The effects of vitamins and selenium mixture against brain tissue induced byd‐galactosamine

Abstract

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.

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

“…[ 63 ] On the other hand, LDH levels of animals injected with 500 mg/kg GalN were found to be higher than that of control. [ 15 ] Present findings are consistent with previously published studies investigating the effects of GalN‐induced oxidative stress on different tissues of rats. [ 17,23 ] In this study, MMSC attenuated GalN‐mediated oxidative injury in brain and cerebellum tissues by not only decreasing activities of AChE, LDH, and XO but also increasing the activities of ArE and CA.…”

“…[ 43,44 ] In line with this, GSH levels were reported to decrease as a result of GalN‐mediated oxidative damage in the brain and lung tissues of rats. [ 15,21 ] In the present work, administration of MMSC gave rise to a progressive rise in the levels of GSH, and diminished AOPP levels‐an indication of a reduction in oxidative stress. The ability of MMSC treatment to restore of both GSH and AOPP levels may be attributed to its antioxidant capacity to neutralize ROS.…”

“…[ 14 ] It has recently been shown up that GalN‐mediated liver toxicity gave rise to brain injury via uncontrolled ROS formation. [ 15 ]…”

Gastroprotective effect of vitamin U in D‐galactosamine‐induced hepatotoxicity

“…LDH, a key enzyme for the last step of glycolysis, can be affected by the excessive ROS, or by the presence of GalN itself, as indicated in serum and tissue data of different studies. [ 12,54 ] According to the results, increased LPO and glycoprotein levels were detected which is explained by the decomposing of the membrane structure. This situation also affects membrane‐associated enzymes like Na + /K + ‐ATPase and GalN administration decreased its activity.…”

“…[8] The stomach is the most affected organ because of elevated ROS production caused by many drugs. [9] GalN has been noted to be a promoter for ROS production in different tissues [10][11][12] as well as causing organ damage.…”