression of the mitochondrial membrane potential, preventing mitochondrial ATP synthesis (Kim et al., 2012). The resulting production of mitochondrial reactive O2 species also contributes to H2S toxicity. In addition, since NADH cannot be oxidized anymore by an already reduced mitochondrial complex I, the NADH/NAD ratio increases and virtually stops the TCA cycle (LaNoue et al., 1972; Liu et al., 2018). This, in turn, also suppresses synthesis of ATP via mitochondrial substrate-level phosphorylation (TCA cycle). The rise in the NADH/NAD ratio also increases the transformation of pyruvate into lactate in the cytoplasm (Burgner and Ray, 1984)."
"However, some manifestations produced by an intoxication by H2S compatible with survival are probably not related to a decrease in intracellular ATP concentration: Recent works on the interaction between H2S and proteins (Paul and Snyder, 2012), including ion channels (Zhang et al., 2012), have revealed much more complex sets of mechanisms potentially leading to an acute neuronal depression (apnea and coma). Such mechanisms include the effects of H2S on cysteine residues of proteins, by direct “sulfhydration” (S-SH bonds) (Mustafa et al., 2009). This mechanism has been put forward to account for the extreme and early toxicity of H2S on Ca2+ channels for instance (Sun et al., 2008; Zhang et al., 2012), including sarcoplasmic reticulum ryanodine receptors (RyR) rich in free cysteine residues. Various ion channels, including K+-ATP (Chen et al., 2012), Ca2+ (Sun et al., 2008; Telezhkin et al., 2010; Zhang et al., 2012), are affected by hydrogen sulfide in the heart and in the central nervous system. Not all the mechanisms of sulfide toxicity require the mitochondrial activity to be critically altered, as shown for the medullary neurons for instance (Greer et al., 1995)."
"H2S has been proposed to contribute to the phosphorylation of NMDA receptor subunits resulting in their activation (Abe and Kimura, 1996; Kimura, 2000) as well as an increase in glutamate production (Garcia-Bereguiain et al., 2008). Perhaps more interestingly, the inhibitory effect of H2S on GABAergic system (Han et al., 2005) may well represent the substratum for many of the clinical symptoms related to neural depression (coma, apnea) observed in sulfide intoxication. The very rapid production of neural inhibition including the brainstem respiratory neurons could be seen as a protective mechanism, which by a reduction in ATP demand could certainly anticipate and limit the consequences of a reduction in ATP production."
"[..]one of the first measurable symptoms of toxicity to an exposure to H2S is a stimulation of breathing, long identified as a result of a stimulation of the arterial chemoreceptors by H2S (Haouzi, 2012; Heymans et al., 1931). As the intoxication progresses this stimulation of breathing is replaced by a depression of breathing always associated with a coma (Beauchamp Jr, et al., 1984; Guidotti, 2010). This coma may be associated with seizures, although generalized seizures appears, at least in un-sedated rats, much less frequent than during cyanide intoxication (Haouzi et al., 2017)."
"The specific approach proposed to treat H2S poisoning has traditionally focused on trapping free H2S using metallo-compounds, e.g. ferric iron contained in methemoglobin (Chenuel et al., 2015; Haouzi and Klingerman, 2013; Van de Louw and Haouzi, 2013) or cobalt compounds such as in hydroxycobalamin (HyCo) (Haouzi, 2011; Smith, 1969; Smith and Gosselin, 1976; Truong et al., 2007; Van de Louw and Haouzi, 2013). Other antidotes are based on empirical observations, such as sodium bicarbonate (Almeida and Guidotti, 1999; Guidotti, 2010) and hyperoxia (Bitterman et al., 1986; Haouzi et al., 2011; Smilkstein et al., 1985; Smith et al., 1976). Vitamin B12 analogues or Nitrite-induced methemoglobinemia (Kohn et al., 2002; Smith, 1967, 1969, 1977; Smith and Gosselin, 1966; Van de Louw and Haouzi, 2013) can however only allow the rapid trapping of H2S outside the cells but have little or no effects on the combined forms after exposure (Haouzi et al., 2014a). In addition, sodium nitrite further decreases arterial blood pressure in subjects already in shock (Hall and Rumack, 1997; Hall et al., 2009) and affects oxygen transport (Ash-Bernal et al., 2004; Smith and Gosselin, 1979, 1966). Cobalt contained in HyCo (Van de Louw and Haouzi, 2013) has several theoretical advantages over methemoglobinemia (Mihajlovic, 1999; Truong et al., 2007), but whether this very large molecule can penetrate cells at sufficient concentrations and rapidly enough (Astier and Baud, 1996) to neutralize the effects of H2S remains to be demonstrated. We found that HyCo reduces the immediate mortality of sulfide in the sheep but only when used within one or 2 min following exposure (Haouzi et al., 2015). In our experience, no clear beneficial effects are demonstrable if administered later on, and more importantly HyCo did not prevent the development of a severe metabolic acidosis or lactate production in the surviving animals (Haouzi et al., 2015). As HyCo has no interaction with the sulfides “fixed” on proteins, new paradigms must be proposed using agents counteracting the deleterious consequences of H2S toxicity, rather than trying to trap soluble H2S. Of interest, recent works on cobinamide, a very soluble modified B12 analog (Brenner et al., 2010), have shown a clear efficacy in animal models receiving this antidotes when a continuous exposure to sulfide a low dose was maintained following a very toxic bout (Brenner et al., 2014; Ng et al., 2018). The effects of this promising agent administered at various timing after the end of a unique bout of H2S remain therefore to be characterized."
