α-tocopherol attenuates acetaminophen-induced testicular dysfunction in adult male rats

Abstract

BACKGROUND: Acetaminophen (Paracetamol) is a widely used over-the-counter analgesic and an antipyretic drug known to inhibit cyclooxygenase II enzyme paramount in the prostaglandin synthesis and essential for normal male reproductive function. α-tocopherol (Vitamin E), an antioxidant has been used in the management of a number of conditions including infertility. However, there is a dearth of information on the role of α-tocopherol in the management of testicular dysfunction. This study was designed to investigate the ameliorative effect of α-tocopherol in acetaminophen-induced testicular dysfunction. MATERIALS AND METHODS: Adult male Wistar rats were randomly allotted into groups; Control 1 (vehicle 1; received 0.2 ml of olive oil), Control 2 (vehicle 2; received 0.2 ml of distilled water), acetaminophen- treated (ACE-treated; received 500 mg/kg b. w), α-tocopherol-treated (AT-treated; received 100 mg/kg b. w), and α-tocopherol + acetaminophen-treated (AT + ACE-treated). The treatment lasted for 14 days, and the administration was given orally. The body weight change was monitored using animal weighing balance (Olympia SCL66110 model, Kent Scientific Corporation, Torrington, CT06790, USA), semen analysis and biochemical assay were performed. RESULTS: The results showed a significant increase in body weight gain and significant alteration of spermatozoa integrity in the acetaminophen-treated group when compared to the vehicle-treated groups. These alterations were associated with decreased hypophyseal-gonadotropic hormones, testosterone, and increased testicular tissue oxidative redox status. Concomitant administration of α-tocopherol during treatment with acetaminophen ameliorated the alterations. CONCLUSION: The present study demonstrates that administration of α-tocopherol during treatment with acetaminophen preserves testicular function. This might be due to its antioxidative effect and enhancement of hypophyseal-gonadotropic hormone secretion.