Male infertility has become a global concern, accounting for 20-70% of infertility. Dysfunctional spermatogenesis is the most common cause of male infertility; thus, treating abnormal spermatogenesis may improve male infertility and has attracted the attention of the medical community. Mitochondria are essential organelles that maintain cell homeostasis and normal physiological functions in various ways, such as mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS transmits electrons through the respiratory chain, synthesizes adenosine triphosphate (ATP), and produces reactive oxygen species (ROS). These mechanisms are vital for spermatogenesis, especially to maintain the normal function of testicular Sertoli cells and germ cells. The disruption of mitochondrial OXPHOS caused by external factors can result in inadequate cellular energy supply, oxidative stress, apoptosis, or ferroptosis, all inhibiting spermatogenesis and damaging the male reproductive system, leading to male infertility. This article summarizes the latest pathological mechanism of mitochondrial OXPHOS disorder in testicular Sertoli cells and germ cells, which disrupts spermatogenesis and results in male infertility. In addition, we also briefly outline the current treatment of spermatogenic malfunction caused by mitochondrial OXPHOS disorders. However, relevant treatments have not been fully elucidated. Therefore, targeting mitochondrial OXPHOS disorders in Sertoli cells and germ cells is a research direction worthy of attention. We believe this review will provide new and more accurate ideas for treating male infertility.
Male ; Humans ; Infertility, Male/metabolism* ; Oxidative Phosphorylation ; Mitochondria/metabolism* ; Spermatogenesis/physiology* ; Sertoli Cells/metabolism* ; Oxidative Stress/physiology* ; Animals ; Reactive Oxygen Species/metabolism*

Objective To study the action and mechanism of Sancai Lianmei Particle on cell apoptosis of liver cells in Type 2 Diabetes Mellitus(T2DM)combined with Non-alcoholic Fatty Liver Disease(NAFLD).Methods High fat and sugar + STZ induced diabetic with fatty liver rats used as models,intervention with Sancai Lianmei Particle,intraperitoneal glucose tolerance test(IPGTT)to assess insulin resistance,ELISA method to detect the mice serum biochemistry,insulin levels;ELISA method to detect inflammatory factors in liver homogenate;SOD and MDA levels were monitored to assess the degree of oxidative stress;ASK1/JNK/NF-κB mRNA expression in liver tissue was monitored by Real-time PCR;apoptotic-related proteins were detected by Western blot,apoptosis of hepatocytes was assayed by TUNEL;HE staining was conducted to observe the liver tissue.Results Sancai Lianmei Particle can obviously reduce the body weight of T2DM with NAFLD model rats;reduce the levels of GHb,INS,TC,TG,LDL-C,ALT,AST,IL-1β,IL-6,TNF-α,MDA;improve insulin resistance and oxidative stress.HE staining of liver tissue showed that Sancai Lianmei Particle could alleviate the vacuolar degeneration of liver and deposition of lipid droplets.Sancai Lianmei Particle can effectively down-regulate the expressions of ASK1,JNK and NF-κB mRNA in liver tissues of model rats.Western Blot results exhibited that Sancai Lianmei Particle could significantly regulate the expression of apoptotic proteins of Bax,Caspase-3,and Bcl-2 and inhibit the apoptosis of hepatocytes.Conclusion This study proved that Sancai Lianmei Particle can improve hepatic insulin resistance and oxidative stress,slow the progression of NAFLD by regulating liver cell apoptosis based on ROS-ASK1-JNK/NF-κB pathway.