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A Case For High ROS, Antioxidants Are Useless And Potentially Harmful!

B

Braveheart

Guest
Sodium selenite supposedly kills cancer cells through oxidation according to studies, if this is the correct way of describing its action. Correct me if I am wrong.

It is only a specific sodium selenite that has anticancer activity according to one of the studies under, quote:

"However, it is now firmly established that only an inorganic sodium selenite with four-valent Se, and not that with six-valent (selenate) cation shows anticancer activity."

Sodium Selenite as an Anticancer Agent. - PubMed - NCBI
Application of Sodium Selenite in the Prevention and Treatment of Cancers
Rationale for the treatment of cancer with sodium selenite. - PubMed - NCBI
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.adelaide.edu.au/directory/graham.lyons?dsn=directory.file;field=data;id=19832;m=view&ved=2ahUKEwjNucaSsr3hAhVBYlAKHdXzBbAQFjADegQIARAB&usg=AOvVaw3vwvD_gA96AWVsm_ihEoRF&cshid=1554620194017 (Document download from university)
https://www.sciencedirect.com/science/article/pii/S0946672X1630075X
Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
https://www.researchgate.net/publication/303893204_Sodium_Selenite_as_an_Anti-Cancer_Agent
Sodium Selenite Benefits Are Numerous
https://www.hindawi.com/journals/omcl/2016/4741694/
https://www.google.com/url?sa=t&sou...WMAJ6BAgJEAE&usg=AOvVaw0COeJ0ZlqWb5fNuEI9zEEd (downloadable document Chinese study)
Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells
Sodium selenite induces apoptosis in colon cancer cells via Bax-dependent mitochondrial pathway
Combined effect of sodium selenite and docetaxel on PC3 metastatic prostate cancer cell line | Estudo Geral
Effect of Sodium Selenite on Gene Expression of SELF, SELW, and TGR Selenoproteins in Adenocarcinoma Cells of the Human Prostate
https://www.redjournal.org/article/S0360-3016(10)00409-8/pdf
Comparative proteomics analysis of sodium selenite-induced apoptosis in human prostate cancer cells - Metallomics (RSC Publishing)
https://www.google.com/url?sa=t&sou...WMAV6BAgAEAE&usg=AOvVaw1cXNRiJrukr87GvSMLvUqb (downloadable document study)
http://europepmc.org/abstract/MED/18405881
https://jhoonline.biomedcentral.com/articles/10.1186/1756-8722-6-7
https://www.google.com/url?sa=t&sou...WMAh6BAgCEAE&usg=AOvVaw3bunZz7Lz5Bc6AoyYx-E2M (downloadable document study, sodium selenite reverses chemotherapy resistance in cancer study)

"Sodium Selenite

Sodium selenite destroys cancer cells by selectively generating toxic free radicals (reactive oxygen species) which target the destruction of the mitochondria in cancer cells, however not in healthy cells.

Sodium selenite helps with the repair of damaged genes (DNA segments). This reduces the risk of new cancers being formed.

Numerous human studies with sodium selenite support the use of this form of selenium as a possible additional treatment for cancer patients and for preventing new or recurring cases of cancer.

In a randomized controlled clinical trial of sodium selenite using 200 mcg per day versus a placebo in patients with aggressive head and neck cancers, patients given the supplement showed an increased ability to destroy cancer cells. In another study it was shown that temporary use of 1,000 mcg of sodium selenite in patients with oral tumors effectively reduced potentially deadly swelling in these patients after surgery. Sodium selenite in patients with newly diagnosed non-Hodgkin's lymphoma increased the response rate to chemotherapy by 50% compared to a placebo group, and significantly increased overall survival time."

Source: https://www.liverdoctor.com/selenium-cancer-fighting-mineral/

And there's many more information, studies and literature to be found on sodium selenite for cancer on the internet. Hope this helps.
good info...thanks!
 

Obi-wan

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@Obi-wan As per travis—-I thought the benefit of selenomethionine wasn’t necessarily it’s role as an anti-oxidant/oxidant in cancer proliferation but rather it’s effect on inhibiting polyamine synthesis??

The more I read the more I become confused

“I think it depends on the person because they have different pharmacokinetics. It has been shown that selenomethionine is four times more effective than selenide for preventing pancreatic degeneration in chicks,⁽¹⁾ perhaps indicating that the pancreatic membranes are highly lipophilic and largely-exclude the water-soluble selenide (or perhaps selenide gets absorbed to far-up the digestive tract; selenomethionine further down). Selenide does seem to reach many body locations quicker, but since the prostate has such a high methionine requirement—for polyamine synthesis—selenomethionine would likely be the better choice for reaching that.”


