"The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid"

[Amazoniac]

- Water, strong ions, and weak ions

Spoiler

"In any aqueous solution in equilibrium, the sum of the positive charges always equals that of the negative charges. For instance, in a solution of NaCl:

[Na+] + [H+] = [Cl−] + [OH−]​

This concept can be expressed graphically, using two columns: one each for positive and negative charges, keeping them equal in height. Gamble developed figures now called ‘Gamblegrams’ to help express the composition of complex solutions such as plasma (Fig. 1)."

"Water has a concentration of 55.3 M at 37°C, which is around 400 times the concentration of any other substance in the body fluids (Fig. 2). However, it is vital to realize that because water dissociates so little, the concentrations of hydrogen ions in body fluids are very small. Hydrogen ion concentrations are measured in NANO moles [nmol, 10^(−9) mol] whereas important ions such as sodium are present in concentrations nearly a million times greater [mmol, 10^(−3) mol] (Fig. 2)."

"Figure 3 shows Gamblegrams for some important body fluids."

 

[Makrosky]

This is normally caused by a lack of pboysterone.

 

[Amazoniac]

- Potassium and intracellular pH

- Potassium and Its Disorders
- Potassium Homeostasis, Oxidative Stress, and Human Disease

@yerrag

 

[yerrag]

- Potassium and intracellular pH

- Potassium and Its Disorders
- Potassium Homeostasis, Oxidative Stress, and Human Disease

@yerrag

I've been trying to read these but the only thing that registers with me, from the second reference, is that sodium does not necessarily have to be conserved, and that in such a condition, the body will excrete sodium instead of potassium, but usually there will be potassium excreted along with the sodium being excreted.

This leads me to think about why sodium needs to be spared and potassium wasted. Not for the reason that sodium is needed for osmolarity, but as to why sodium has to be conserved if sodium were plentiful in the body. This leads me to ask - how to do we know whether sodium is deficient or not?

And if sodium is deficient, then there would be the need for aldosterone to conserve sodium and to waste potassium.

I want to keep in mind also that when sodium is deficient, the blood volume would be deficient since sodium is needed for attract water (but serum albumin is needed also to attract and hold on to sodium).

It would then not be a coincidence that aldosterone is needed when blood volume is low, because aldosterone would keep sodium from further being reduced, and this would lead to further reduction in blood volume. But instead of aldosterone being associated with low blood volume, aldosterone would usually be associated only with high blood pressure - perhaps it's because blood pressure can be measured, and blood volume can't.

So, would it not be a good idea to increase intake of sodium chloride in order for blood volume to increase, assuming there isn't anything in the way of building blood volume other than sodium chloride? This would lead to a state where blood volume is enough, and salt not being deficient, and there being no need to conserve salt, such that aldosterone won't be needed. And at this state, there would be no high blood pressure condition because the higher blood pressure isn't needed to compensate for low blood volume.

Of course, there would be other factors involved that would stand in the way of such an easy solution to low blood volume and high blood pressure. But I'm just making a hypothetical case in a perfect world.

Does this make sense? It seems all along I have forgotten to ask why sodium chloride needs to be conserved. That article was helpful in getting me to consider why it has to be. And it doesn't - if sodium chloride weren't deficient. Perhaps I am deficient in sodium chloride, and I need to begin a protocol of slowly building up my sodium stores.

After all, why do we talk about building our magnesium and potassium and calcium stores, but we don't talk about building our sodium stores? Is it because we are burdened by the conventional idea that sodium chloride is bad?

 

[yerrag]

I've been trying to read these but the only thing that registers with me, from the second reference, is that sodium does not necessarily have to be conserved, and that in such a condition, the body will excrete sodium instead of potassium, but usually there will be potassium excreted along with the sodium being excreted.

This leads me to think about why sodium needs to be spared and potassium wasted. Not for the reason that sodium is needed for osmolarity, but as to why sodium has to be conserved if sodium were plentiful in the body. This leads me to ask - how to do we know whether sodium is deficient or not?

And if sodium is deficient, then there would be the need for aldosterone to conserve sodium and to waste potassium.

I want to keep in mind also that when sodium is deficient, the blood volume would be deficient since sodium is needed for attract water (but serum albumin is needed also to attract and hold on to sodium).

It would then not be a coincidence that aldosterone is needed when blood volume is low, because aldosterone would keep sodium from further being reduced, and this would lead to further reduction in blood volume. But instead of aldosterone being associated with low blood volume, aldosterone would usually be associated only with high blood pressure - perhaps it's because blood pressure can be measured, and blood volume can't.

So, would it not be a good idea to increase intake of sodium chloride in order for blood volume to increase, assuming there isn't anything in the way of building blood volume other than sodium chloride? This would lead to a state where blood volume is enough, and salt not being deficient, and there being no need to conserve salt, such that aldosterone won't be needed. And at this state, there would be no high blood pressure condition because the higher blood pressure isn't needed to compensate for low blood volume.

