I hope this post is not taken as somehow trying to promote the use of DMSO. I am simply pointing out the connection between the two since the actual compound used (Dimethylsulfoniopropionates - DMSP used int he study is rapidly metabolized in vivo into a number of chemicals, but mostly DMSO.
Dimethylsulfoniopropionate - Wikipedia
"...This is probably due to the non-linear abiotic and microbial uptake of methanethiol in seawater, and the comparatively low reactivity of DMS. However, a significant portion of DMS in seawater is oxidized to dimethyl sulfoxide(DMSO)."
It is not known at this time whether DMSO will have the same effects as DMSP but the beneficial effects on cancer noted in studies on DMSO is likely not a coincidence. I think @burtlancast and @Wagner83 will find this interesting.
Anyways, the study protocol was treatment for only 10 days with DMSP doses in the range of HED 2.2mg/kg - 16mg/kg. While all doses used had therapeutic effects only the highest dose of HED 16mg/kg completely eradicated the cancer. The cancer used to inoculate the mice was Ehrlich ascites carcinoma, which has guaranteed lethality in mice in about 2 weeks, thus exceeding the lethality of melanoma and pancreatic cancers in humans. As the study also mentioned, DMSP also completely cured chronic liver cancers in rats. The proposed mechanism of action for both cancers is stimulation of the immune system induced by DMSP, as well as activation of stem cells that invade the tumor and convert it back to normal tissue. The stem cell mechanism is akin to the famous salamander example Peat once wrote about. The salamanders, which have much higher stem cell activity than humans which allows them to regenerate on demand, transplanted with human tumors invariably turn them into normal tissue. However, I also suspect that DMSP inhibits fatty acid oxidation in a manner similar to the drug Mildronate. The structure of DMSP is virtually identical to newly discovered successors to Mildronate that are active in much lower concentrations. DMSP is known as member of the sulfobetaine class of chemicals and they are know to inhibit carnitine transport just like Mildronate does (Inhibition of mitochondrial carnitine-acylcarnitine translocase by sulfobetaines. - PubMed - NCBI).
Finally, as the study itself note, DMSP has no side effects and no toxicity unlike another therapeutic chemical (TG) used as active control comparison in both studies.
Anticancer effects of a tertiary sulfonium compound, dimethylsulfoniopropionate, in green sea algae on Ehrlich ascites carcinoma-bearing mice. - PubMed - NCBI
Sulfobetaine (dimethylsulfoniopropionate) and glycine betaine show incompatible involvement in crucial Ehrlich ascites carcinoma in mice. - PubMed - NCBI
A tertiary sulfonium compound, dimethylsulfoniopropionate in green sea algae, completely suppresses crucial Ehrlich ascites carcinoma in mice. - PubMed - NCBI
"...In conclusion, our results demonstrate that 70 mM DMSP completely eradicated crucial Ehrlich ascites carcinoma in mice. This finding is likely attributable to the function of recruited and resided activated macrophages and to the regeneration of tissue specific stem cells in the local microenvironments without a cytokine interference and, in particular, with no side effects."
"...In addition, we demonstrated that free ingestion of 10- and 20-mM DMSP solutions (av. 104 and 208 mg/day/rat) for up to 33 weeks completely healed chronic cancer, 3’-methyl-4-dimethylamino-azobenzene induced-liver cancer in rats with no abnormality in other viscera, showing liver weights and liver weights (/body wt.) with significant difference (p<0.05, by Tukey-Kramer test) from controls, cancerous rats fed with 10 mM DMSP and 20 mM DMSP solutions (10,20). In this experiments, the activity of a liver marker enzyme, γ-GTP, in serum of cancerous rats was very high as well (10, 20)."
"...Ehrlich ascites carcinoma cells elicit solid cancers in organs when subcutaneously-(s.c.) injected and free cell cancers in the peritoneal cavity when i.p.-injected in mice (9). In particular, the latter causes prompt death of all the mice with large volume of ascites fluid for about 2 weeks (9)."