"Methylene blue (MB), a dye that was synthetized at the end of the 19th century (Clifton and Leikin, 2003; Ginimuge and Jyothi, 2010), appears to exert interesting antidotal properties against severe intoxications by H2S with very relevant neurological benefits in animal models. MB appears to act through a unique modality of action, resulting from its very distinctive cyclic redox properties. These properties are currently used to treat methemoglobinemia, restoring the ability of hemoglobin to carry O2 (Clifton and Leikin, 2003; Ginimuge and Jyothi, 2010; Mayer et al., 1993; Wright et al., 1999)."
"MB diffuses extremely rapidly and accumulates in all tissues including in the brain (Peter et al., 2000)."
"As soon as it enters the blood, MB, with a redox potential around zero, is reduced into leucomethylene blue (LMB)
"[..]MB appears to increase the pool of “trapped” H2S in red cells through a mechanism very similar to the mechanisms involved in the restoration of electron chain
LUH 3417
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@Amazoniac
Any updates?
Any updates?
Amazoniac
Member
- The contribution of alliaceous and cruciferous vegetables to dietary sulphur intake
- Calorie restriction and methionine restriction in control of endogenous hydrogen sulfide production by the transsulfuration pathway
"The sulphur intake determined from analysis of each 24-h food diary analysed ranged from 390 mg to 1414 mg total sulphur consumed in a 24-h period, and enabled the identification of low (<750 mg/day), moderate (between 750 and 1250 mg/day) and high sulphur intake (>1250 mg/day) diets across the 41 diet dairies analysed."
"[..]the analysis of sulphur content and partitioning in commonly consumed foods and vegetables undertaken in this study indicates as much as 89.5% of the total sulphur consumed in a typical diet may not be derived from SAA. Significant sulphur intake was also achieved from consumption of wheat and starchy foods, dairy and vegetables. If only SAA intake is monitored the significant contribution to total sulphur intake from these other foods will be disregarded. Alliaceous and cruciferous vegetables are shown to be an important source of sulphur in the diet."
"[..]the analysis of sulphur content and partitioning in commonly consumed foods and vegetables undertaken in this study indicates as much as 89.5% of the total sulphur consumed in a typical diet may not be derived from SAA. Significant sulphur intake was also achieved from consumption of wheat and starchy foods, dairy and vegetables. If only SAA intake is monitored the significant contribution to total sulphur intake from these other foods will be disregarded. Alliaceous and cruciferous vegetables are shown to be an important source of sulphur in the diet."
- Calorie restriction and methionine restriction in control of endogenous hydrogen sulfide production by the transsulfuration pathway
You mean, chris (op)?
LUH 3417
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I meant with your research. I read through some of the recommendations and find them helpful. Wondering if you’ve come across anything else regarding inability to handle sulfur. Also...some of the symptoms have a cross over with oxalate toxicity. I’m curious if there is a link.
