Table 1 Sources of reactive oxygen species (ROS), their mechanism of generation and effects on male reproductive hormones
From: Reactive oxygen species and male reproductive hormones
Sources of ROS | Mechanism of ROS generation | Effects on male reproductive hormones |
|---|---|---|
Exogenous sources | ||
 Psychological stress | By increasing stress hormone (cortisol) levels and activating the immune–inflammatory system | Decreases serum testosterone and LH levels by suppressing androgen synthesis and inducing Leydig cells apoptosis |
 Heat stress | By decreasing antioxidant enzyme activities, increasing NADPH oxidase activity and disrupting mitochondrial homeostasis | Disrupts Sertoli cell functions, decreases testosterone and LH levels |
 Environmental toxicants | By activating inflammatory mechanisms and cellular death | Decreases Leydig and Sertoli cell functions, hormonal biosynthesis |
 Electromagnetic radiations | By decreasing total antioxidant capacity | Decreases serum testosterone and LH levels |
 Long-term heavy exercise | By stimulating mitochondrial enzymes including NOX and XO | Decreases LH, FSH, and testosterone levels |
 Obesity | By increasing leptin levels in human endothelial cells and increasing mitochondrial fatty acid oxidation | Activation of the HPG axis stimulates FSH and LH release. Leptin can directly affect the gonads due to its receptor isoforms in gonadal tissue and stimulate steroid secretion, through increasing the GnRH |
 High-fat and high-protein food | By decreasing natural food antioxidants and free radical scavengers | Decreases testosterone biosynthesis, LH secretion and androgen profile |
 Alcohol | By stimulating cytochrome P450s enzyme activities in the liver, altering levels of necessary metals in the body, and reducing antioxidant levels | Increases Sertoli cells and Leydig cells apoptosis, reduces serum testosterone, LH and FSH levels |
 Marijuana and narcotic drugs | By increasing inflammation and cytochrome p53-induced apoptotic cell death | Inhibits GnRH release and LH production, inhibits HPG axis, reduces testosterone level, and increases SHBG level |
 Smoking | By decreasing oxygen delivery to the testis and the high metabolic requirements of spermatogenesis, releasing a large number of mutagens and metabolites, weakening of the antioxidant defense systems. Stimulation of NOX enzymes | Alters plasma levels of testosterone, prolactin, estradiol, FSH, LH and SHBG by affecting the Leydig and Sertoli cells |
 Anabolic steroids | By stimulating mitochondrial respiratory chain complexes, inflammatory cytokine release and cellular apoptosis | Disrupts Leydig cell functions, suppresses HPG axis, reduces LH release and thus testicular testosterone biosynthesis |
Endogenous sources | ||
 Aging | By decreasing the activities of antioxidant enzymes, alteration in the mitochondrial membrane potential | Increases lipid peroxidation of Leydig cells, LH sensitivity by diminishing LH receptors, reduces the rate of steroidogenesis, testosterone biosynthesis and secretion |
 Infections of the reproductive tract | Bacterial strains that colonize the male reproductive tract causes inflammatory damage by inducing leukocyte migration, release of cytokines and other inflammatory mediators, activation of macrophages, lymphocytes and other immunoreactive cells | Reduces serum testosterone levels by disrupting the hormonal axis, increase in LH and FSH levels |