I recall also Travis saying that selenomethionine inhibits polyamine synthesis but feel it is an antioxidant at low dosage but would be an oxidant at high dosage. Per the study sodium selenite is better as it inhibits the antioxidant system of cancer cells and because it contains selenium would still inhibit polyamine synthesis. Plus it makes Docetaxel much more effective.
 

TreasureVibe

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Messages
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This is very interesting as I had stopped taking Selenomethionine due to it being an antioxidant. So now we know that inorganic Selenite is not an antioxidant but possesses oxidizing properties.

In the study at https://estudogeral.sib.uc.pt/bitstream/10316/20321/1/Combined effect of sodium selenite and docetaxel on PC3 metastatic prostate cancer cell line(BiochemBiophysREsComm2011).pdf

"Docetaxel and sodium selenite inhibit prostate cancer cells
(PC3) growth in a dose and time dependent-manner.
Half maximal inhibitory concentration values (IC50) of docetaxel
(Fig. 1A) and sodium selenite (Fig. 1B) were reached for
approximately 500 nM (Rsqr: 0.998) and 10 lM (Rsqr: 0.991),
respectively, after 24 h incubation. However, when we treat the
cells with 100 nM docetaxel and 2.5 lM sodium selenite simultaneously,
we observed a synergistic antiproliferative effect
(Fig. 1C). In fact, sodium selenite and docetaxel combination have
a synergistic effect on cell growth inhibition (67%) compared with
docetaxel (22%) and sodium selenite (24%) alone."

"On the other hand cell death may be related with oxidative
stress induction. In fact docetaxel has been recently associated to
an increase of ROS in the prostate cancer DU-145 cells [27]. Surprisingly,
we found ROS depletion after 24 h treatment (Fig. 4).
Moreover, it could be a result of peroxides conversion into hydroxyl
radicals. However, data not shown indicate that sodium selenite
and docetaxel alone, or in combination, did not interfere on
PC3 peroxides production after 6 h treatment. Therefore, we admit
that sodium selenite could inhibit the antioxidant system leading
to oxidative lesion by reactive hydroxyl radicals and consequent
cell death."

"Reduced glutathione (GSH), counteract oxidative stress by directly
quenching reactive oxygen species and has been associated
to resistance to apoptosis and radiation in prostate cancer cells
[28]. Besides sodium selenite supplies selenium for synthesis of seleno-
proteins such as the antioxidant defenses glutathione peroxidase
(Gl-Px) and thioredoxin reductase, higher concentrations are
related with increased oxidative stress by decreasing reduced glutathione/
oxidized glutathione (GSH/GSSG) ratio and also by altering
MnSOD subcellular distribution. These observations are
related with an increase of ROS levels and cell sensitization to
apoptosis [13–15,29]."
Combination of carmustine and selenite effectively inhibits tumor growth by targeting androgen receptor, androgen receptor-variants, and Akt in preclinical models: New hope for patients with castration resistant prostate cancer.
Thamilselvan V, et al. Int J Cancer. 2016.
Show full citation
Abstract
Despite established androgen receptor (AR) antagonists, AR/AR-variants signaling remain a major obstacle for the successful treatment of castration resistant prostate cancer (CRPC). In addition, CRPC cells adapt to survive via AR-independent pathways to escape next generation therapies. Therefore, there is an urgent need for drugs that can target these signaling pathways in CRPC. In this study, we sought to determine whether carmustine and selenite in combination could induce apoptosis and inhibit growth of CRPC in-vitro and in-vivo. CRPC (22Rv1, VCaP, and PC-3) cell lines in culture and xenograft mouse were used. Combination of carmustine and selenite treatment significantly increased reactive oxygen species, apoptosis and growth inhibition in CRPC cells with down regulation of anti-apoptotic (Bcl-2 and Mcl-1) and proliferative proteins (c-Myc and cyclin-D1). This effect was associated with complete reduction of AR/AR-variants, AR-V7, PSA and significant induction of p27Kip1. Combination treatment substantially abolished phospho-Akt, phospho-GSK-3β, and anchorage-independent growth in AR-positive and AR-negative cells. Consistent with in-vitro results, combination treatment effectively induced apoptosis and completely inhibited xenograft tumor growth and markedly reduced AR/AR-variants, AR-V7, PSA, and Bcl-2 in xenograft tumors without causing genotoxicity in host mice. Individual agent treatment showed only partial effect. The combination treatment showed a significant synergistic effect. The present study is the first to demonstrate that the combination of carmustine and selenite treatment completely suppressed CRPC tumor growth by reducing AR/AR-variants and Akt signaling. Our findings suggest that the combination of carmustine and selenite could constitute a promising next-generation therapy for successful treatment of patients with CRPC.

