TCDD and corticosterone on testicular steroidogenesis and antioxidant system of epididymal sperm in rats

Abstract

2,3,7,8-Tetrachloro dibenzo-p-dioxin (TCDD), an endocrine-disrupting environmental pollutant, has been found to cause male reproductive toxicity. Glucocorticoids have been found to influence the metabolic pathway of TCDD. Stress, which affects the male reproductive function, is marked by an increase in the level and activity of glucocorticoids in the body. The present study was carried out to understand the effect of TCDD on testicular steroidogenesis and sperm antioxidant system under the influence of increased level of corticosterone in the body. Adult male rats were treated with either TCDD (100 ng/kg bw/ day) or corticosterone (3 mg/kg bw/day) or both for 15 days. Treatment with either TCDD or corticosterone was found to suppress the levels of steroidogenic acute regulatory protein and androgen-binding protein and reduce the activities of steroidogenic enzymes in testis while increasing oxidative stress in ventral prostate, seminal vesicles and epididymal sperm. In rats treated with both TCDD and corticosterone, the suppression of testicular steroidogenesis and increase in oxidative stress observed in ventral prostate, seminal vesicles and epididymal sperm were significant as compared to TCDD alone treated rats. The levels of Fas and FasL proteins were also increased in rats subjected to either TCDD or corticosterone treatment. In rats treated with both compounds, the increase observed in testicular levels of Fas and FasL was significant as compared to TCDD alone treated rats. Effect of TCDD on testicular steroidogenesis and antioxidant system of epididymal sperm may get enhanced under increased level of glucocorticoids in the body.

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.…”

Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

“…We previously reported that prenatal exposure to dexamethasone (DEX), a widely used synthetic glucocorticoid, induced programmed hypertension in adult offspring [6,7]. Glucocorticoids have been found to influence the metabolic pathway of TCDD [8]. On the other hand, both glucocorticoids and TCDD can activate the aryl hydrocarbon receptor (AHR) signaling pathway [9,10].…”

Effects of dioxin on testicular histopathology, sperm parameters, and CatSper2 gene and protein expression in Naval Medical Research Institute male mice

“…One of the possible mechanisms is that dioxin has oestrogenic activity and it causes disruption in hormonal signalling pathways. Therefore, it affects the sperm parameters through effect on hormone levels (Dhanabalan, Mathur, & Latha, ). In addition, dioxin increases sperm injury by increasing the free radical levels (Ciftci, Aydin, Ozdemir, & Vardi, ).…”