Methylmethionine sulfonium chloride
January 20 2016

This nutrient is used for ulcer treatment. S-Methylmethionine is sometimes called vitamin U but it is not recognized as a vitamin by traditional nutrition science.

Protoplasma. 2015. Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties. The aim of present study was to investigate the effect of vitamin U (vit U, S-methylmethionine) on oxidative stress, inflammation, and fibrosis within the context of valproic acid (VPA)-induced renal damage. In this study, female Sprague Dawley rats were randomly divided into four groups: Group I consisted of intact animals, group II was given vit U (50 mg/kg/day, by gavage), group III was given VPA (500 mg/kg/day, intraperitonally), and group IV was given VPA + vit U. The animals were treated by vit U 1 h prior to treatment with VPA every day for 15 days. The following results were obtained in vit U + VPA-treated rats: (i) the protective effect of vit U on renal damage was shown by a significant decrease in histopathological changes and an increase in Na+/K+-ATPase activity; (ii) anti-oxidant property of vit U was demonstrated by a decrease in malondialdehyde levels and xanthine oxidase activity and an increase in glutathione levels, catalase and superoxide dismutase activities; (iii) anti-inflammatory property of vit U was demonstrated by a decrease in tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1 levels, and adenosine deaminase activity; (iv) anti-fibrotic effect of vit U was shown by a decrease in transforming growth factor-β, collagen-1 levels, and arginase activity. Collectively, these data show that VPA is a promoter of inflammation, oxidative stress, and fibrosis which resulted in renal damage. Vitamin U can be proposed as a potential candidate for preventing renal damage which arose during the therapeutic usage of VPA.

Pharmacology. 1992. Sulphydryl-containing agents stimulate the healing of duodenal ulceration in man.
This prospective randomized double-blind study examined whether sulphydryl-containing agents stimulate the healing and prevent the recurrence of duodenal ulceration in man. To this end, DL-methionine methyl sulphonium chloride (MMSC, 500 mg four times daily) or DL-cysteine (200 mg four times daily) were orally administered with cimetidine. Symptomatic endoscopy-proven duodenal ulcer patients who were smokers and social drinkers were randomized to receive for 8 weeks cimetidine (400 mg b.d.), cimetidine (400 mg b.d.) with MMSC, or cimetidine (400 mg b.d.) with cysteine. These patients were then kept on their respective oral regimens (except for cimetidine which was changed to 400 mg at bedtime) for 1 year (maintenance) and followed up for another. After 8 weeks of treatment, the ulceration healed in 65 patients (74%) given cimetidine alone but in all the patients given MMSC (n = 87) or cysteine (n = 86) with cimetidine. During the maintenance year, 15 patients (29%) given cimetidine at night relapsed. Addition of MMSC or cysteine to cimetidine incurred a significantly lower relapse rate. During the year following maintenance therapy, the relapse rate in the group that had been previously treated with cimetidine alone (63%, n = 51) was significantly (p less than 0.001) higher than that in the groups previously treated with MMSC and cimetidine (6%, n = 67) or cysteine with cimetidine (6%, n = 64). The results suggest that sulphydryl-containing agents stimulate the healing and protect against the recurrence of duodenal ulceration.

Can J Surg. 1993. Sulfhydryl-containing agents in the treatment of gastric bleeding induced by nonsteroidal anti-inflammatory drugs.
In a double-blind study involving 172 patients, the author investigated the effect of sulfhydryl-containing agents (cysteine and methylmethionine sulfonium chloride [MMSC]) on hematemesis resulting from erosive gastritis induced by nonsteroidal anti-inflammatory drugs. The 56 patients who received cysteine (200 mg orally four times a day) and the 59 patients who received MMSC (500 mg orally four times a day) were significantly more hemodynamically stable, with no rebleeding, than the 57 patients who made up a control group. Endoscopy carried out 48 hours after admission demonstrated that gastric erosions were still present in a significantly higher number of patients in the control group (20 [35%]) than in patients receiving cysteine (6 [11%]) and in patients receiving MMSC (7 [12%]). Eighteen patients (32%) in the control group required blood transfusion because of continued bleeding or rebleeding compared with only 3 patients (5%) receiving cysteine and 2 patients (3%) receiving MMSC. Emergency surgery was necessary in 13 patients (23%) in the control group and in 1 patient (2%) in the group receiving cysteine who had rebleeding. Four patients in the control group died postoperatively. The results show that sulfhydryl-containing agents stimulate the healing of erosive gastritis induced by nonsteroidal anti-inflammatory drugs and protect against the complications of bleeding produced by the gastritis.

