RESUMO
Several causes of infertility have been identified, and several papers have documented some compounds that cause infertility. One of the compounds reported to be toxic to the reproductive system is cyanide. In the management of infertility, various mechanisms ranging from synthetic drugs, natural products and supplements have been employed. Quercetin is an antioxidant supplement that has been used in the treatment of a variety of ailments. This work is aimed at investigating the role of quercetin in attenuating spermato-toxicity and testicular-histopathology induced by cyanide. Seventy-two (72) male wistar rat (weight 190 g ± 10 g) were divided into nine groups (n = 8) except for groups 4 and 5 with (n = 16). Group 1 (control) received physiological saline while Groups 2 and 3 received 0.5 and 1 mg/kg body weight (bwt) cyanide respectively for 56 days, groups 4 and 5 received 0.5 and 1 mg/kg bwt cyanide respectively for 30 days. At day 30, eight animals were sacrificed from Groups 4 and 5 and the remaining eight (8) rats were subdivided into groups (6 and 7) and were given 20 and 40 mg/kg bwt of quercetin respectively for twenty-six days. Co-administration of cyanide and quercetin at a dose of 0.5 mg/kg cyanide +20 mg/kg quercetin and 1 mg/kg cyanide +40 mg/kg quercetin were given to group 8 and 9 respectively for 56 days. Significant decreases in sperm parameters (count, motile and normal sperm) and increases in malondiadehyde concentration were observed in the cyanide treated groups. Testicular histoarchitecture showed few to no spermatozoa in the lumen of rats treated with cyanide. All these effects were attenuated by quercetin. In conclusion, quercetin regulates testicular histopathology induced by cyanide in Wistar rats. Data from this work suggests potential preventive or therapeutic applications of quercetin for individuals subjected to cyanide environmental pollution.
RESUMO
Hibiscus sabdariffa (HS) is native to tropical and subtropical regions, and its enrichment as a source of antioxidants and phytoestrogen has been documented. The present study investigated effects of HS on ovarian toxicity induced by cadmium. Adult female Wistar rats were grouped into 4 (n=5/group): Group A received HS (100 mg/kg), group B received cadmium sulphate (5 mg/kg), group C received cadmium sulphate and HS, and group D (control) received 1 ml of distilled water. Cadmium sulphate was administered for five days (i.p) followed by oral administration of HS for 28 days. Results showed distortion in the cytoarchitecture of the follicular cells in the ovary of cadmium-treated rats while there was mild or no distortion recorded for the ovary of the rats treated with cadmium and HS. There was also a significant reduction in the serum level of Luteinizing and follicle stimulating hormone of the rats treated with cadmium (group B) when compared with control rats. However, these alterations were attenuated when treated with HS. We concluded that HS has an ovarian protective effect in cadmium-treated adult female rats. Hence the present results suggest that HS extract would be a potential therapeutic agent in ovarian dysfunction.