Of course, there would be other factors involved that would stand in the way of such an easy solution to low blood volume and high blood pressure. But I'm just making a hypothetical case in a perfect world.

Does this make sense? It seems all along I have forgotten to ask why sodium chloride needs to be conserved. That article was helpful in getting me to consider why it has to be. And it doesn't - if sodium chloride weren't deficient. Perhaps I am deficient in sodium chloride, and I need to begin a protocol of slowly building up my sodium stores.

After all, why do we talk about building our magnesium and potassium and calcium stores, but we don't talk about building our sodium stores? Is it because we are burdened by the conventional idea that sodium chloride is bad?

Last night I took 10 grams of salt and today I have much higher blood pressure.

So that's it. Taking salt isn't the solution to my high blood pressure.

But I have another idea. Why is it that I'm urinating 1 liter (3 liters instead of 2) more of urine each day, and this excess is all urinated at night? Hmmm...

It's just as if when I'm asleep the body is trying to increase my blood volume, by increasing my plasma volume . And each night it is failing, so it is dumping exactly the same volume of urine that my I'm lacking in plasma. The body has enough sodium chloride and enough water to build up the volume of plasma that's lacking. It's just that it's lacking albumin to get the job done. So each night it is dumping that water, and probably the salt, and that is why I am urinating a lot and having to wake up for it.

I have got to keep the albumin from being excreted in urine so I can slowly build back my blood volume. I may have to try something: increased b1. Maybe with increased b1, the pentose phosphate pathway can make enough NADPH for use in making NADPH oxidase in order to support more the production of ROS. This would make phagocytosis more effective in eating up immune complexes in my kidneys. Perhaps my phagocytic powers are lacking, and the immune complexes are staying put in my kidneys, and the inflammation they bring keeps using up my albumin stores.

 

[yerrag]

- Potassium and intracellular pH

- Potassium and Its Disorders
- Potassium Homeostasis, Oxidative Stress, and Human Disease

@yerrag

From "Potassium and Its Disorders:"

Toluene is thought to lead to potassium wasting by causing renal tubular acidosis (RTA) [22].

Licorice and herbal cough mixtures contain glycyrrhizic and glycyrrhetinic acids. They are thought to exert mineralocorticoid effects leading to hypokalemia [22].

Bicarbonaturia results from metabolic alkalosis, distal RTA or treatment with proximal RTA.

Increased distal tubular bicarbonate delivery increases potassium secretion.

@Amazoniac Doesn't this explain why taking too much bicarbonates would lead to potassium wasting. No wonder I was losing potassium and perhaps even urinating a lot when I was on excessive bicarbonate supplementation.

 

[Amazoniac]

- Impact of the diet on net endogenous acid production and acid-base balance (!)
- The hydrogen ion in normal metabolism: a review (!)

---

- The relation of sulfur metabolism to acid-base balance and electrolyte excretion: the effects of DL-methionine in normal man

---

- Calculation of titratable acidity from urinary stone risk factors

 

[yerrag]

Increased distal tubular bicarbonate delivery increases potassium secretion.

@Amazoniac

Is this the meaning of the sentence: Carbonic acid dissociates into H+ and HCO3- in the distal tubule where H+ goes into the blood, and K+ goes into the collecting duct for excretion, along with bicarbonate?

 

[yerrag]

Last night I took 10 grams of salt and today I have much higher blood pressure.

So that's it. Taking salt isn't the solution to my high blood pressure.

But I have another idea. Why is it that I'm urinating 1 liter (3 liters instead of 2) more of urine each day, and this excess is all urinated at night? Hmmm...

It's just as if when I'm asleep the body is trying to increase my blood volume, by increasing my plasma volume . And each night it is failing, so it is dumping exactly the same volume of urine that my I'm lacking in plasma. The body has enough sodium chloride and enough water to build up the volume of plasma that's lacking. It's just that it's lacking albumin to get the job done. So each night it is dumping that water, and probably the salt, and that is why I am urinating a lot and having to wake up for it.

I have got to keep the albumin from being excreted in urine so I can slowly build back my blood volume. I may have to try something: increased b1. Maybe with increased b1, the pentose phosphate pathway can make enough NADPH for use in making NADPH oxidase in order to support more the production of ROS. This would make phagocytosis more effective in eating up immune complexes in my kidneys. Perhaps my phagocytic powers are lacking, and the immune complexes are staying put in my kidneys, and the inflammation they bring keeps using up my albumin stores.

No, this isn't right.

I think what's happening is that the mitochondria is producing plenty of H2O2 but is unable to use the H2O2 into ROS such as HOCl- for lack of NADPH oxidase to carry out the reaction to completion. So there is excess H2O2 and it gets to be converted to water by glutathione peroxidase. This is why I'm urinating a lot.

At the same time the phagocytes cannot eat up the immune complexes in my kidneys, yet it keeps trying and it's like Groundhog Day each and every day, with my immune system contantly attacking the immune complexes with no effect except to cause inflammation and oxidative stress, which keeps consuming my supply of albumin, using it as an antioxidant to quell the inflammation and the oxidative stress.

