Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5559970 | Food and Chemical Toxicology | 2017 | 12 Pages |
â¢Prepubertal exposure to rosuvastatin diminished sperm quality and increased sperm DNA fragmentation at adulthood.â¢Rosuvastatin exposure at prepuberty impaired testicular and epididymal morphology and reduced serum testosterone concentrations during sexual maturity.â¢Exposure to the higher dose of rosuvastatin provoked augmented post-implantation loss after natural mating.â¢Ascorbic acid supplementation alleviated the reproductive damage induced by rosuvastatin.
Pediatric obesity is closely associated with dyslipidemias and environmental factors, such as diet and lack of physical exercises, which may alter lipid profile in children. Rosuvastatin decreases serum total cholesterol and triglycerides concentrations. Vitamin C (ascorbic acid) plays an important role on sperm integrity and fertility. Juvenile male rats were distributed into six experimental groups that received saline solution 0.9%, 3 or 10Â mg/kg/day of rosuvastatin, 150Â mg/day of ascorbic acid, or 3 or 10Â mg/kg/day of rosuvastatin co-administered with 150Â mg/day of ascorbic acid from PND23 until PND53 and then the rats were maintained until sexual maturity. Rosuvastatin-exposed groups showed lower sperm quality, androgen depletion and germ cell death. Ascorbic acid was capable to prevent partially the reproductive adverse effects provoked by rosuvastatin. In conclusion, prepubertal exposure to rosuvastatin provokes long-term reproductive damages at sexual maturity and ascorbic acid supplementation at prepuberty may be a preventive mode against these reproductive adverse effects.