Attenuation of sodium arsenite mediated ovarian DNA damage, follicular atresia, and oxidative injury by combined application of vitamin E and C in post pubertal Wistar rats.

Arsenic being a toxic metalloid ubiquitously persists in environment and causes several health complications including female reproductive anomalies. Epidemiological studies documented birth anomalies due to arsenic exposure. Augmented reactive oxygen species (ROS) generation and quenched antioxidant pool are foremost consequences of arsenic threat. On the contrary, Vitamin E (VE) and C (VC) are persuasive antioxidants and conventionally used in toxicity management. Present study was designed to explore the extent of efficacy of combined VE and VC (VEC) against Sodium arsenite (NaAsO2) mediated ovarian damage. Thirty-six female Wistar rats were randomly divided into three groups (Grs) and treated for consecutive 30 days; Gr I (control) was vehicle fed, Gr II (treated) was gavaged with NaAsO2 (3 mg/kg/day), Gr III (supplement) was provided with VE (400 mg/kg/day) & VC (200 mg/kg/day) along with NaAsO2. Marked histological alterations were evidenced by disorganization in oocyte, granulosa cells and zona pellucida layers in treated group. Considerable reduction of different growing follicles along with increased atretic follicles was noted in treated group. Altered activities ofΔ5 3ß-Hydroxysteroid dehydrogenase and 17ß-Hydroxysteroid dehydrogenase accompanied by reduced luteinizing hormone, follicle-stimulating hormone and estradiol levels were observed in treated animals. Irregular estrous cyclicity pattern was also observed due to NaAsO2 threat. Surplus ROS production affected ovarian antioxidant strata as evidenced by altered oxidative stress markers. Provoked oxidative strain further affects DNA status of ovary. However, supplementation with VEC caused notable restoration from such disparaging effects of NaAsO2 toxicities. Antioxidant and antiapoptotic attributes of those vitamins might be liable for such restoration.

Vitamin C and E supplementation can ameliorate NaF mediated testicular and spermatozoal DNA damages in adult Wistar rats.

OBJECTIVE: Present study was designed to explore the efficacy of vitamin C and E (VC&VE) against fluoride mediated testicular, epididymal and spermatozoal anomalies. MATERIALS AND METHODS: Thirty two adult Wistar rats were divided into four groups. Group-I was control; Group-II received sodium fluoride (NaF) at 15 mg/kg/day dose; Group-III was provided with VC (200 mg/kg/day) and VE (400 mg/kg/day) plus NaF; Group-IV received only VC&VE. Structural integrity and oxidative stress markers (superoxide dismutase, catalase, malondialdehyde and protein carbonyl) of testis and epididymis were assessed. Spermatozoal parameters (count, motility, viability and hypo-osmotic swelling) were evaluated. Testicular functional maker enzymes (acid phosphatase, alkaline phosphatase and lactate dehydrogenase) were also assessed. Integrity of testicular and spermatozoal DNA was evaluated. Testicular fluoride content was measured. RESULT: Fluoride induced structural changes and alterations of oxidative stress markers were observed in testis and epididymis. Spermatozoal potentials were altered and reduced activities of testicular functional marker enzymes were observed. Fluoride caused testicular and spermatozoal DNA damages. VC&VE supplementation resulted in protection from all fluoride mediated alterations and helped in attenuating testicular fluoride accumulation. CONCLUSION: Antioxidant properties of VC&VE ameliorated fluoride mediated reproductive damages but only supplementation did not exhibit any notable effect compared to control rats.