So I would need to enable more NADPH production to make more NADPH oxidase available to create more ROS.

 

[Amazoniac]

- Fluid resuscitation after an otherwise fatal hemorrhage: I. Crystalloid solutions

Spoiler

@Amazoniac

Is this the meaning of the sentence: Carbonic acid dissociates into H+ and HCO3- in the distal tubule where H+ goes into the blood, and K+ goes into the collecting duct for excretion, along with bicarbonate?

From what I understand, it's not necessary to be from the dissociation of craponic acid in kidney cells, it can be derived from filtered blood and its recovery inhibited for having too much of it. It's going to reach the distal parts needing a cation to maintain ion neutrality.

I may get to the potassium articles later.

I think what's happening is that the mitochondria is producing plenty of H2O2 but is unable to use the H2O2 into ROS such as HOCl- for lack of NADPH oxidase to carry out the reaction to completion. So there is excess H2O2 and it gets to be converted to water by glutathione peroxidase. This is why I'm urinating a lot.

If you mean that the water generated through this means is the source increasing the volume excreted (rather than a signal acting like an irritant that makes you urinate more), it's unlikely given that the contribution from all metabolic processes is only responsible for about 10% of daily water input (something like 250 ml from 2500 ml).
- Metabolic water

 

[yerrag]

Increased distal tubular bicarbonate delivery increases potassium secretion.

@Amazoniac

Is this the meaning of the sentence: Carbonic acid dissociates into H+ and HCO3- in the distal tubule where H+ goes into the blood, and K+ goes into the collecting duct for excretion, along with bicarbonate?

From what I understand, it's not necessary to be from the dissociation of craponic acid in kidney cells, it can be derived from filtered blood and its recovery inhibited for having too much of it. It's going to reach the distal parts needing a cation to maintain ion neutrality.

Is this what you're saying?:

"...it's not necessary to be from the dissociation of carbonic acid in kidney cells; the potassium can be derived from the kidney filtrate and its reabsorption inhibited for having too much of it. It's going to reach the distal parts needing a cation to maintain ion neutrality."

If so, question: if the filtrate contains potassium bicarbonate (after all the cation in question is potassium, and the anion is bicarbonate), and it reaches the distal tubule, why is it going to need a cation to maintain net neutrality when potassium bicarbonate is already ion neutral?

I think what's happening is that the kidney filtrate contains carbonic acid, and when it reaches the distal tubule, the carbonic acid will dissociate into bicarbonate and H+, and the H+ will will resorb into the lumen in exchange for potassium (K+) and the bicarbonate ion and potassium ion will go into the collecting duct. After all, the bicarbonate is in excess, and because it is in excess and the ecf is alkaline as a result, the kidney will want to hold on to the H+ and get rid of K+ - because H+ is more acidic.

I think what's happening is that the mitochondria is producing plenty of H2O2 but is unable to use the H2O2 into ROS such as HOCl- for lack of NADPH oxidase to carry out the reaction to completion. So there is excess H2O2 and it gets to be converted to water by glutathione peroxidase. This is why I'm urinating a lot.

I have to dorrect this to:
I think what's happening is that the mitochondria is producing plenty of H2O2 but is unable to convert the H2O2 into ROS adequately for lack of myeloperoxidase (HOCl- ROS as well as lack of NADPH oxidase generation. So there is excess H2O2 and unused H2O2 gets converted to water by catalase. This may be why I'm urinating a lot.

If you mean that the water generated through this means is the source increasing the volume excreted (rather than a signal acting like an irritant that makes you urinate more), it's unlikely given that the contribution from all metabolic processes is only responsible for about 10% of daily water input (something like 250 ml from 2500 ml).

That assumes a state where there is no need for the mitochondria to downregulate from full ATP production. The mitochondria downregulates when it needs to produce more ROS to support its immune system defenses, instead of producing more ATP. So it will produce more superoxide which turns into H2O2, with the intention to use hydrogen peroxide to create more ROS for use in the respiratory burst of phagocytosis.

But if there is not enough enzymes to enable the full conversion of available hydrogen peroxide to ROS, the excess H2O2 gets converted to water by catalase.

 

[Amazoniac]

The conversions between craponate species are usually represented this way, giving the impression that it's necessary to pass through the toxin in the middle:

H2O + CO2 ⇌ H2CO3 ⇌ HCO3− + H+​

H2O + CO2 and H2CO3 are considered interchangeable, and we know that craponic annihilase is responsible for speeding up the reaction.

- 2.1: About Carbonic Anhydrase | Bioinorganic Chemistry (Bertini)

The dissociation of water (bound to craponic annihilase) is often omitted as well, yet the enzyme relies on the hydroxide ion (obtained from releasing a hydrogen ion from a water molecule) for its function.

Spoiler

Source: the internet.

The hydrogen ion doesn't participate in the reaction, it's discarded from what I can tell. This makes the process a hydroxylation of crapon dioxide rather than hydration. How can its product be H2CO3 if one hydrogen atom was lost to the medium?

