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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