"...In the present work, we found that initial i.p. supplementation (0.5 ml) of 10-70 mM DMSP solutions almost linearly restricted accumulation of ascites fluid in a dose-dependent manner. The linear-fitted curve indicates that increasing DMSP doses causes a parallel relation with a decrease of the volume of ascitic fluid and thus with a decline of the death rate of test mice. In fact, the supplementation of 70 mM DMSP solution to EAC bearing-mice completely suppressed the proliferation of EAC cells with no accumulation of ascites fluid in the peritoneal cavity, exhibiting the same body weights as those in control mice."
"...Only initial i.p. administration of 50 and 70 mM DMSP solutions to EAC-bearing mice resulted in same body weights as those in the control group for up to10 days. Of great interest, a single i.p. injection of DMSP (180 mM, 1 ml) to juvenile mice, single i.p. supplementation of a large amount of DMSP (3.2 M, 1 ml) to rats (8) or oral and sequential administration of a high dose of DMSP (208 mg/day/rat) for up to 33 weeks to young rats (10), caused no toxicity in rodents for a long time. These findings indicate that it is possible to administer i.p. and orally higher frequent-doses of DMSP to animals suffering from acute and chronic cancers without side-effects in vivo, which strongly suggests that DMSP mitigates and heals different kinds of cancers in different types of animals."
"...In contrast, it was found that DMSP activated delayed-type hypersensitive immune reaction in rats (10) and mice (8, 10). Moreover we showed that administration of DMSP to EAC-bearing mice restored the abnormal immune systems to normal levels with decreased ascites fluids at 10 days (10). This re-establishment is likely attributable to increased numbers of macrophages at early rearing time since these cells play a major role in ameliorating inflammation caused by cancer (12-15, 18, 19). In fact, we found that i.p. administrations of DMSP into normal 4-week-old mice accumulated large numbers of macrophages in the peritoneal cavity without giving any damage to various viscera of the peritoneal cavity 3 days after the injection, greatly distinguishing from TG causing inflammation and cell death of all viscera in the cavity."
"...Taken together, our results and other findings suggest it is likely that resident and multi-potent stem cells formed from hematopoietic progenitor stem cells are regenerated by EAC cells leading to a subsequent differentiation of these progenitors to lineage cellular populations in inflamed and/or damaged cells and tissues (13-15, 18), which is accompanied by the up-regulation of the innate immune systems due to high potential of activated macrophages (12, 18-19, 21) via the DMSP signaling through complex and yet unspecified ways."
Dimethylsulfoniopropionate - Wikipedia
"...This is probably due to the non-linear abiotic and microbial uptake of methanethiol in seawater, and the comparatively low reactivity of DMS. However, a significant portion of DMS in seawater is oxidized to dimethyl sulfoxide(DMSO)."
It is not known at this time whether DMSO will have the same effects as DMSP but the beneficial effects on cancer noted in studies on DMSO is likely not a coincidence. I think @burtlancast and @Wagner83 will find this interesting.
Anyways, the study protocol was treatment for only 10 days with DMSP doses in the range of HED 2.2mg/kg - 16mg/kg. While all doses used had therapeutic effects only the highest dose of HED 16mg/kg completely eradicated the cancer. The cancer used to inoculate the mice was Ehrlich ascites carcinoma, which has guaranteed lethality in mice in about 2 weeks, thus exceeding the lethality of melanoma and pancreatic cancers in humans. As the study also mentioned, DMSP also completely cured chronic liver cancers in rats. The proposed mechanism of action for both cancers is stimulation of the immune system induced by DMSP, as well as activation of stem cells that invade the tumor and convert it back to normal tissue. The stem cell mechanism is akin to the famous salamander example Peat once wrote about. The salamanders, which have much higher stem cell activity than humans which allows them to regenerate on demand, transplanted with human tumors invariably turn them into normal tissue. However, I also suspect that DMSP inhibits fatty acid oxidation in a manner similar to the drug Mildronate. The structure of DMSP is virtually identical to newly discovered successors to Mildronate that are active in much lower concentrations. DMSP is known as member of the sulfobetaine class of chemicals and they are know to inhibit carnitine transport just like Mildronate does (Inhibition of mitochondrial carnitine-acylcarnitine translocase by sulfobetaines. - PubMed - NCBI).
Finally, as the study itself note, DMSP has no side effects and no toxicity unlike another therapeutic chemical (TG) used as active control comparison in both studies.
