Protective role of Actovegin against Cisplatin-evoked testicular damage: evidence from a rat model.

Abstract

Testicular dysfunction and infertility are major concerns for men on Cisplatin. Excess reactive oxygen species produced by Cisplatin cause oxidative stress, impairing sperm quality. Actovegin is a deproteinized calf blood extract containing more than 200 bioactive components that may affect multiple biochemical and signaling pathways. Consequently, this study examines Actovegin's protective effects against Cisplatin -induced testicular toxicity and its potential to reduce oxidative stress. This study used 24 male Wistar rats, divided into 3 groups of 8 rats each. Sixteen rats received intraperitoneal Cisplatin to induce testicular injury on days 6, 13, and 20. Eight of these rats received saline five days before the first Cisplatin dose and for 21 days afterward. In contrast, eight rats received Actovegin daily, starting five days before the first Cisplatin dose and continuing until day 21. Additionally, normal control rats received saline daily for 26 days. Blood, semen, and testes were collected on the 22nd day after Cisplatin administration to assess testicular weight and length and to perform biochemical analyses of testosterone levels, inflammatory markers, and oxidative and antioxidant indicators. Histopathological examination of testicular specimens was performed, and semen was also analyzed. In addition to mitigating inflammation, reducing oxidative stress, and improving semen quality, Actovegin increased testicular weight and length compared to the untreated Cisplatin -exposed group. Moreover, it restored the normal testicular morphology and architecture. Actovegin efficiently reduces Cisplatin -induced testicular dysfunction by controlling oxidative stress, suggesting that it may be a preventive therapy against Cisplatin -related infertility.