Effects of corticosterone and 2,3,7,8‐tetrachloro‐ dibenzo‐p‐dioxin on epididymal antioxidant system in adult rats

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an endocrine disruptor, causes epididymal toxicity by inducing oxidative stress. Glucocorticoids have been found to influence TCDD action in vitro and in vivo. The present experiments were set up to analyze the effects of TCDD on rat epididymal antioxidant system under the influence of increased corticosterone level. Adult male Wistar/NIN rats (70-80 days old) numbering 24 (six per group) were used in the study. Corticosterone (3 mg/kg body weight per day) or TCDD (100 ng/kg body weight per day) were administered or coadministered to rats for 15 days. Treatment with corticosterone or TCDD decreased the levels of serum testosterone significantly. In caput, corpus, and cauda fractions, administration of corticosterone or TCDD increased the levels of lipid peroxidation and hydrogen peroxide and decreased the activities of superoxide dismutase and catalase significantly. Coadministration of corticosterone and TCDD to rats decreased the levels of serum testosterone significantly as compared with rats treated with TCDD alone. In caput, corpus, and cauda fractions, the levels of lipid peroxidation and hydrogen peroxide were increased and activities of superoxide dismutase and catalase were decreased significantly as compared with rats treated with TCDD alone. Stress, characterized by increased glucocorticoid levels and activity, may enhance TCDD-induced epididymal toxicity.

Effect of exogenous testosterone on oxidative status of the testes in adult male rats

“…In contrast, exogenous testosterone seems to increase the oxidative stress via a decrease in intra‐testicular endogenous testosterone (Aitken & Shaun, ). Another study found that stress through increase in corticosterone decreases testosterone production and significantly increases the oxidative stress in the epididymis (Dhanabalan et al ., ). Whether the change in oxidative stress is casual due to decreased testosterone levels, or whether other mechanisms are involved, remains unknown.…”

Impact of adrenalectomy and dexamethasone treatment on testicular morphology and sperm parameters in rats: insights into the adrenal control of male reproduction

“…Although the role of the epididymis in facilitating sperm chromatin condensation is unclear, this organ possesses several antioxidant defense systems that may protect sperm DNA from the harmful effects of oxidative stress (Hinton et al, 1995). High glucocorticoid circulating levels induced by stress or treatment with corticosterone increased lipid peroxidation and hydrogen peroxide (H 2 O 2 ) formation, while decreased the activity of ROS scavenging enzymes in the rat testis, epididymis and in epididymal spermatozoa (Dhanabalan et al, 2010(Dhanabalan et al, , 2011(Dhanabalan et al, , 2013. Thus, it is possible that the excess of glucocorticoids may disrupt sperm DNA integrity by inducing oxidative stress during spermatogenesis and sperm maturation.…”

“…For example, it is well established that conditions associated with high levels of circulating glucocorticoids, as observed in stress, Cushing syndrome, and long-term therapy with synthetic glucocorticoids, disrupt male fertility (Gabrilove et al, 1974;Sapolsky, 1985;Cooke et al, 2004;Hardy et al, 2005). High plasma levels of glucocorticoids induce reproductive dysfunction by multiple mechanisms, such as suppression of testicular response to gonadotropins (Welsh et al, 1982;Sapolsky, 1985;Orr & Mann, 1992), down-regulation of genes encoding testosterone biosynthetic enzymes (Hales & Payne, 1989;Payne & Sha, 1991;Badrinarayanan et al, 2006), induction of Leydig cell and germ cell apoptosis (Yazawa et al, 2000;Gao et al, 2002Gao et al, , 2003, and induction of oxidative stress in the epididymis (Balasubramanian et al, 1987;Dhanabalan et al, 2010Dhanabalan et al, , 2011Dhanabalan et al, , 2013.…”

Immunolocalisation of 11β‐HSD‐1 and ‐2, glucocorticoid receptor, mineralocorticoid receptor and Na+K+‐ATPase during the postnatal development of the rat epididymis

“…Glucocorticoid and mineralocorticoid hormones can modulate a range of functions in the epididymis, including carbohydrate and lipid metabolism (Balasubramanian et al 1983, 1987), expression of secretory proteins (Courty, 1991), and ion and fluid transport (Munck et al 1984). Glucocorticoids have also been linked to oxidative stress through their effects on the antioxidant defence system (Dhanabalan et al 2010), and excess glucocorticoid exposure has been implicated in the overproduction of reactive oxygen species (Iuchi et al 2003; Ozmen, 2005; Bjelakovic et al 2007). As sperm have limited antioxidant defences of their own (Aitken & Delulis, 2010), the epididymis functions to protect sperm from the detrimental effects of oxidative stress through specialised antioxidant defence mechanisms (Veri et al 1994; Latchoumycandane et al 2002; Vernet et al 2004; Martin‐DeLeon, 2006).…”