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The effects of vitamins and selenium mixture against brain tissue induced by d ‐galactosamine
Author(s) -
Tunali Sevim,
Catal Tunc,
Bolkent Sehnaz,
Yanardag Refiye
Publication year - 2019
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22347
Subject(s) - selenium , chemistry , brain tissue , galactosamine , food science , biochemistry , biophysics , medicine , biology , organic chemistry , glucosamine
Brain damage is a major complication of fulminant hepatic failure. d ‐Galactosamine ( d ‐GalN)‐induced liver toxicity causes damage to brain. The effects of vitamins and selenium mixture against d ‐GalN stimulated brain injury were investigated in this study. Sprague‐Dawley female rats aged 2.0‐2.5 months were used for the study. The rats were divided into four categories. A 0.9% NaCl solution was intraperitoneally given to the experimental rats in the first group. Using gavage technique, the second group of animals were subjected to a formulation consisting of 100 mg·kg −1 ·day −1 vitamin C, 15 mg·kg −1 ·day −1 of β‐carotene, 100 mg·kg −1 ·day −1 of α‐tocopherol in addition to 0.2 mg·kg −1 ·day −1 of sodium selenate for 3 days. The third group was given a single dose of d ‐GalN hydrochloride at the concentration of 500 mg·kg −1 through a saline injection. The final group was given similar concentrations of both the antioxidant combination and d ‐GalN. Tissue samples were collected under ether anesthesia. The rats treated with d ‐GalN showed brain damage; increased myeloperoxidase, catalase, glutathione peroxidase, glutathione‐S‐transferase, lactate dehydrogenase, and superoxide dismutase activities; and decreased glutathione levels. Treatment with vitamins and selenium combination resulted in alleviation of these alterations in the rats. These findings suggest that administration of the vitamins and selenium combination suppresses oxidative stress and protects brain cells from injury induced by d ‐GalN.