OH− + CO2 -CA→ H2CO3 (?)​

It would have to yield hydrocraponate:

OH− + CO2 -CA→ HCO3−​

And what's the fate for the hydrogen ion released? It's instantly buffered by hydrocraponate available in the surroundings? Do they count on one hydrogen ion being taken up by the formed hydrocraponate as soon as it's displaced from the enzyme by water to restart the cycle, and this is what explains the hydration?

H+ + OH− + CO2 -CA→ HCO3− + H+ ⇌ H2CO3

- Role of Carbonic Anhydrases and Inhibitors in Acid–Base Physiology: Insights from Mathematical Modeling

"[..]most CO2-related carbon in the human body—aside from the carbonates in structures such as bone and tooth enamel—is present in the form of HCO3−. In fact, for a pH of 7.40—the value of normal, human arterial plasma at 37 °C—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 20 times the concentration of dissolved CO2. For a pH of 7.20—a representative value of normal intracellular pH of most cells—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 12.6 times the concentration of dissolved CO2."​

But then, what about the reverse process? What they refer to as 'dehydration of craponic acid'. If the activity of the enzyme depends on the hydroxide ion, how can it yield CO2 and H2O starting from H2CO3? It's the opposite case of the questionable line above.

H2CO3 -CA→ OH− (?) + CO2​

Saving for later:
- H2CO3 as Substrate for Carbonic Anhydrase in the Dehydration of HCO3-

- Chronic Metabolic Acidosis Destroys Pancreas [sensationalism: :10:]

⮤ [10] The origin and secretion of pancreatic juice bicarbonate
⮤ [11] The source of pancreatic juice bicarbonate

Is this what you're saying?:

"...it's not necessary to be from the dissociation of carbonic acid in kidney cells; the potassium can be derived from the kidney filtrate and its reabsorption inhibited for having too much of it. It's going to reach the distal parts needing a cation to maintain ion neutrality."

If so, question: if the filtrate contains potassium bicarbonate (after all the cation in question is potassium, and the anion is bicarbonate), and it reaches the distal tubule, why is it going to need a cation to maintain net neutrality when potassium bicarbonate is already ion neutral?

I think what's happening is that the kidney filtrate contains carbonic acid, and when it reaches the distal tubule, the carbonic acid will dissociate into bicarbonate and H+, and the H+ will will resorb into the lumen in exchange for potassium (K+) and the bicarbonate ion and potassium ion will go into the collecting duct. After all, the bicarbonate is in excess, and because it is in excess and the ecf is alkaline as a result, the kidney will want to hold on to the H+ and get rid of K+ - because H+ is more acidic.

No, I was referring to the 'distal tubular bicarbonate delivery', that this 'bicarbonate' can come from filtered blood rather than created locally.

That assumes a state where there is no need for the mitochondria to downregulate from full ATP production. The mitochondria downregulates when it needs to produce more ROS to support its immune system defenses, instead of producing more ATP. So it will produce more superoxide which turns into H2O2, with the intention to use hydrogen peroxide to create more ROS for use in the respiratory burst of phagocytosis.

But if there is not enough enzymes to enable the full conversion of available hydrogen peroxide to ROS, the excess H2O2 gets converted to water by catalase.

Catalase turning two H2O2 molecules into two of H2O simplifies things. An absurd scenario based on the value provided here, '500 nmol of H2O/min/g of liver wet wt' would be '0.009 mg of H2O/min/g of liver' or '0.54 mg of H20/h/g of liver'. In 24 h, if all (!) of your body weight was contributing evenly at such insane rate of production, it would yield 900 g or ml of water.

One liter of water is a lot to have that as origin, like it was pointed out, metabolic processes generate only about 250 ml of water per day. Once oxygen is inside the cell, good metabolism will also turn it into water, perhaps more effectively than when it's used for other purposes or when it's attacking molecules randomly and having its availability decreased.

 

[yerrag]

The conversions between craponate species are usually represented this way, giving the impression that it's necessary to pass through the toxin in the middle:

H2O + CO2 ⇌ H2CO3 ⇌ HCO3− + H+​

H2O + CO2 and H2CO3 are considered interchangeable, and we know that craponic annihilase is responsible for speeding up the reaction.

- 2.1: About Carbonic Anhydrase | Bioinorganic Chemistry (Bertini)

The dissociation of water (bound to craponic annihilase) is often omitted as well, yet the enzyme relies on the hydroxide ion (obtained from releasing a hydrogen ion from a water molecule) for its function.

Spoiler

View attachment 22083

Spoiler

Source: the internet.​

​

The hydrogen ion doesn't participate in the reaction, it's discarded from what I can tell. This makes the process a hydroxylation of crapon dioxide rather than hydration. How can its product be H2CO3 if one hydrogen atom was lost to the medium?

