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Objective: To investigate the potential of N-acetylcysteine (NAC) and zinc sulphate (ZnSO4) in mitigating reproductive dysfunction caused by di-2-ethylhexyl phthalate (DEHP) in rats and to understand the underlying mechanisms, specifically oxidative stress and sex hormone receptor activity. Methods: Thirty-five male Wistar rats were randomly divided into five equal groups (n=7 per group). Group 1 was administered 0.5 mL of distilled water and served as the control group. Group 2 was given only DEHP (750 mg/kg/day), while group 3, 4 and 5 were given DEHP (750 mg/kg/day) plus NAC (100 mg/kg/day), DEHP (750 mg/kg/day) plus ZnSO4 (0.5 mg/kg/day), and DEHP (750 mg/kg/day) plus NAC (100 mg/kg/day) as well as ZnSO4 (0.5 mg/kg/day), respectively. All treatments lasted for 21 days. Samples were obtained after the rats were sacrificed, and hormones levels in the serum and markers of oxidative stress in the testicles were analyzed using the enzyme-linked immunosorbent assay. The amount of androgen receptors in the testicles was determined by immunohistochemistry, and the susceptibility of testosterone and DEHP to bind to androgen receptor and 5α-reductase was determined by molecular docking studies. Results: DEHP decreased reproductive hormones, testicular antioxidant enzymes, increased malondialdehyde levels, and negatively impacted histology of the pituitary and testes. NAC or ZnSO4 treatment showed a marked improvement in testicular antioxidant status and hormone levels, as well as a positive effect on the histology of the pituitary and testes. The combination of both treatments appeared to be more effective. The affinity of DEHP to bind to androgen receptors may lead to disruption of androgen receptor signaling, which can further result in dysfunction of hormones related to androgen. However, NAC is more likely to form stronger binding interactions with follicle stimulating hormone and luteinizing hormone receptors, as well as gonadotropin-releasing hormone receptors, when compared to DEHP. Conclusions: The possibility that NAC and ZnSO4 could downregulate DEHP-induced sex hormone changes is suggested by their potential to reduce toxicity.

Conclusion: Treatment with Zn and/or vitamin E reverses BLCO-induced neurobehavioural alterations via modulation of oxidative stress, inflammation and neurotransmitters.

Abstract Background Heavy metals are well documented to induce reproductive toxicity. This study was designed to investigate the role of vitamin E and quercetin on reproductive toxicity mediated by lead acetate in male Wistar rats. Thirty male adult Wistar rats were grouped into six (n = 5 per group) as follows: Group 1 (Control); Group 2 and 3 were administered with 100 mg/kg vitamin E and quercetin, respectively; Group 4 was administered with 30 mg/kg lead acetate; Groups 5 and 6 received lead acetate with vitamin E and lead acetate with quercetin, respectively. Results Lead acetate significantly increased (p

Objective: To investigate the hepatic and reproductive toxicity of dichlorvos and lead acetate on male Wistar rats. Methods: Fifteen adult male Wistar rats (170-190 g) were randomly divided into three groups, with 5 rats in each group. Group 1 received 0.5 mL distilled water orally and served as the control group, while groups 2 and 3 were orally treated with 2 mg/kg body weight (b.w.) dichlorvos and 10 mg/kg b.w. lead acetate, respectively, for 55 days. Epididymal sperm, serum follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone concentrations, testicular 17 β-hydroxysteroid dehydrogenase activity (17β-HSD), androgen receptor expression, aspartate aminotransferase (AST), alanine aminotransferase (ALT), testicular oxidant and antioxidant enzymes were evaluated with standard methods. Results: Sperm count, motility, morphology, FSH, LH, testosterone levels, 17β-HSD, androgen receptor expression, and catalase activity were significantly reduced in the dichlorvos and lead acetate treated groups as compared with the control group (P