Combination of carmustine and selenite effectively inhibits tumor growth by targeting androgen receptor, androgen receptor-variants, and Akt in precl... - PubMed - NCBI


[Influence of sodium selenite on carcinogenesis of the prostate and other organs induced by methylnitrosourea and testosterone in rats].
Bespalov VG, et al. Vopr Onkol. 2011.
Show full citation
Abstract
Influence of selenium on induced carcinogenesis of the prostate and other organs was studied in male Wistar rats. Carcinogenesis was induced (68) by using our modification of a combined double-stage model including surgical castration, single administration of N-methyl-N-nitrosourea (MNU) and long-term promotion by a mix of testosterone ethers (MTE). Seven days after MNU injection the rats were randomized to form 2 groups. Controls were fed drinking water while the study group - water containing sodium selenite 4mg/l, daily - till the end of the experiment. Controls (12) were not exposed to any treatment. They were followed up for 55 weeks until sacrificed. Apparent benign prostatic hyperplasia developed in rats subjected to castration, MNU and MTE. Also, such precancerous lesions as prostatic intraepithelial neoplasia (PIN) and prostate cancer including metastatic one were detected. Malignant lymphoma, other than in target tissues, was the most frequent. Prostate pathological changes and lymphomas were not registered in intact rats. Unlike rats treated with MNU and MTE and fed untreated drinking water, selenium did not influence significantly the development of prostate intraepithelial neoplasia but reduced multiplicity of prostate cancer by 44.6%. Simultaneously, the incidence of induced malignant lymphomas decreased by 26.4%.

[Influence of sodium selenite on carcinogenesis of the prostate and other organs induced by methylnitrosourea and testosterone in rats]. - PubMed - NCBI

Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles in cancer cells generates potent therapeutic effects.
Zhao G, et al. Free Radic Biol Med. 2018.
Show full citation
Abstract
We have previously demonstrated that selenium nanoparticles (SeNPs) administered via oral route possess similar capacities of increasing selenoenzyme activities as the extensively examined sodium selenite, selenomethionine and methylselenocysteine, and yet display the lowest toxicity among these selenium compounds in mouse models. However, the low toxicity of SeNPs found in mammalian systems would lead to the interpretation that the punctate distribution of elemental selenium found in cultured cancer cells subjected to selenite treatment that triggers marked cytotoxicity represents a detoxifying mechanism. The present study found that SeNPs could be reduced by the thioredoxin- or glutaredoxin-coupled glutathione system to generate ROS. Importantly, ROS production by SeNPs in these systems was more efficient than by selenite, which has been recognized as the most redox-active selenium compound for ROS production. This is because multiple steps of reduction from selenite to selenide anion are required; whereas only a single step reduction from the elemental selenium atom to selenide anion is needed to trigger redox cycling with oxygen to produce ROS. We thus speculated that accumulation of SeNPs in cancer cells would result in a strong therapeutic effect, rather than serves a detoxification function. Indeed, we showed herein that preformed SeNPs generated a potent therapeutic effect in a mouse model due to rapid, massive and selective accumulation of SeNPs in cancer cells. Overall, for the first time, we demonstrate that SeNPs have a stronger pro-oxidant property than selenite and hyper-accumulation of SeNPs in cancer cells can generate potent therapeutic effects.

Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles ... - PubMed - NCBI

Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells
Article (PDF Available) in Cancer Chemotherapy and Pharmacology 63(2):351-62 · May 2008 with 32 Reads
DOI: 10.1007/s00280-008-0745-3 · Source: PubMed
Weixiong Zhong
39.83
University of Wisconsin–Madison

Abstract
Studies have demonstrated that selenium supplementation reduces the incidence of cancer, particularly prostate cancer. Evidence from experimental studies suggests that apoptosis is a key event in cancer chemoprevention by selenium and reactive oxygen species play a role in induction of apoptosis by selenium compounds. The current study was designed to investigate the role of superoxide and mitochondria in selenite-induced apoptosis in human prostate cancer cells. LNCaP cells were transduced with adenoviral constructs to overexpress four primary antioxidant enzymes: manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), catalase (CAT), or glutathione peroxidase 1 (GPx1). Cell viability, apoptosis, and superoxide production induced by sodium selenite were analyzed by the MTT assay, chemiluminescence, flow cytometry, western blot analysis, and Hoechst 33342 staining following overexpression of these antioxidant enzymes. Our study shows the following results: (1) selenite induced cancer cell death and apoptosis by producing superoxide radicals; (2) selenite-induced superoxide production, cell death, and apoptosis were inhibited by overexpression of MnSOD, but not by CuZnSOD, CAT, or GPx1; and (3) selenite treatment resulted in a decrease in mitochondrial membrane potential, release of cytochrome c into the cytosol, and activation of caspases 9 and 3, events that were suppressed by overexpression of MnSOD. This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite. The data suggest that superoxide production in mitochondria is, at least in part, a key event in selenium-induced apoptosis in prostate cancer cells.

https://www.researchgate.net/public...endent_pathway_in_human_prostate_cancer_cells
Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells. - PubMed - NCBI
 

Collden

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Joined
Oct 6, 2012
Messages
630
Several years ago there was a post on DavidIckes forum that spoke at length about how oxidative stress was crucial to male health and that the modern culture pushing men to consume more raw fruits/veggies and less meat, fat, alcohol and cooked foods was a major cause of the feminization of men in modern society. Always wondered if there wasn't something to what it said about the misunderstood role of oxidative stress especially in men.
 
Last edited:

Obi-wan

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Thread starter
Joined
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Messages
1,120
In the study at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436308/pdf/zbc30625.pdf regarding Fenbendazole

"FZ-induced ROS generation could be associated with the transcriptional activation of ROS-related genes. Our data show PIG3 induction upon FZ treatment. PIG3 is a p53-inducible gene homolog of oxidoreductase and is reported to be associated with p53-induced elevation of ROS production (51). Proteasomal inhibition is likely to accumulate mitochondrial damage and generate oxidative stress inside the cell(52). Oxidative stress can, in turn, affect proteasome function either by producing excessive levels of damaged proteins, causing unfolded protein response or by reducing the levels of ATP production. Proteasome inhibitors have been previously reported to elicit ER stress response (53, 54). Certain compounds selectively kill cancer cells by induction of ER stress ROS, because cancer cells are expected to rely strongly on the ROS stress response pathway as compared with normal cells (55–58). Altogether, our results indicate that FZ induces cytotoxicity in cancer cells via impairment of proteasomel function and induction of unfolded protein response. The ubiquitin-proteasome system is integral to cellular protein homeostasis. The growing recognition of the fundamental importance of this pathway to normal cell function and in disease has prompted an in depth search for small-molecule inhibitors that selectively block the function of these pathways. Therefore, we propose FZ as a novel drug candidate that targets the ubiquitin-proteasome pathway and effectively kills cancer cells.
 

Obi-wan

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Thread starter
Joined
Mar 16, 2017
Messages
1,120
Combination of carmustine and selenite effectively inhibits tumor growth by targeting androgen receptor, androgen receptor-variants, and Akt in preclinical models: New hope for patients with castration resistant prostate cancer.
Thamilselvan V, et al. Int J Cancer. 2016.
Show full citation
Abstract
Despite established androgen receptor (AR) antagonists, AR/AR-variants signaling remain a major obstacle for the successful treatment of castration resistant prostate cancer (CRPC). In addition, CRPC cells adapt to survive via AR-independent pathways to escape next generation therapies. Therefore, there is an urgent need for drugs that can target these signaling pathways in CRPC. In this study, we sought to determine whether carmustine and selenite in combination could induce apoptosis and inhibit growth of CRPC in-vitro and in-vivo. CRPC (22Rv1, VCaP, and PC-3) cell lines in culture and xenograft mouse were used. Combination of carmustine and selenite treatment significantly increased reactive oxygen species, apoptosis and growth inhibition in CRPC cells with down regulation of anti-apoptotic (Bcl-2 and Mcl-1) and proliferative proteins (c-Myc and cyclin-D1). This effect was associated with complete reduction of AR/AR-variants, AR-V7, PSA and significant induction of p27Kip1. Combination treatment substantially abolished phospho-Akt, phospho-GSK-3β, and anchorage-independent growth in AR-positive and AR-negative cells. Consistent with in-vitro results, combination treatment effectively induced apoptosis and completely inhibited xenograft tumor growth and markedly reduced AR/AR-variants, AR-V7, PSA, and Bcl-2 in xenograft tumors without causing genotoxicity in host mice. Individual agent treatment showed only partial effect. The combination treatment showed a significant synergistic effect. The present study is the first to demonstrate that the combination of carmustine and selenite treatment completely suppressed CRPC tumor growth by reducing AR/AR-variants and Akt signaling. Our findings suggest that the combination of carmustine and selenite could constitute a promising next-generation therapy for successful treatment of patients with CRPC.