OH− + CO2 -CA→ H2CO3 (?)​

It would have to yield hydrocraponate:

OH− + CO2 -CA→ HCO3−​

And what's the fate for the hydrogen ion released? It's instantly buffered by hydrocraponate available in the surroundings? Do they count on one hydrogen ion being taken up by the formed hydrocraponate as soon as it's displaced from the enzyme by water to restart the cycle, and this is what explains the hydration?

H+ + OH− + CO2 -CA→ HCO3− + H+ ⇌ H2CO3​

​

- Role of Carbonic Anhydrases and Inhibitors in Acid–Base Physiology: Insights from Mathematical Modeling​

​

"[..]most CO2-related carbon in the human body—aside from the carbonates in structures such as bone and tooth enamel—is present in the form of HCO3−. In fact, for a pH of 7.40—the value of normal, human arterial plasma at 37 °C—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 20 times the concentration of dissolved CO2. For a pH of 7.20—a representative value of normal intracellular pH of most cells—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 12.6 times the concentration of dissolved CO2."​

But then, what about the reverse process? What they refer to as 'dehydration of craponic acid'. If the activity of the enzyme depends on the hydroxide ion, how can it yield CO2 and H2O starting from H2CO3? It's the opposite case of the questionable line above.

H2CO3 -CA→ OH− (?) + CO2​

Saving for later:
- H2CO3 as Substrate for Carbonic Anhydrase in the Dehydration of HCO3-



⮤ [10] The origin and secretion of pancreatic juice bicarbonate
⮤ [11] The source of pancreatic juice bicarbonate



No, I was referring to the 'distal tubular bicarbonate delivery', that this 'bicarbonate' can come from filtered blood rather than created locally.


Catalase turning two H2O2 molecules into two of H2O simplifies things. An absurd scenario based on the value provided here, '500 nmol of H2O/min/g of liver wet wt' would be '0.009 mg of H2O/min/g of liver' or '0.54 mg of H20/h/g of liver'. In 24 h, if all (!) of your body weight was contributing evenly at such insane rate of production, it would yield 900 g or ml of water.

One liter of water is a lot to have that as origin, like it was pointed out, metabolic processes generate only about 250 ml of water per day. Once oxygen is inside the cell, good metabolism will also turn it into water, perhaps more effectively than when it's used for other purposes or when it's attacking molecules randomly and having its availability decreased.

Thanks for taking the time.

 

[Jam]

The conversions between craponate species are usually represented this way, giving the impression that it's necessary to pass through the toxin in the middle:

H2O + CO2 ⇌ H2CO3 ⇌ HCO3− + H+​

H2O + CO2 and H2CO3 are considered interchangeable, and we know that craponic annihilase is responsible for speeding up the reaction.

- 2.1: About Carbonic Anhydrase | Bioinorganic Chemistry (Bertini)

The dissociation of water (bound to craponic annihilase) is often omitted as well, yet the enzyme relies on the hydroxide ion (obtained from releasing a hydrogen ion from a water molecule) for its function.

Spoiler

View attachment 22083

Spoiler

Source: the internet.​

​

The hydrogen ion doesn't participate in the reaction, it's discarded from what I can tell. This makes the process a hydroxylation of crapon dioxide rather than hydration. How can its product be H2CO3 if one hydrogen atom was lost to the medium?

OH− + CO2 -CA→ H2CO3 (?)​

It would have to yield hydrocraponate:

OH− + CO2 -CA→ HCO3−​

And what's the fate for the hydrogen ion released? It's instantly buffered by hydrocraponate available in the surroundings? Do they count on one hydrogen ion being taken up by the formed hydrocraponate as soon as it's displaced from the enzyme by water to restart the cycle, and this is what explains the hydration?

H+ + OH− + CO2 -CA→ HCO3− + H+ ⇌ H2CO3​

​

- Role of Carbonic Anhydrases and Inhibitors in Acid–Base Physiology: Insights from Mathematical Modeling​

​

"[..]most CO2-related carbon in the human body—aside from the carbonates in structures such as bone and tooth enamel—is present in the form of HCO3−. In fact, for a pH of 7.40—the value of normal, human arterial plasma at 37 °C—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 20 times the concentration of dissolved CO2. For a pH of 7.20—a representative value of normal intracellular pH of most cells—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 12.6 times the concentration of dissolved CO2."​

But then, what about the reverse process? What they refer to as 'dehydration of craponic acid'. If the activity of the enzyme depends on the hydroxide ion, how can it yield CO2 and H2O starting from H2CO3? It's the opposite case of the questionable line above.

H2CO3 -CA→ OH− (?) + CO2​

Saving for later:
- H2CO3 as Substrate for Carbonic Anhydrase in the Dehydration of HCO3-



⮤ [10] The origin and secretion of pancreatic juice bicarbonate
⮤ [11] The source of pancreatic juice bicarbonate



No, I was referring to the 'distal tubular bicarbonate delivery', that this 'bicarbonate' can come from filtered blood rather than created locally.


Catalase turning two H2O2 molecules into two of H2O simplifies things. An absurd scenario based on the value provided here, '500 nmol of H2O/min/g of liver wet wt' would be '0.009 mg of H2O/min/g of liver' or '0.54 mg of H20/h/g of liver'. In 24 h, if all (!) of your body weight was contributing evenly at such insane rate of production, it would yield 900 g or ml of water.