LUH 3417
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The Down Side to High Oxalates – Problems with Sulfate, B6, Gut, and Methylation
The big idea with oxalate toxicity is it causes problems in the liver and kidney – our two most important organs of detoxification. While high oxalates will cause liver problems and a loss of B6, it is in the kidney where the oxalate causes us to lose much of our precious sulfate. The kidney is a critical player with any sulfate problem because it is the organ responsible for keeping our sulfate levels in balance.22 The kidney must swap a molecule of oxalate for a molecule of sulfate through the Sat1 transporter, and when oxalates are high it causes a loss of sulfate into the urine. Urine sulfate levels have been a confusing subject for many patients, researchers and doctors who study methylation and genetic pathways. Everyone wants to know where this sulfate is coming from, and I believe the answer has to do with oxalates and kidney polymorphisms.
The idea that kidneys swap 1 sulfate for 1 oxalate molecule is like the standard swapping of Na for K in cells. Not sure what to make of it or what it means.
The big idea with oxalate toxicity is it causes problems in the liver and kidney – our two most important organs of detoxification. While high oxalates will cause liver problems and a loss of B6, it is in the kidney where the oxalate causes us to lose much of our precious sulfate. The kidney is a critical player with any sulfate problem because it is the organ responsible for keeping our sulfate levels in balance.22 The kidney must swap a molecule of oxalate for a molecule of sulfate through the Sat1 transporter, and when oxalates are high it causes a loss of sulfate into the urine. Urine sulfate levels have been a confusing subject for many patients, researchers and doctors who study methylation and genetic pathways. Everyone wants to know where this sulfate is coming from, and I believe the answer has to do with oxalates and kidney polymorphisms.
The idea that kidneys swap 1 sulfate for 1 oxalate molecule is like the standard swapping of Na for K in cells. Not sure what to make of it or what it means.
Amazoniac
Member
Sulfur compounds might poison you for profits:
- The antabuse effect of hydrogen sulfide
- Is aldehyde dehydrogenase inhibited by sulfur compounds? In vitro and in vivo studies
If it applies to poisonal, they could end up inducing a functional 'deficiency' of poison A.
- Reactive Sulfur Species: A New Redox Player in Cardiovascular Pathophysiology
- The antabuse effect of hydrogen sulfide
"Disulfiram (DS) has been clinically used to treat recovering alcoholics for over 50 years. It exerts its pharmacologic effect by inhibiting hepatic aldehyde dehydrogenase (ALDH). It has been proposed that DS inhibits ALDH by forming an intermolecular mixed disulfide, presumably with the active site thiols. It has also been shown that reactive sulfur species are produced during DS and H2S metabolism. Here, we have shown that H2S, at or above 50 µM inhibits yeast ALDH, in an in vitro system. There was a dose-response relationship for this effect as increasing H2S concentration further decreased ALDH activity. The decrease in ALDH activity is enhanced if H2S is incubated with ALDH for 30 minutes. Cytochrome C, a hemoprotein and/or some metal cations increased ALDH inactivation by H2S. H2S is, therefore, a weak inhibitor of ALDH and requires a catalyst to convert it into a more active species. It is postulated that heme or metal cations catalyse the oxidation of H2S to reactive sulfur species which can form persulfides with the ALDH cystein at the catalytic site and inhibit its activity. ALDH activity was restored by adding reducing agents such as dithiothreitol and glutathione to reduce the cysteine persulfide moiety of the enzyme. H2S also increased the cytotoxicity of acetaldehyde and/or 2-chloroacetaldehyde in the presence of the alcohol dehydrogenase inhibitor 4-methylpyrazole towards freshly isolated rat hepatocytes. ALDH inhibition by H2S indicates that the H2S must have an “antabuse” effect which would suggest unpleasant reactions to alcohol in the people exposed to H2S gas."
- Is aldehyde dehydrogenase inhibited by sulfur compounds? In vitro and in vivo studies
If it applies to poisonal, they could end up inducing a functional 'deficiency' of poison A.
- Reactive Sulfur Species: A New Redox Player in Cardiovascular Pathophysiology
Thank you, that's cool. I can't remember if I read about this before, but didn't make the connection. We have to put low killcium intake or its malabsorption as a potential culprits. Sparing sulfur and maximizing its use are good measures.
"Shell membrane fibres consist of collagens (type I, V and X) and cysteine-rich eggshell membrane proteins (CREMPs) (Arias et al., 1991; Kodali et al., 2011)."