Combination of carmustine and selenite effectively inhibits tumor growth by targeting androgen receptor, androgen receptor-variants, and Akt in precl... - PubMed - NCBI


[Influence of sodium selenite on carcinogenesis of the prostate and other organs induced by methylnitrosourea and testosterone in rats].
Bespalov VG, et al. Vopr Onkol. 2011.
Show full citation
Abstract
Influence of selenium on induced carcinogenesis of the prostate and other organs was studied in male Wistar rats. Carcinogenesis was induced (68) by using our modification of a combined double-stage model including surgical castration, single administration of N-methyl-N-nitrosourea (MNU) and long-term promotion by a mix of testosterone ethers (MTE). Seven days after MNU injection the rats were randomized to form 2 groups. Controls were fed drinking water while the study group - water containing sodium selenite 4mg/l, daily - till the end of the experiment. Controls (12) were not exposed to any treatment. They were followed up for 55 weeks until sacrificed. Apparent benign prostatic hyperplasia developed in rats subjected to castration, MNU and MTE. Also, such precancerous lesions as prostatic intraepithelial neoplasia (PIN) and prostate cancer including metastatic one were detected. Malignant lymphoma, other than in target tissues, was the most frequent. Prostate pathological changes and lymphomas were not registered in intact rats. Unlike rats treated with MNU and MTE and fed untreated drinking water, selenium did not influence significantly the development of prostate intraepithelial neoplasia but reduced multiplicity of prostate cancer by 44.6%. Simultaneously, the incidence of induced malignant lymphomas decreased by 26.4%.

[Influence of sodium selenite on carcinogenesis of the prostate and other organs induced by methylnitrosourea and testosterone in rats]. - PubMed - NCBI

Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles in cancer cells generates potent therapeutic effects.
Zhao G, et al. Free Radic Biol Med. 2018.
Show full citation
Abstract
We have previously demonstrated that selenium nanoparticles (SeNPs) administered via oral route possess similar capacities of increasing selenoenzyme activities as the extensively examined sodium selenite, selenomethionine and methylselenocysteine, and yet display the lowest toxicity among these selenium compounds in mouse models. However, the low toxicity of SeNPs found in mammalian systems would lead to the interpretation that the punctate distribution of elemental selenium found in cultured cancer cells subjected to selenite treatment that triggers marked cytotoxicity represents a detoxifying mechanism. The present study found that SeNPs could be reduced by the thioredoxin- or glutaredoxin-coupled glutathione system to generate ROS. Importantly, ROS production by SeNPs in these systems was more efficient than by selenite, which has been recognized as the most redox-active selenium compound for ROS production. This is because multiple steps of reduction from selenite to selenide anion are required; whereas only a single step reduction from the elemental selenium atom to selenide anion is needed to trigger redox cycling with oxygen to produce ROS. We thus speculated that accumulation of SeNPs in cancer cells would result in a strong therapeutic effect, rather than serves a detoxification function. Indeed, we showed herein that preformed SeNPs generated a potent therapeutic effect in a mouse model due to rapid, massive and selective accumulation of SeNPs in cancer cells. Overall, for the first time, we demonstrate that SeNPs have a stronger pro-oxidant property than selenite and hyper-accumulation of SeNPs in cancer cells can generate potent therapeutic effects.

Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles ... - PubMed - NCBI

Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells
Article (PDF Available) in Cancer Chemotherapy and Pharmacology 63(2):351-62 · May 2008 with 32 Reads
DOI: 10.1007/s00280-008-0745-3 · Source: PubMed
Weixiong Zhong
39.83
University of Wisconsin–Madison

Abstract
Studies have demonstrated that selenium supplementation reduces the incidence of cancer, particularly prostate cancer. Evidence from experimental studies suggests that apoptosis is a key event in cancer chemoprevention by selenium and reactive oxygen species play a role in induction of apoptosis by selenium compounds. The current study was designed to investigate the role of superoxide and mitochondria in selenite-induced apoptosis in human prostate cancer cells. LNCaP cells were transduced with adenoviral constructs to overexpress four primary antioxidant enzymes: manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), catalase (CAT), or glutathione peroxidase 1 (GPx1). Cell viability, apoptosis, and superoxide production induced by sodium selenite were analyzed by the MTT assay, chemiluminescence, flow cytometry, western blot analysis, and Hoechst 33342 staining following overexpression of these antioxidant enzymes. Our study shows the following results: (1) selenite induced cancer cell death and apoptosis by producing superoxide radicals; (2) selenite-induced superoxide production, cell death, and apoptosis were inhibited by overexpression of MnSOD, but not by CuZnSOD, CAT, or GPx1; and (3) selenite treatment resulted in a decrease in mitochondrial membrane potential, release of cytochrome c into the cytosol, and activation of caspases 9 and 3, events that were suppressed by overexpression of MnSOD. This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite. The data suggest that superoxide production in mitochondria is, at least in part, a key event in selenium-induced apoptosis in prostate cancer cells.

https://www.researchgate.net/public...endent_pathway_in_human_prostate_cancer_cells
Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells. - PubMed - NCBI

"selenite treatment resulted in a decrease in mitochondrial membrane potential, release of cytochrome c into the cytosol, and activation of caspases 9 and 3, events that were suppressed by overexpression of MnSOD. This study demonstrates that selenite induces cell death and apoptosis by production of superoxide in mitochondria and activation of the mitochondrial apoptotic pathway and MnSOD plays an important role in protection against prooxidant effects of superoxide from selenite. The data suggest that superoxide production in mitochondria is, at least in part, a key event in selenium-induced apoptosis in prostate cancer cells."

"It has been reported that selenite-induced cell death or apoptosis is inhibited by SOD mimics or by stable overexpression of MnSOD in several types of cancer cells [13,14,17-20,26]. It has been shown that cancer cells usually have lower levels of MnSOD than their normal counterparts [35]. Recent studies demonstrated that normal prostatic epithelial cells had higher levels of MnSOD and lower sensitivity to selenite compared to prostate cancer cells [36,37].These observations suggest that high levels of MnSOD may protect normal cells against superoxide generated apoptosis by Se."

" In conclusion, we have demonstrated that selenite induced cell death in LNCaP prostate cancer cells in association with superoxide production and apoptosis. Superoxide production was mainly in or adjacent to mitochondria and triggered the mitochondrial pathway of apoptosis. Only overexpression of MnSOD suppressed selenite-induced superoxide production and apoptosis. Our study suggests that levels of MnSOD in prostate and other cancer cells may influence the efficacy of Se in supplementation in cancer chemoprevention. Since cancer cells usually have lower levels of MnSOD, they should be more sensitive to Se than their normal cell counterparts. Therefore, in cancer prevention, Se may be found to selectively induce apoptosis of cancer cells without causing significant damage to normal cells."

Similar to FZ induced ROS. Selenite produces ROS down the same pathway. I now take Sodium Selenite.
 

Obi-wan

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Joined
Mar 16, 2017
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Great case for using Vit E Succinate at http://clincancerres.aacrjournals.org/content/clincanres/8/3/863.full.pdf

ABSTRACT -

Tocopheryl succinate (-TOS), a redox-inactive analogue of vitamin E, is a strong inducer of apoptosis, whereas -tocopherol (-TOH) lacks apoptogenic activity (J. Neuzil et al., FASEB J., 15: 403–415, 2001). Here we investigated the possible antineoplastic activities of -TOH and -TOS and further explored the potential of -TOS as an antitumor agent. Using nude mice with colon cancer xenografts, we found that -TOH exerted modest antitumor activity and acted by inhibiting tumor cell proliferation. In contrast, -TOS showed a more profound antitumor effect, at both the level of inhibition of proliferation and induction of tumor cell apoptosis. -TOS was nontoxic to normal cells and tissues, triggered apoptosis in p53/ and p21Waf1/Cip1(/)
cancer cells, and exerted a cooperative proapoptotic activity with tumor necrosis factor-related apoptosis-inducing ligand (Apo2 ligand) due to differences in proapoptotic signaling. Finally, -TOS cooperated with tumor necrosis factor-related apoptosis-inducing ligand in suppression of tumor growth in vivo. Vitamin E succinate is thus a potent and highly specific anticancer agent and/or adjuvant of considerable therapeutic potential.

