Hepatitis B virus surface protein induces oxidative stress by increasing peroxides and inhibiting antioxidant defences in human spermatozoa

作者：Lin Cheng, Pingnan Sun, Xiaoling Xie, Dongmei Sun, Qi Zhou, Shaozhe Yang, Qing‐Dong Xie, Xiaoling Zhou · 发表于：Reproduction Fertility and Development · 年份：2020 · DOI：10.1071/rd20130 · 被引用次数：13 · 研究领域：Hepatitis B Virus Studies、Sperm and Testicular Function、Hepatitis Viruses Studies and Epidemiology

Hepatitis B virus (HBV) infection may affect sperm motility in patients with HBV. HBV surface protein (HBs) decreases mitochondrial membrane potential, impairs motility and induces apoptotic-like changes in human spermatozoa. However, little is known about how human spermatozoa respond to reactive oxygen species (ROS; mainly peroxides) induced by HBs. In this study, HBs induced supraphysiological ROS levels in human spermatozoa and reduced the formation of 2-cell embryos (obtained from hamster oocytes and human spermatozoa). HBs induced a pre-apoptotic status in human spermatozoa, as well as antioxidant defences by increasing glutathione peroxidase 4 (GPX4) and peroxiredoxin 5 (PRDX5) levels. These results highlight the molecular mechanism responsible for the oxidative stress in human spermatozoa exposed to HBV and the antioxidant defence response involving GPX4 and PRDX5.