co-administration of vitamin e and homtamin ginseng prevented and reversed sodium fluoride-induced testicular dysfunction through inhibition of oxidative influx and hormonal modulation mechanism in wistar rats

Background: reproductive damage from sodium fluoride exposure is a concern, but there’s limited scientific data on the synergistic effect of homtamin ginseng and vitamin e. a potential remedy could include homtamin ginseng and vitamin e supplementation, but further research is needed. this research was conducted to investigate the effects of homtamin ginseng and vitamin e on the reproductive damage induced by sodium fluoride exposure. different treatment protocols were employed, such as administering drugs alone, preventive measures, and reversal approaches. methods: in the drug alone or preventive-protocol, rats received oral treatment of saline (2 ml/kg), homtamin ginseng (40 mg/kg/day), vitamin e (150 mg/kg/day) or both alone repeatedly for 28 days, or in combination with sodium fluoride (100 ppm/kg/p.o./day) from days 15-28. in the reversal-protocol, the animals received naf for 28 days prior to saline, homtamin ginseng, vitamin e or homtamin ginseng + vitamin e from days 15-28. results: the result showed a (p < 0.05) increase in testicular malondialdehyde and a decrease in the activities of testicular superoxide dismutase, catalase and glutathione peroxidase in the group exposed to sodium fluoride. these changes were significantly (p < 0.05) ameliorated by vitamin e and homtamin ginseng. more so, sodium fluoride altered testicular and brain weight, spermatogenesis, hormonal profile, fertility test as well as testicular architecture negatively following treatment with sodium fluoride. however, homtamin ginseng and vitamin e or combination of both prevented and reversed the effects of sodium fluoride on spermatogenesis, hormonal profile, fertility and mating indices in rats. conclusion: in conclusion, homtamin ginseng and vitamin e prevented and reversed sodium fluoride-induced testicular dysfunction through inhibition of oxidative influx and hormonal modulation mechanism in wistar rats.