Document Type : Original Article
Authors
1
physiology department, Faculty of vetrinary medicine, Cairo university, Egypt,Giza
2
physiology department, Faculty of vetrinary medicine, Cairo univerisity, Egypt, Giza
3
Pharmacology Department, Faculty of Veterinary Medicine, Cairo University, Egypt
4
Department of physiology, Faculty of veterinary medicine, Cairo university, 12211 Giza, Egypt
Abstract
Sodium valproate (SVP) is a commonly prescribed antiepileptic drug that has been associated with reproductive toxicity. The core objective of the current study is to evaluate the prospective role of oxidative stress in SVP-induced testicular damage and evaluate the protective effects of vitamin E supplementation. Male Wistar rats were divided into Control, SVP-treated, Vitamin E-treated, and SVP+Vitamin E-treated groups. Serum samples were collected to measure levels of testosterone, FSH, and LH hormones, and total antioxidant capacity (TAC). The testes were taken to determine their weight, semen analysis, redox status, and histopathological findings. The findings revealed that oral administration of SVP caused testicular degeneration, deteriorated spermatogenic parameters, elevation in Malondialdehyde (MDA) levels as well as depletion of reduced glutathione (GSH) levels and reduction of total antioxidant capacity (TAC) besides a decline in the activity of superoxide dismutase (SOD) and catalase (CAT) enzymes. The administration of Vit. E pretreatment in SVP-intoxicated rats has increased the relative weight of the tests as well as spermatogenic parameters. Serum testosterone and FSH hormonal levels were elevated. Testicular redox status and degenerative abnormalities were significantly improved. This study demonstrates that SVP administration induced testicular oxidative stress, leading to structural damage and impaired spermatogenesis. However, co-administration of vitamin E protects against SVP-induced damage via preserving testicular structure and function. These results advocate that vitamin E supplementation could have a therapeutic effect in mitigating reproductive toxicity associated with Sodium valproate (SVP) treatment. Further investigations are warranted to elucidate the underlying mechanisms and optimize the vitamin E supplementation dosage regimen in this context.
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