L-Carnitine Ameliorates Toxic Effect of Short- and Long-Time Use of Buprenorphine on Male Reproductive System in a Rat Model Publisher



Salehi M¹ ; Shirian S^{2, 3} ; Nazari H⁴ ; Ahmadi E⁴ ; Farahmandfar M¹ Show Affiliations
Source: Comparative Clinical Pathology Published:2024

Abstract

Stress-oxidative-induced sexual dysfunction has been widely reported to be associated with drug use disorders, particularly buprenorphine (Bu). This study aimed to evaluate the protective effect of L-carnitine (LC) in ameliorating stress-induced oxidative sexual dysfunction in a rat model of Bu addiction. Forty-eight adult male Wistar rats were randomly divided into three equal groups (n = 16) including the control (received tap water), Bu, and Bu + LC groups. On days 28 and 56 (as short and long time use of Bu, respectively) from the start of the study, eight rats from each group were randomly selected. Blood samples were collected for sex hormonal assays, including free testosterone (FT), total testosterone (TT), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) using ELISA. To analyze the sperm parameters, testicular anti-oxidant capacity, histological, immunohistochemical, and molecular analysis, the rats were sacrificed after collecting blood samples. The long-term Bu group exhibited the lowest sperm parameter index, mRNA and protein expression levels of BCL2, antioxidant activity, as well as the highest mRNA expression levels of caspase-3 and BAX, protein expression of BAX, and histological and hormonal changes. The LC + Bu group showed the higher and lower sperm parameter index, mRNA and protein expression level of BCL2, and antioxidant activity than those of the Bu and control groups, respectively. In addition, LC + Bu showed the lowest and highest mRNA expression levels of caspase-3 and BAX, protein expression of BAX, and histological and hormonal changes than those of the Bu and control groups, respectively. The administration of LC showed promising results in alleviating Bu-induced testicular degeneration by increasing testicular antioxidant capacity and inhibiting the apoptosis pathway. © The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature 2024.