Last edited:
Amazoniac
Member
- 17. Alcohols and Phenols - Organic Chemistry (McMurry) | LibreTexts.org
- Thiol - Wikipedia
- Omca Demirkol | ResearchGate
↳ Biologically Important Thiols in Various Vegetables and Fruits
↳ Impact of Food Disinfection on Beneficial Biothiol Contents in Vegetables
↳ Biologically important thiols in various organically and conventionally grown vegetables
- Beneficial Role of L-Cysteine and H2S Rich Fruits and Vegetables in Diabetic Pathophysiology
"Molecules of alcohols contain one or more hydroxyl groups (OH groups) substituted for hydrogen atoms along the carbon chain. The structure of the simplest alcohol, methanol (methyl alcohol), can be derived from that of methane by putting an OH in place of one of the H’s:
The name, too, is derived from the name methane by replacing the final e with ol (for alcohol). The general formula for an alcohol may be written as R—OH, where R represents the hydrocarbon (alkane) portion of the molecule and is called an alkyl group. In methanol, R is the methyl group CH3."
The name, too, is derived from the name methane by replacing the final e with ol (for alcohol). The general formula for an alcohol may be written as R—OH, where R represents the hydrocarbon (alkane) portion of the molecule and is called an alkyl group. In methanol, R is the methyl group CH3."
- Thiol - Wikipedia
"A thiol (/ˈθaɪɒl/) or thiol derivative is any organosulfur compound of the form R−SH, where R represents an alkyl or other organic substituent. The –SH functional group itself is referred to as either a thiol group or a sulfanyl ["sulf(h)ydryl"] group. Thiols are the sulfur analogue of alcohols (that is, sulfur takes the place of oxygen in the hydroxyl group of an alcohol), and the word is a portmanteau of "thio-" + "alcohol", with the first word deriving from Greek θεῖον (theion) meaning "sulfur"."
"Thiols are sometimes referred to as mercaptans. The term "mercaptan" /mərˈkæptæn/ was introduced in 1832 by William Christopher Zeise and is derived from the Latin mercurium captāns (capturing mercury) because the thiolate group (RS−) bonds very strongly with mercury compounds."
"According to hard/soft acid/base (HSAB) theory, sulfur is a relatively soft (polarizable) atom. This explains the tendency of thiols to bind to soft elements and ions such as mercury, lead, or cadmium. The stability of metal thiolates parallels that of the corresponding sulfide minerals."
"Many thiols have strong odors resembling that of garlic. The odors of thiols, particularly those of low molecular weight, are often strong and repulsive. The spray of skunks consists mainly of low-molecular-weight thiols and derivatives."
"Thiols are also responsible for a class of wine faults caused by an unintended reaction between sulfur and yeast and the "skunky" odor of beer that has been exposed to ultraviolet light."
"Not all thiols have unpleasant odors. For example, furan-2-ylmethanethiol contributes to the aroma of roasted coffee, whereas grapefruit mercaptan, a monoterpenoid thiol, is responsible for the characteristic scent of grapefruit. The effect of the latter compound is present only at low concentrations. The pure mercaptan has an unpleasant odor."
"Natural gas distributors were required to add thiols, originally ethanethiol, to natural gas (which is naturally odorless) after the deadly New London School explosion in New London, Texas, in 1937. Many gas distributors were odorizing gas prior to this event. Most gas odorants utilized currently contain mixtures of mercaptans and sulfides, with t-butyl mercaptan as the main odor constituent in natural gas and ethanethiol in liquefied petroleum gas (LPG, propane)."
"In situations where thiols are used in commercial industry, such as liquid petroleum gas tankers and bulk handling systems, an oxidizing catalyst is used to destroy the odor. A copper-based oxidation catalyst neutralizes the volatile thiols and transforms them into inert products."
"The S−H bond in thiols is weak compared to the O−H bond in alcohols."
"In industry, methanethiol is prepared by the reaction of hydrogen sulfide with methanol."
"Thiols are easily deprotonated. Relative to the alcohols, thiols are more acidic. The conjugate base of a thiol is called a thiolate." "[..]thiolates can be obtained from thiols by treatment with alkali metal hydroxides."
"Akin to the chemistry of alcohols, thiols form sulfides, thioacetals, and thioesters, which are analogous to ethers, acetals, and esters respectively. Thiols and alcohols are also very different in their reactivity, thiols being more easily oxidized than alcohols. Thiolates are more potent nucleophiles than the corresponding alkoxides."
