vitamin-u and Brain-Injuries

Amiodarone (AMD) is a powerful antiarrhythmic drug preferred for treatments of tachycardias. Brain can be affected negatively when some drugs are used, including antiarrhythmics. S-methyl methionine sulfonium chloride (MMSC) is a well-known sulfur containing substance and a novel powerful antioxidant. It was intended to investigate the protective effects of MMSC on amiodarone induced brain damage. Rats were divided to four groups as follows, control (given corn oil), MMSC (50 mg/kg per day), AMD (100 mg/kg per day), AMD (100 mg/kg per day) + MMSC (50 mg/kg per day). The brain glutathione and total antioxidant levels, catalase, superoxide dismutase, glutathione peroxidase, paraoxonase, and Na+/K+-ATPase activities were decreased, lipid peroxidation and protein carbonyl, total oxidant status, oxidative stress index and reactive oxygen species levels, myeloperoxidase, acetylcholine esterase and lactate dehydrogenase activities were increased after AMD treatment. Administration of MMSC reversed these results. We can conclude that MMSC ameliorated AMD induced brain injury probably due to its antioxidant and cell protective effect.

Topics: Amiodarone; Animals; Antioxidants; Brain; Brain Injuries; Chlorides; Glutathione; Oxidative Stress; Rats; Rats, Wistar; Superoxide Dismutase; Vitamin U

Pentylenetetrazole (PTZ) is preferred for experimental epilepsy induction. PTZ damages brain and other organs by elevating oxidative substances. Vitamin U (Vit U) is sulfur derivative substance that proved to be an excellent antioxidant. The current study was intended to determine the protective role of Vit U on PTZ-induced brain damage. Male Sprague-Dawley rats were separated into four groups. The Control group (Group I), was given saline for 7 days intraperitoneally (i.p); Vit U (Group II) was given as 50 mg/kg/day for 7 days by gavage; PTZ was injected into animals (Group III) at a single dose of 60 mg/kg, by i.p; PTZ + Vit U group (Group IV) was administered PTZ and Vit U in same dose and time as aforementioned. After the experiment was terminated, brain tissues were taken for the preparation of homogenates. In the PTZ group, glutathione and lipid peroxidation levels, alkaline phosphatase, myeloperoxidase, xanthine oxidase, acetylcholine esterase, antioxidant enzyme activities, total oxidant status, oxidative stress index, reactive oxygen species, and nitric oxide levels were increased. However, total antioxidant capacity was decreased in the PTZ group. Vit U ameliorated these effects in the PTZ-induced brain damage. Consequently, we can suggest that Vit U protected brain tissue via its antioxidant feature against PTZ kindling epilepsy.

Topics: Alkaline Phosphatase; Animals; Antioxidants; Brain; Brain Injuries; Epilepsy; Glutathione; Male; Nitric Oxide; Oxidants; Oxidative Stress; Pentylenetetrazole; Peroxidase; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Sulfur; Vitamin U; Xanthine Oxidase