One liter of water is a lot to have that as origin, like it was pointed out, metabolic processes generate only about 250 ml of water per day. Once oxygen is inside the cell, good metabolism will also turn it into water, perhaps more effectively than when it's used for other purposes or when it's attacking molecules randomly and having its availability decreased.

 

[yerrag]

Catalase turning two H2O2 molecules into two of H2O simplifies things. An absurd scenario based on the value provided here, '500 nmol of H2O/min/g of liver wet wt' would be '0.009 mg of H2O/min/g of liver' or '0.54 mg of H20/h/g of liver'. In 24 h, if all (!) of your body weight was contributing evenly at such insane rate of production, it would yield 900 g or ml of water.

One liter of water is a lot to have that as origin, like it was pointed out, metabolic processes generate only about 250 ml of water per day. Once oxygen is inside the cell, good metabolism will also turn it into water, perhaps more effectively than when it's used for other purposes or when it's attacking molecules randomly and having its availability decreased.

Thanks for the calculations, which I can't understand and thank you also for making me think for other causes. And now I have:

catalase action by bacteria, and the redox process involving anti-oxidants neutralizing the oxidative stresses of inflammation.

Catalase Action -When the immune system, using neutrophils and macrophages tries to eat up antigens, they are blocked from doing so by the catalase enzyme. A periodontal pathogen called A. Actinomycetemcomitans releases it and causes the hydrogen peroxide to turn into water, thereby making the immune cells (neutrophils and macrophages.) unable to create the respiratory burst of phagocytosis - because ROS cannot be made.

A. Actinomycetemcomitans is a bacteria that is catalase-positive, meaning it produces catalase to change H2O2 to H2O. It is probably the only bacteria in a symbiotic periodontal milieu that protects the milieu from the effects of hydrogen peroxide, as shown in this example: Aggregatibacter actinomycetemcomitans mediates protection of Porphyromonas gingivalis from Streptococcus sanguinis hydrogen peroxide production in multi-species biofilms

While initially I referred to catalase action as a result of having excess hydrogen peroxide from perhaps a lack of the enzymes NADPH peroxidase and myeloperoxidase to effect the use of hydrogen peroxide to produce ROS for phagocytosis, the cause could simply be catalase action from bacteria causing H2O2 to be converted to water.

Redox Involving Antioxidants Against Oxidative Stress - I am not sure, perhaps you know something about this, where water is a by-product of this redox reaction? It seems if antioxidants are being oxidized, and oxidants are being reduced, there usually is some H2O product in the end.

​

 

[yerrag]

The conversions between craponate species are usually represented this way, giving the impression that it's necessary to pass through the toxin in the middle:

H2O + CO2 ⇌ H2CO3 ⇌ HCO3− + H+
H2O + CO2 and H2CO3 are considered interchangeable, and we know that craponic annihilase is responsible for speeding up the reaction.

- 2.1: About Carbonic Anhydrase | Bioinorganic Chemistry (Bertini)

The dissociation of water (bound to craponic annihilase) is often omitted as well, yet the enzyme relies on the hydroxide ion (obtained from releasing a hydrogen ion from a water molecule) for its function.

Spoiler

Source: the internet.

The hydrogen ion doesn't participate in the reaction, it's discarded from what I can tell. This makes the process a hydroxylation of crapon dioxide rather than hydration. How can its product be H2CO3 if one hydrogen atom was lost to the medium?

OH− + CO2 -CA→ H2CO3 (?)
It would have to yield hydrocraponate:

OH− + CO2 -CA→ HCO3−
And what's the fate for the hydrogen ion released? It's instantly buffered by hydrocraponate available in the surroundings? Do they count on one hydrogen ion being taken up by the formed hydrocraponate as soon as it's displaced from the enzyme by water to restart the cycle, and this is what explains the hydration?

H+ + OH− + CO2 -CA→ HCO3− + H+ ⇌ H2CO3

- Role of Carbonic Anhydrases and Inhibitors in Acid–Base Physiology: Insights from Mathematical Modeling

"[..]most CO2-related carbon in the human body—aside from the carbonates in structures such as bone and tooth enamel—is present in the form of HCO3−. In fact, for a pH of 7.40—the value of normal, human arterial plasma at 37 °C—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 20 times the concentration of dissolved CO2. For a pH of 7.20—a representative value of normal intracellular pH of most cells—the Henderson–Hasselbalch equation predicts that the concentration of HCO3− is approximately 12.6 times the concentration of dissolved CO2."
But then, what about the reverse process? What they refer to as 'dehydration of craponic acid'. If the activity of the enzyme depends on the hydroxide ion, how can it yield CO2 and H2O starting from H2CO3? It's the opposite case of the questionable line above.