Pharmacology. 1992.
Role of sulphydryl-containing agents in the management of recurrent attacks of ulcerative colitis. A new approach.
This double-blind randomised study investigated the role of sulphydryl-containing agents in the management of recurrent attacks of ulcerative colitis. To this end, DL-cysteine (200 mg 4 times daily) and DL-methionine-methyl sulphonium chloride (MMSC, 500 mg 4 times daily) were administered orally. Patients with recurrent attacks of moderate proctosigmoidal ulcerative colitis, despite prophylaxis by oral sulphasalazine (2 g daily), were given prednisolone by mouth, 10 mg four times a day, sulphasalazine by mouth, 500 mg four times a day, and morning and evening retention enema (Predsol 20 mg) alone or with cysteine or MMSC. After 2 weeks of treatment with sulphasalazine and prednisolone, 51% of patients (n = 45) were symptom free. Addition of cysteine (n = 46) or MMSC (n = 47) to this regimen controlled the symptoms within 2 weeks in 85% of patients. During 12 months of prophylactic treatment, 5% of patients (n = 42) receiving sulphasalazine (2 g daily) and cysteine and 5% of patients (n = 41) taking sulphasalazine (2 g daily) and MMSC relapsed, relative to 27% of cases with sulphasalazine (2 g daily) alone. These results demonstrate that sulphydryl-containing agents play a key role in the treatment of and protection against ulcerative colitis.

J Gastroenterol Hepatol. 2009.
Effects of combination treatment with famotidine and methylmethionine sulfonium chloride on the mucus barrier of rat gastric mucosa.
In the present study, the effects of co-administration of methylmethionine sulfonium chloride (MMSC) and famotidine on rat gastric mucus cells were investigated using both biochemical and histological methods. Rats were divided into four groups: controls were given carboxymethylcellulose orally once daily for 7 days and the second, third and fourth groups were treated similarly with famotidine (famotidine group), MMSC (MMSC group) or famotidine plus MMSC (combination group). After killing the rats on the 8th day, the stomachs were removed and the biosynthesis and amount of mucin in different areas of the gastric mucosa were compared among groups. Using anti-mucin monoclonal antibodies, the mucin content and immunoreactivity were also compared. Both the biosynthesis and accumulation of mucin were significantly decreased in the famotidine group, but increased in the MMSC and combination groups. The amount and immunoreactivity of surface mucus cell-derived mucin were both reduced in the famotidine group, and increased in the MMSC and combination groups. There was no difference among the groups in the content and immunoreactivity of gland mucus cell-derived mucin. Famotidine-induced suppression of gastric surface mucus cell function is prevented by combined treatment with MMSC, raising the possibility of a more effective cure of PUD.

Food Chem Toxicol. 2012. Effects of vitamin U (S-methyl methionine sulphonium chloride) on valproic acid induced liver injury in rats.S In this study, we aimed to investigate the effects of vitamin U (Vit U) on valproic acid (VPA)-induced liver damage. Female Sprague Dawley rats were randomly divided into four groups. Group I was intact control animals. Group II was control rats given Vit U (50 mg/kg/day) for fifteen days. Group III was given only VPA (500 mg/kg/day) for fifteen days. Group IV was given VPA+Vit U (in same dose and time). Vit U was given to rats by gavage and VPA was given intraperitoneally. On the 16th day of experiment, all the animals were fasted overnight and then sacrificed under ether anesthesia. Liver tissue was taken from animals, homogenized in 0.9% saline to make up to 10% homogenate. Liver aspartate and alanine transaminases, alkaline phosphatase, lactate dehydrogenase, myeloperoxidase, sorbitol dehydrogenase, glutamate dehydrogenase and xanthine oxidase activities and lipid peroxidation levels were increased and paraoxonase activity and glutathione levels were decreased in VPA group. Treatment with Vit U reversed these effects. These results demonstrated that administration of Vit U is a potentially beneficial agent to reduce the liver damage in VPA induced hepatotoxicity, probably by decreasing oxidative stress.