"Thiols, especially in the presence of base, are readily oxidized by reagents such as bromine and iodine to give an organic disulfide (R−S−S−R)."
"Oxidation by more powerful reagents such as sodium hypochlorite or hydrogen peroxide can also yield sulfonic acids (RSO3H)."
"Oxidation can also be effected by oxygen in the presence of catalysts[.]"
"Free radicals derived from mercaptans, called thiyl radicals, are commonly invoked to explain reactions in organic chemistry and biochemistry."
"Many cofactors (non-protein-based helper molecules) feature thiols. The biosynthesis and degradation of fatty acids and related long-chain hydrocarbons is conducted on a scaffold that anchors the growing chain through a thioester derived from the thiol Coenzyme A."
"Thiols are sometimes referred to as mercaptans. The term "mercaptan" /mərˈkæptæn/ was introduced in 1832 by William Christopher Zeise and is derived from the Latin mercurium captāns (capturing mercury) because the thiolate group (RS−) bonds very strongly with mercury compounds."
"According to hard/soft acid/base (HSAB) theory, sulfur is a relatively soft (polarizable) atom. This explains the tendency of thiols to bind to soft elements and ions such as mercury, lead, or cadmium. The stability of metal thiolates parallels that of the corresponding sulfide minerals."
"Many thiols have strong odors resembling that of garlic. The odors of thiols, particularly those of low molecular weight, are often strong and repulsive. The spray of skunks consists mainly of low-molecular-weight thiols and derivatives."
"Thiols are also responsible for a class of wine faults caused by an unintended reaction between sulfur and yeast and the "skunky" odor of beer that has been exposed to ultraviolet light."
"Not all thiols have unpleasant odors. For example, furan-2-ylmethanethiol contributes to the aroma of roasted coffee, whereas grapefruit mercaptan, a monoterpenoid thiol, is responsible for the characteristic scent of grapefruit. The effect of the latter compound is present only at low concentrations. The pure mercaptan has an unpleasant odor."
"Natural gas distributors were required to add thiols, originally ethanethiol, to natural gas (which is naturally odorless) after the deadly New London School explosion in New London, Texas, in 1937. Many gas distributors were odorizing gas prior to this event. Most gas odorants utilized currently contain mixtures of mercaptans and sulfides, with t-butyl mercaptan as the main odor constituent in natural gas and ethanethiol in liquefied petroleum gas (LPG, propane)."
Diffusion through the skin must be possible.
"In situations where thiols are used in commercial industry, such as liquid petroleum gas tankers and bulk handling systems, an oxidizing catalyst is used to destroy the odor. A copper-based oxidation catalyst neutralizes the volatile thiols and transforms them into inert products."
"The S−H bond in thiols is weak compared to the O−H bond in alcohols."
"In industry, methanethiol is prepared by the reaction of hydrogen sulfide with methanol."
"Thiols are easily deprotonated. Relative to the alcohols, thiols are more acidic. The conjugate base of a thiol is called a thiolate." "[..]thiolates can be obtained from thiols by treatment with alkali metal hydroxides."
"Akin to the chemistry of alcohols, thiols form sulfides, thioacetals, and thioesters, which are analogous to ethers, acetals, and esters respectively. Thiols and alcohols are also very different in their reactivity, thiols being more easily oxidized than alcohols. Thiolates are more potent nucleophiles than the corresponding alkoxides."
Below are postulated intermediate metabolites in converting poisonal to poisonoic acid, we have momentealiraely sulfur compounds:
- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity
- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity
"Thiols, especially in the presence of base, are readily oxidized by reagents such as bromine and iodine to give an organic disulfide (R−S−S−R)."
Was is Gerson in carotenoid bath + iodine attack?
"Oxidation by more powerful reagents such as sodium hypochlorite or hydrogen peroxide can also yield sulfonic acids (RSO3H)."
"Oxidation can also be effected by oxygen in the presence of catalysts[.]"
"Free radicals derived from mercaptans, called thiyl radicals, are commonly invoked to explain reactions in organic chemistry and biochemistry."