Conclusions.

In this study, we show that (a) -TOS inhibited growth of colon carcinoma by almost 80%, and -TOH inhibited growth of colon carcinoma by 35%; (b) -TOS-treated mice showed increased apoptosis and decreased proliferation, whereas -TOH inhibited proliferation only; (c) -TOS efficiently killed cancer cells deficient in p53 and p21Waf1/Cip1;( d) -TOS cooperated with TRAIL in apoptosis induction and inhibition of tumor growth; (e) -TOS accumulated in tissues and was partially hydrolyzed to -TOH; and (f) -TOS was nontoxic to normal murine organs and to normal cells. Our data strongly suggest that -TOS is a nontoxic antineoplastic agent that cooperates with TRAIL in vivo and suggest an explanation why -TOH is often found to be inefficient in cancer treatment (57). We propose that this semisynthetic vitamin E analogue is a promising anticancer agent or adjuvant, which warrants its testing in other models of cancer with a realistic prospect of its use in human therapy.

Profound...having or showing great knowledge or insight.
 

TreasureVibe

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  • Limonene increases the ability of docetaxel to induce apoptosis in prostate cancer cells. More reactive oxygen species are produced in the cancer cells, while the amount of glutathione, an antioxidant that inhibits tumor growth, is significantly reduced. The activity of caspase, an enzyme involved in triggering apoptosis, is also increased [4].
Source: 10 Surprising Health Benefits of Limonene + Side Effects - SelfHacked
 

Obi-wan

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I recall also Travis saying that selenomethionine inhibits polyamine synthesis but feel it is an antioxidant at low dosage but would be an oxidant at high dosage. Per the study sodium selenite is better as it inhibits the antioxidant system of cancer cells and because it contains selenium would still inhibit polyamine synthesis. Plus it makes Docetaxel much more effective.



It is a study that says that Cabergoline,an Prolactine-inhibitor,actually cured the disease.
It is a very safe medication.Maybe you should try it.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6641560/pdf/nihms-1039812.pdf

REVERSAL OF PROSTATE CANCER BY CABERGOLINE.JPG
 
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..excerpt from the above:

The patient had received androgen ablation treatment that included
hormone therapy, chemotherapy, and radiation therapy. The androgen-dependent malignancy
was terminated.

..
However, androgen-independent malignancy developed; which likely is due to prolactin.
Based on that expectation, cabergoline treatment (dopamine agonist; Casodex) was
employed to inhibit the pituitary production of prolactin. Prior to treatment, the patient’s
CTC (circulating tumor cell) count=5.4; which is indicative of survival for ~21 months.
After 7 weeks treatment with cabergoline, the circulating tumor cell count=0.
Correspondingly, the plasma prolactin concentration decreased 88% (11.3 to 1.3 ug/ml).
This corroborates that prolactin, not impaired androgen receptor, is the required target for
treating advanced prostate cancer.




i would go for it,on top of the other possible medications.
It is a very gentle medication,will raise dopamine also.
 
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How does a D2 agonist raise Dopamine levels?

it doesnt,its a rethoric formulation for those that maybe are not in the know?
It will raise Dopamine action by binding to the dopamine-action mediating Dopamine Receptor.
 

Texon

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Nov 28, 2016
Messages
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Hey amazoniac, how would you recomend getting acetoacetate, I assume you are not referring to ketosis, ethyl/methyl acetoacetate? Or something else?
I'm pretty sure I recall that very high doses of vitamin c such as iv treatments are pro oxidant.
 

GelatinGoblin

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Several years ago there was a post on DavidIckes forum that spoke at length about how oxidative stress was crucial to male health and that the modern culture pushing men to consume more raw fruits/veggies and less meat, fat, alcohol and cooked foods was a major cause of the feminization of men in modern society. Always wondered if there wasn't something to what it said about the misunderstood role of oxidative stress especially in men.
Hmmmm... It's not that Oxidative Stress is good but too much antioxidants disturbing is bad
 

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