H2CO3 -CA→ OH− (?) + CO2
Saving for later:
- H2CO3 as Substrate for Carbonic Anhydrase in the Dehydration of HCO3-


⮤ [10] The origin and secretion of pancreatic juice bicarbonate
⮤ [11] The source of pancreatic juice bicarbonate

I know you're trying to inject some humor into this boring field of self-help on health, but it's hard to add another layer of parsing for your humorous wordsmithing here.

I can't read this because the subject is hard enough, and you're not making it easier. But thanks for the effort at educating me with learning with laughter.

 

[yerrag]

No, I was referring to the 'distal tubular bicarbonate delivery', that this 'bicarbonate' can come from filtered blood rather than created locally.

Let's try again, but never mind. We're going in circles.

 

[Amazoniac]

- Effects of plant food potassium salts (citrate, galacturonate or tartrate) on acid-base status and digestive fermentations in rats

Spoiler

"D-galacturonate is a major component of plant cell wall polysaccharides such as pectins, and free galacturonate is found in small amounts in fruits and vegetables and it also originates from pectin breakdown by the colonic microflora (Dongowski et al. 2002). In contrast to malate or citrate, the galacturonate anion is poorly absorbed in the small intestine (Pajor, 1999) but is well metabolized by the large intestine microflora (Mortensen et al. 1988; Aprikian et al. 2003). Tartrate is essentially found, in its natural L(+) form, in grapes. Some tartrate ions bypass the small intestine and are fermented by colonic bacteria, which utilize the ions for the production of SCFA, just as dietary fibre is used (Spiller et al. 2003). It has also been shown that around 30% of ingested tartrate appears unchanged in the urine (Chadwick et al. 1978), reflecting some absorption in the small intestine."

"The amounts of organic anions generated by microbial fermentations of unavailable carbohydrates in the large intestine, predominantly SCFA (namely acetate, propionate and butyrate), may be 5–10-fold greater than the amounts of ingested organic anions (Demigné et al. 2004a). Their alkalinizing potential is still a matter of discussion since they are not systematically absorbed in parallel with cations: they may be absorbed as protonated forms or in exchange with bicarbonate, as well as anionic species through a paracellular route (Sellin, 1999; Vidyasagar et al. 2004)."

"To further investigate the actual impact of various K salts on low-grade metabolic acidosis and on digestive fermentations, Wistar rats were adapted to an acidogenic diet (relatively high in protein and sodium, and poor in K and alkalinizing anions) which was supplemented with different K salts, of inorganic or organic anions."

"It is noteworthy that the KCl diet led to an acidification of the caecal content although this diet would not provide additional fermentable substrate. Cl2 concentrations were not enhanced in the caecal lumen or the ileum (data not shown), but the organic anion profile measured with this diet (high lactate/low SCFA) is characteristic of highly acidic fermentations (Rémésy et al. 1993)."

"In the present study, the caecal anion profile was characterized by a relatively high concentration of succinate in all the diet groups, likely due to the presence of inulin in the diet which promotes acidic fermentations (Rémésy et al. 1993). Succinate, an intermediate in the fermentation process of microbiota, is generally metabolized to SCFA (as a major precursor of propionate) by cross-feeding species in the ecosystem and it does not usually accumulate to a substantial extent in the bowel (Bernalier et al. 1999). Nevertheless, some data suggest that sizeable amounts of succinate may be detected in the large intestine when adequate techniques are used (Morita et al. 1998; Aprikian et al. 2003)."

Let's try again, but never mind. We're going in circles.

When there's an excess of hydrocraponate ion (HCO3−) in plasma that's not being normalized through the lungs, it's going to be filtered by the kidneys and not recovered from the filtrate. Since hydrocraponate was already in plasma and not dissociated from crapon dioxide in cells, it's probably already paired by the edemium ion (Na+).

 

[Amazoniac]

- Distal renal tubular acidosis associated with non-autoimmune hypothyroidism

"Functionally, hypothyroidism is associated with impaired renal bicarbonate reabsorption after bicarbonate loading, reduced hydrogen secretion in the distal nephron, a decreased urinary-blood PCO2 gradient typical of distal renal tubular acidosis and the impaired ability to acidify urine and excrete ammonium after an acute ammonium chloride load."​

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- Is Bypassing the Stomach a Means to Optimize Sodium Bicarbonate Supplementation? A Case Study With a Postbariatric Surgery Individual

- A Novel Ingestion Strategy for Sodium Bicarbonate Supplementation in a Delayed-Release Form: a Randomised Crossover Study in Trained Males

"Given that bicarbonate is lost in the neutralisation of gastric acid [8], large oral doses (200–300 mg/kg body mass) are required to induce meaningful elevations in the blood."​

 

[Amazoniac]

- Respiratory alkalosis may impair the production of vitamin D and lead to significant morbidity, including the fibromyalgia syndrome (hypothesis)

Spoiler

"Hyperventilation caused by physical and/or psychological stress may lead to significant respiratory alkalosis and an elevated systemic pH. The alkalotic pH may in turn suppress the normal renal release of phosphate into the urine, thereby interrupting the endogenous production of 1,25-dihydroxyvitamin D (calcitriol)."

