vitamin b ameliorates sodium fluoride induced oxidative stress in wistar rats

Background: exposure to sodium fluoride (naf) via sources such as the environment, use of toothpaste, and pesticides causes toxicity in the liver, kidneys, and brain, where it induces oxidative stress. vitamin b plays an important role in the body by participating in metabolism and scavenging free radicals, thereby protecting the body against oxidative stress. therefore, the present study aimed to determine the ameliorative effect of vitamin b on naf-induced hepato-renal and brain damage.methods: a total of 20 adult male wistar rats were used for the experiment. they were randomly divided into four groups of five rats each. g group i was administered distilled water, group ii received naf at 600 ppm, group iii received naf at 600 ppm plus vitamin b (10 ml/kg/day), and group iv was administered vitamin b (10 ml/kg/day) orally, daily for four weeks. hematology, serum biochemical markers, and oxidative stress markers in the liver, kidneys, and brain were analyzed. results: the wbc, rbc, pcv, and hemoglobin were decreased in the naf group. moreover, serum alt, ast, alp, urea, and creatinine were significantly increased (p<0.05). there was a significant decrease (p<0.05) in catalase, glutathione peroxidase, and superoxide dismutase levels in the liver, kidneys, and brain. in addition, there was a significant increase (p<0.05) in liver, kidney, and brain malondialdehyde (mda) in the naf group compared to other groups. conclusion: the administration of vitamin b alone did not cause any biochemical alterations in the liver, kidney, or brain. co-administration of naf and vitamin b for four weeks ameliorated the oxidative changes induced by naf in the liver, kidney, and brain.