- The Reactive Sulfur Species Concept: 15 Years On
- Reactive sulfur species (RSS): persulfides, polysulfides, potential, and problems
- Biogenesis of reactive sulfur species for signaling by hydrogen sulfide oxidation pathways
- Reactive sulfur species (RSS): persulfides, polysulfides, potential, and problems
- Biogenesis of reactive sulfur species for signaling by hydrogen sulfide oxidation pathways
"Many cofactors (non-protein-based helper molecules) feature thiols. The biosynthesis and degradation of fatty acids and related long-chain hydrocarbons is conducted on a scaffold that anchors the growing chain through a thioester derived from the thiol Coenzyme A."
- Omca Demirkol | ResearchGate
↳ Biologically Important Thiols in Various Vegetables and Fruits
↳ Impact of Food Disinfection on Beneficial Biothiol Contents in Vegetables
↳ Biologically important thiols in various organically and conventionally grown vegetables
- Beneficial Role of L-Cysteine and H2S Rich Fruits and Vegetables in Diabetic Pathophysiology
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Amazoniac
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- A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility
- Role of Thiamin in Health and Disease
- Sulfate-reducing microorganisms - Wikipedia
- Vitamin B1 Dosage
- The Basics of Thiols and Cysteines in Redox Biology and Chemistry
"Colonic mucin O-glycans contain glycosidic linkages distinct from plant fibers and also covalently linked sulfate. In further support of increased bacterial degradation of the host mucus on the FF diet, we detected significantly increased bacterial enzymes (sulfatase and α-fucosidase) in the mice subjected to the FF diet on either a chronic or intermittent basis (Fig. 3C). In contrast, enzymes targeting linkages in fiber polysaccharides (β-glucosidase) were significantly reduced in the mice fed the fiber-deficient diets, while others involved in xylan and α-galactan degradation trended similarly without significance (Fig. 3C).Despite the dramatic change in microbiota species abundance and transcriptional response, there was only one significant change (succinate) in SCFA and organic acids in the FF diet fed mice (Fig. 3D). Overall, the transcriptomic and enzyme analyses support the conclusion that a fiber-deprived gut microbiota synergistically and progressively expresses CAZymes, sulfatases and proteases to attack mucus polysaccharides when the diet lacks complex plant fiber."
- Role of Thiamin in Health and Disease
"Causes of thiamin deficiency include the use of the diuretic furosemide, the presence of chronic kidney disease on hemodialysis, diabetes mellitus with increased urinary excretion of thiamin, malignant neoplasms, acquired immunodeficiency syndrome, hyperemesis gravidarum, and diseases and surgeries of the gastrointestinal tract, including bariatric surgery.[1,7,9,30] Bariatric surgeries increase the risk of thiamin deficiency through several mechanisms, including lower vitamin intake, higher prevalence of postoperative vomiting, and impaired absorption, mainly in patients who have undergone Roux-en-Y gastric bypass surgery. In these patients, the bypass of the small intestine, the preferred location for thiamin absorption, and bacterial overgrowth are important causes of thiamin deficiency.[31-33]"
- Sulfate-reducing microorganisms - Wikipedia
- Vitamin B1 Dosage
- The Basics of Thiols and Cysteines in Redox Biology and Chemistry
Highserotonin90
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- Mar 24, 2018
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B1 Have sulfur
Amazoniac
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Some of these nutrients are excreted chiefly intact (taurine, thiamine, biotin, and so on), therefore they don't require specific metabolism of sulfur that could explain diverse molecules leading to the same adversity, it's possibly due to gut issues (that might be present as consequence of something else).
I don't know if the region for active and passive uptakes are different for thiamine, because if the active process occurs earlier in the tract, it justifies taking 1 mg at a time on multiple occasions to target the liver without fueling the problem. On repeating this 5 times, the person would be getting far more than what's usual to obtain from diet. But if extreme doses are need'd, it would be safer to cover the basics this way and get extra through the skin. It should be a good practice and I'm not aware of anything protective in the residual excess from digestion.
Seeking bacterial thiaminase is irrelevant here, it's possible to have trouble from competition rather than degradation.
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- 17β-Estradiol nongenomically induces vascular endothelial H2S release by promoting phosphorylation of cystathionine γ-lyase
- Hydrogen Sulfide in the Adipose Tissue—Physiology, Pathology and a Target for Pharmacotherapy (@chrismturner89)
- Hydrogen Sulfide in Pharmacotherapy, Beyond the Hydrogen Sulfide-Donors
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Highserotonin90
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- Mar 24, 2018
- Messages
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Se non sbaglio, un gene SLC è responsabile del suo trasporto ...