---

"Respiratory alkalosis is one of the four major types of acid-base disturbances in physiology. It is caused by hyperventilation, the simple act of breathing faster and/or more deeply than normal. This results first in a lowered partial pressure of carbon dioxide (pCO2) in the blood; if continued, it will lead to an elevated systemic pH [1]. A variety of physical and/or psychological stresses may lead to hyperventilation. Hypoxia can cause it, as can pain, fever, drugs, hormones, or an emotional state, such as anxiety or fear [2,3]. Since breathing is a mostly unconscious activity, those who hyperventilate may remain largely unaware of it. Most cases of hyperventilation do not last very long, and this may account for the relatively benign reputation of respiratory alkalosis. But if the hyperventilation is severe enough and/or lasts long enough, the resulting respiratory alkalosis may bring with it some untoward consequences."

"One such consequence might be a risk to the human body's natural production of the form of vitamin D known as 1,25 dihydroxyvitamin D, or calcitriol."

"[..]calcitriol has as its primary function the regulation of ionized calcium levels in the body. When these levels drop below a certain set point, a short and tightly-regulated chain of events is set into motion: a burst of parathyroid hormone (PTH) is released into the blood; PTH causes the kidneys to discharge phosphate into the urine; the loss of phosphate, or phosphaturia, induces the kidneys to produce a very specific enzyme, which in turn finally creates calcitriol. This hormone then causes increased absorption of calcium from the small intestine and/or its mobilization from bone, and a return of ionized calcium levels to normal [4]."

"This self-regulatory process for the maintenance of normal calcium levels may be upset by significant hyperventilation. At some point following the initial fall in pCO2, continuing hyperventilation will begin to overwhelm the buffering capacity of the body. This will cause the systemic pH to climb quickly from a normal of 7.4 towards one of 7.6 or even higher [5]. In responding to this situation, the body is at a disadvantage because significant respiratory alkalosis effectively disables two of the three mechanisms (buffers, lungs, and kidneys) it uses to defend itself against pH change."

"The buffering system will already have been pushed to the point of exhaustion, and the lungs, if forced to continue the hyperventilation, will drive the systemic pH even higher. The only remaining method the body has for correcting the elevated pH of respiratory alkalosis is for the kidneys to excrete what has effectively become an excess load of bicarbonate. This happens to be a very uncommon task for the kidneys. Normally they are engaged in recovering as much filtered bicarbonate as possible from the tubular fluid by excreting one acid ion (H+) into the tubular fluid in exchange for every bicarbonate ion (HCO3−) recovered from it [6]. But here that situation is reversed, and the challenge is to excrete bicarbonate rather than to reabsorb it [7]. This does occur naturally in respiratory alkalosis, but it does not happen quickly. It may take hours or even days for the kidneys to excrete enough bicarbonate to correct the pH imbalance [8]. During this relatively long period of time, one of the kidneys' vital functions may be impaired. That function is the excretion of phosphate in response to PTH. This seemingly minor task happens to be of major importance, because it is the rate-limiting step in the body's production of calcitriol [9]."

"In humans, the elimination of phosphate from the body is carried out almost entirely by the kidneys [10]. The process begins in the proximal renal tubules, where the type II sodium-phosphate co-transporters are located. These co-transporters are important in the excretion of phosphate, but they have a somewhat counterintuitive method of action: they release phosphate passively into the tubular fluid when they are inactive, but reabsorb it back into the body when they are active. Whether the co-transporters are inactive or active depends heavily on the pH: they are inactivated as the pH falls, and activated as it rises. The end result is that phosphate excretion by this route would be progressively inhibited by the rising pH of respiratory alkalosis [11]. There is at least one other route for phosphate elimination. It could be excreted into the distal tubules should it be needed as a buffer for the excretion of excess acid [12]. But if the pH is elevated, as in respiratory alkalosis, there would be no excess acid to excrete, and thus no need for phosphate as a buffer."

"Both routes of phosphate excretion would therefore be increasingly blocked by the rising pH of respiratory alkalosis. This situation would presumably persist until the kidneys could, by excreting bicarbonate, lower the pH to the point at which meaningful phosphaturia could occur, and the normal production of calcitriol could be resumed. Should this not happen in a timely fashion, a variety of adverse consequences might ensue."

"It would, for example, disturb the normal reciprocal relationship that exists between cortisol and calcitriol: a rise in cortisol level decreases calcium absorption from the gut [16], thereby lowering ionized calcium levels in the blood, which should in turn cause a rise in calcitriol production. If this could not occur because of an alkalosis-induced depression of the parathyroid axis, the body would simply be forced into a default mode that could temporarily disrupt endocrine autoregulation. Repeated insults in the form of episodic bouts of hyperventilation might reinforce this pattern, and make full recovery increasingly difficult. All of this pathology might result from the kidneys' inability to correct the pH of respiratory alkalosis quickly enough to avoid causing a shortfall in the body's production of calcitriol."