Oxidative brain and cerebellum injury induced byd‐galactosamine: Protective effect ofS‐methyl methionine sulfonium chloride

Abstract

The objective of this study was to examine the protective effects of S-methyl methionine sulfonium chloride (MMSC) against galactosamine (GalN)-induced brain and cerebellum injury in rats. A total of 22 female Sprague-Dawley rats were randomly divided into four groups as follows: Group I (n = 5), intact animals; Group II (n = 6), animals received 50 mg/kg/day of MMSC by gavage technique for 3 consecutive days; Group III (n = 5), animals injected with a single dose of 500 mg/kg of GalN intraperitoneally (ip); and Group IV (n = 6), animals injected with the same dose of GalN 1 h after MMSC treatment. After 6 h of the last GalN treatment (at the end of the experiments), all animals were killed under anesthesia, brain and cerebellum tissues were dissected out. Reduced glutathione, total antioxidant status levels, and antioxidant enzymes (catalase, superoxide dismutase, and glutathionerelated enzymes), aryl esterase, and carbonic anhydrase activities remarkably declined whereas advanced oxidized protein products, reactive oxygen species, total oxidant status, oxidative stress index levels, and myeloperoxidase, acetylcholinesterase, lactate dehydrogenase, and xanthine oxidase activities were significantly elevated in the GalN group compared with intact rats. In contrast, the administration of MMSC to GalN groups reversed these alterations. In conclusion, we may suggest that MMSC has protective effects against GalN-induced brain and cerebellar toxicity in rats.galactosamine, brain and cerebellum, antioxidant effect, oxidative stress, S-methyl methionine sulfonium chloride | INTRODUCTIONGalactosamine (GalN) is an important amino derivative of D-galactose, it is extremely toxic when excessively formed or accumulated in an organism.In experimental animal models, it acts as a hepatotoxin and triggers hepatocellular damage and inflammation. [1][2][3] GalN interacts with uracilcontaining nucleotides in hepatocytes, thereby causing clinically similar effects like that of viral hepatitis and hepatic necrosis. [4] The resultant liver dysfunction may affect more than 500 metabolic processes, compromise detoxification processes, and thereafter result in the damage

Purification and characterization of thioredoxin reductase enzyme from commercial Spirulina platensis tablets by affinity chromatography and investigation of the effects of some chemicals and drugs on enzyme activity

“…39 In some in vitro studies, vitamin U exhibited protective effect, such as in pentylenetetrazole-induced brain damage, 40 d-galactosamine-induced hepatotoxicity, 41 valproic acid-induced lens injury, 42 and in oxidative brain and cerebellum damage induced by d-galactosamine. 43 In the present research, vitamin B 6 exhibited the lowest IC 50 value for TrxR inhibition activity among tested vitamins. The amounts of vitamin B 3 , vitamin B 6 , vitamin C, and vitamin U required for 50% inhibition effects were 582.…”

“…Due to its sulfonium functional group, this cation is an intermediate in several metabolic processes 39 . In some in vitro studies, vitamin U exhibited protective effect, such as in pentylenetetrazole‐induced brain damage, 40 d ‐galactosamine‐induced hepatotoxicity, 41 valproic acid‐induced lens injury, 42 and in oxidative brain and cerebellum damage induced by d ‐galactosamine 43 . In the present research, vitamin B 6 exhibited the lowest IC 50 value for TrxR inhibition activity among tested vitamins.…”

Association between human blood metabolites and cerebral cortex architecture: evidence from a Mendelian randomization study

“…Therefore, it protects the cerebral cortex from mitochondrial damage and oxidative stress ( 17 ). Mahmarzayeva et al ( 18 ) revealed that methionine metabolites could protect against galactosamine-induced encephalotoxicity by reversing the antioxidant enzyme content and antioxidant status levels. In addition, existing research has confirmed that heavy metal deposits, such as Pb and Ni, can lead to a reduction in the volume of the cerebral cortex.…”

Oxidative Brain Injury Induced by Amiodarone in Rats: Protective Effect of S‐Methyl Methionine Sulfonium Chloride

“…6,[12][13][14][15][16] In addition, the most amazing and breath-taking attention of this sulfur containing compound is its antioxidant property, which has been proven by many researchers. [17][18][19] In the current study, the protective effects of MMSC on amiodarone induced brain damage was investigated.…”