Amazoniac
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Amazoniac
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- Thiols And Thioethers | Master Organic Chemistry
Joined these:
- Handheld Dissolved Hydrogen Sulfide (H2S) Meter | Edaphic Scientific
- Buffering in acute respiratory acid-base disturbances | Deranged Physiology
- Transport of H2S and HS(-) across the human red blood cell membrane: rapid H2S diffusion and AE1-mediated Cl(-)/HS(-) exchange
Joined these:
- Handheld Dissolved Hydrogen Sulfide (H2S) Meter | Edaphic Scientific
- Buffering in acute respiratory acid-base disturbances | Deranged Physiology
- Transport of H2S and HS(-) across the human red blood cell membrane: rapid H2S diffusion and AE1-mediated Cl(-)/HS(-) exchange
Amazoniac
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- Endogenous and Exogenous Hydrogen Sulfide Promotes Resolution of Colitis in Rats
- Hydrogen sulphide production in eggs and egg products as a result of heating
- Starch and ICUMSA color removal in sugarcane juice clarified by carbonatation
- methionine cysteine milk light degradation off flavor - Google Search
- Hydrogen sulphide production in eggs and egg products as a result of heating
- Starch and ICUMSA color removal in sugarcane juice clarified by carbonatation
- methionine cysteine milk light degradation off flavor - Google Search
Amazoniac
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- Amino Acid Content And Profile Of Some Proteinaceous Foods
- Preparation and potential applications of casein–polysaccharide conjugates: a review
Just an overview for the next articles.
- Casein‐Based Powders: Characteristics and Rehydration Properties
- Modifications of structures and functions of caseins: a scientific and technological challenge
- Preparation and potential applications of casein–polysaccharide conjugates: a review
Just an overview for the next articles.
- Casein‐Based Powders: Characteristics and Rehydration Properties
- Modifications of structures and functions of caseins: a scientific and technological challenge
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Amazoniac
Member
Funny how these contrast:
- Sulfur - Wikipedia
"Sulfur forms several polyatomic molecules. The best-known allotrope is octasulfur, cyclo-S8." "Octasulfur is a soft, bright-yellow solid that is odorless, but impure samples have an odor similar to that of matches."
- Hydrogen sulfide - Wikipedia
- Hydrogen selenide - Wikipedia
- Sulfur - Wikipedia
"When burned, sulfur melts to a blood-red liquid and emits a blue flame."
"Sulfur forms several polyatomic molecules. The best-known allotrope is octasulfur, cyclo-S8." "Octasulfur is a soft, bright-yellow solid that is odorless, but impure samples have an odor similar to that of matches."
- Hydrogen sulfide - Wikipedia
"It is a colorless chalcogen hydride gas with the characteristic foul odor of rotten eggs."
- Hydrogen selenide - Wikipedia
Amazoniac
Member
From the Wikipedia page:
There was a member who mentioned that after having to wear masks, the person could detect a foul breath that wasn't noticeable before.
People here avoid taking reduced forms of coenzymes, yet H2S will be metabolized as such. It might be rescuing some impairment that's upstream of ubiquinone and will need it (and what follows) adequate to be more helpful than harmful. It would be interesting to know if veins dilate when this toxin isn't being cleared at enough rate.
It might also work through similar principles:
- "The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid" (first link)
Each of the variations below adds a relevant detail that can give us a clearer idea of the process.
- Crustacean Bioenergetics: Mitochondrial Adaptive Molecular Responses to Face Environmental Challenges
- Molecular Characterization of Hydrogen Sulfide Role in Vascular System and Method of Endogenous Production Detections with Common Ion Channels Used to Produce Its Biological Effect
- The novel mitochondria-targeted hydrogen sulfide (H2S) donors AP123 and AP39 protect against hyperglycemic injury in microvascular endothelial cells in vitro
- Sulfur as a Signaling Nutrient Through Hydrogen Sulfide (!)
