Fig. 1

Sources of reactive oxygen species (ROS) and their impact on the complex endocrine network regulating male reproduction. a High levels of ROS impact upon the HPG axis which results in decreased secretion of male reproductive hormones. b Through the HPA axis, ROS increases the release of the stress hormone cortisol, which through the HPA-HPG axes cross-talk, further decreases LH secretion. c Elevated ROS also affects the HPT axis which results in decreased T3 production from the thyroid gland, which through the cross-talk between HPT and HPG axes, again decreases testosterone synthesis. ROS also affects the other endocrine glands which interfere with these endocrine axes to result in decreased testosterone production. Increased oxidative stress (OS), in different conditions, decreases insulin production from the pancreas which again reduces T3 production from the thyroid gland and through HPT-HPG axes cross-talk decreases testosterone biosynthesis. ROS production in obesity also increases circulating leptin levels which directly reduces testosterone synthesis in the testis. Reduced melatonin in OS, and increased production of pro-inflammatory cytokines during reproductive tract infections, affects the HPG axis to reduce testosterone biosynthesis. OS also increases prolactin secretion from the anterior pituitary and E2 synthesis from the testis. These two hormones reduce GnRH secretion from the hypothalamus and testosterone biosynthesis from the testis, respectively