Anticancer effects of a tertiary sulfonium compound, dimethylsulfoniopropionate, in green sea algae on Ehrlich ascites carcinoma-bearing mice. - PubMed - NCBI
Sulfobetaine (dimethylsulfoniopropionate) and glycine betaine show incompatible involvement in crucial Ehrlich ascites carcinoma in mice. - PubMed - NCBI
A tertiary sulfonium compound, dimethylsulfoniopropionate in green sea algae, completely suppresses crucial Ehrlich ascites carcinoma in mice. - PubMed - NCBI
"...In conclusion, our results demonstrate that 70 mM DMSP completely eradicated crucial Ehrlich ascites carcinoma in mice. This finding is likely attributable to the function of recruited and resided activated macrophages and to the regeneration of tissue specific stem cells in the local microenvironments without a cytokine interference and, in particular, with no side effects."
"...In addition, we demonstrated that free ingestion of 10- and 20-mM DMSP solutions (av. 104 and 208 mg/day/rat) for up to 33 weeks completely healed chronic cancer, 3’-methyl-4-dimethylamino-azobenzene induced-liver cancer in rats with no abnormality in other viscera, showing liver weights and liver weights (/body wt.) with significant difference (p<0.05, by Tukey-Kramer test) from controls, cancerous rats fed with 10 mM DMSP and 20 mM DMSP solutions (10,20). In this experiments, the activity of a liver marker enzyme, γ-GTP, in serum of cancerous rats was very high as well (10, 20)."
"...Ehrlich ascites carcinoma cells elicit solid cancers in organs when subcutaneously-(s.c.) injected and free cell cancers in the peritoneal cavity when i.p.-injected in mice (9). In particular, the latter causes prompt death of all the mice with large volume of ascites fluid for about 2 weeks (9)."
"...In the present work, we found that initial i.p. supplementation (0.5 ml) of 10-70 mM DMSP solutions almost linearly restricted accumulation of ascites fluid in a dose-dependent manner. The linear-fitted curve indicates that increasing DMSP doses causes a parallel relation with a decrease of the volume of ascitic fluid and thus with a decline of the death rate of test mice. In fact, the supplementation of 70 mM DMSP solution to EAC bearing-mice completely suppressed the proliferation of EAC cells with no accumulation of ascites fluid in the peritoneal cavity, exhibiting the same body weights as those in control mice."
"...Only initial i.p. administration of 50 and 70 mM DMSP solutions to EAC-bearing mice resulted in same body weights as those in the control group for up to10 days. Of great interest, a single i.p. injection of DMSP (180 mM, 1 ml) to juvenile mice, single i.p. supplementation of a large amount of DMSP (3.2 M, 1 ml) to rats (8) or oral and sequential administration of a high dose of DMSP (208 mg/day/rat) for up to 33 weeks to young rats (10), caused no toxicity in rodents for a long time. These findings indicate that it is possible to administer i.p. and orally higher frequent-doses of DMSP to animals suffering from acute and chronic cancers without side-effects in vivo, which strongly suggests that DMSP mitigates and heals different kinds of cancers in different types of animals."
"...In contrast, it was found that DMSP activated delayed-type hypersensitive immune reaction in rats (10) and mice (8, 10). Moreover we showed that administration of DMSP to EAC-bearing mice restored the abnormal immune systems to normal levels with decreased ascites fluids at 10 days (10). This re-establishment is likely attributable to increased numbers of macrophages at early rearing time since these cells play a major role in ameliorating inflammation caused by cancer (12-15, 18, 19). In fact, we found that i.p. administrations of DMSP into normal 4-week-old mice accumulated large numbers of macrophages in the peritoneal cavity without giving any damage to various viscera of the peritoneal cavity 3 days after the injection, greatly distinguishing from TG causing inflammation and cell death of all viscera in the cavity."
"...Taken together, our results and other findings suggest it is likely that resident and multi-potent stem cells formed from hematopoietic progenitor stem cells are regenerated by EAC cells leading to a subsequent differentiation of these progenitors to lineage cellular populations in inflamed and/or damaged cells and tissues (13-15, 18), which is accompanied by the up-regulation of the innate immune systems due to high potential of activated macrophages (12, 18-19, 21) via the DMSP signaling through complex and yet unspecified ways."
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