"Sulfur is derived from the Latin word sulpur, which was Hellenized to sulphur in the erroneous belief that the Latin word came from Greek. This spelling was later reinterpreted as representing an /f/ sound and resulted in the spelling sulfur, which appears in Latin toward the end of the Classical period. The true Greek word for sulfur, θεῖον, is the source of the international chemical prefix thio-. In 12th-century Anglo-French, it was sulfre. In the 14th century, the erroneously Hellenized Latin -ph- was restored in Middle English sulphre. By the 15th century, both full Latin spelling variants sulfur and sulphur became common in English. The parallel f~ph spellings continued in Britain until the 19th century, when the word was standardized as sulphur. On the other hand, sulfur was the form chosen in the United States, whereas Canada uses both. The IUPAC adopted the spelling sulfur in 1990 or 1971, depending on the source cited, as did the Nomenclature Committee of the Royal Society of Chemistry in 1992, restoring the spelling sulfur to Britain. Oxford Dictionaries note that "in chemistry and other technical uses ... the -f- spelling is now the standard form for this and related words in British as well as US contexts, and is increasingly used in general contexts as well."
There was a member who mentioned that after having to wear masks, the person could detect a foul breath that wasn't noticeable before.
People here avoid taking reduced forms of coenzymes, yet H2S will be metabolized as such. It might be rescuing some impairment that's upstream of ubiquinone and will need it (and what follows) adequate to be more helpful than harmful. It would be interesting to know if veins dilate when this toxin isn't being cleared at enough rate.
It might also work through similar principles:
- "The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid" (first link)
Each of the variations below adds a relevant detail that can give us a clearer idea of the process.
"In mammals, CoQ is a lipid-soluble present in all cell membranes and is involved in multiple metabolic functions. One of these functions is to shuttle electrons in the first reaction of the H2S oxidation pathway, catalyzed by SQOR (Figure 1). Our studies in human fibroblasts confirm that low levels of CoQ cause decrease of SQOR protein levels, proportionally to the degree of CoQ deficiency (Luna-Sanchez et al., 2017; Ziosi et al., 2017)."
- Crustacean Bioenergetics: Mitochondrial Adaptive Molecular Responses to Face Environmental Challenges
- Molecular Characterization of Hydrogen Sulfide Role in Vascular System and Method of Endogenous Production Detections with Common Ion Channels Used to Produce Its Biological Effect
- The novel mitochondria-targeted hydrogen sulfide (H2S) donors AP123 and AP39 protect against hyperglycemic injury in microvascular endothelial cells in vitro
- Sulfur as a Signaling Nutrient Through Hydrogen Sulfide (!)
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Amazoniac
Member
Some minerals can react with hydrogen sulfide and make it colorful.
- Testing sulfide ion, Qualitative Analysis S2- ion | chemistryscl.com
Bismuth is a known one..
- Hydrogen sulfide is a novel potential virulence factor of Mycoplasma pneumoniae: characterization of the unusual cysteine desulfurase/desulfhydrase HapE
- InTech-Microbiological diagnosis for periodontal diseases
Some people report their crap darkening from such precipitation.
- Sulfate‐reducing bacteria slow intestinal transit in a bismuth‐reversible fashion in mice
- Site of Bismuth Absorption from Bismuth Subsalicylate
- Bismuth subsalicylate markedly decreases hydrogen sulfide release in the human colon
- The Effect of 5-Aminosalicylic Acid–Containing Drugs on Sulfide Production by Sulfate-Reducing and Amino Acid–Fermenting Bacteria
- 5-Aminosalyclic Acid (5-ASA): A Unique Anti-Inflammatory Salicylate
- Molecule of the Month: Hydrogen Sulphide | University of Bristol
- Testing sulfide ion, Qualitative Analysis S2- ion | chemistryscl.com
Bismuth is a known one..
- Hydrogen sulfide is a novel potential virulence factor of Mycoplasma pneumoniae: characterization of the unusual cysteine desulfurase/desulfhydrase HapE
- InTech-Microbiological diagnosis for periodontal diseases
Some people report their crap darkening from such precipitation.
- Sulfate‐reducing bacteria slow intestinal transit in a bismuth‐reversible fashion in mice
- Site of Bismuth Absorption from Bismuth Subsalicylate
- Bismuth subsalicylate markedly decreases hydrogen sulfide release in the human colon
- The Effect of 5-Aminosalicylic Acid–Containing Drugs on Sulfide Production by Sulfate-Reducing and Amino Acid–Fermenting Bacteria
- 5-Aminosalyclic Acid (5-ASA): A Unique Anti-Inflammatory Salicylate
- Molecule of the Month: Hydrogen Sulphide | University of Bristol
EMF Mitigation - Flush Niacin - Big 5 Minerals
