Industrial Dioxin as an Endocrine Disruptor: Combined Effects with Hyperglycemia on Male Reproductive Health

Abstract

Background: Industrial pollutants like dioxins, known endocrine disruptors, pose significant risks to reproductive health, particularly when combined with metabolic disorders such as hyperglycemia. This study evaluated the synergistic effects of dioxin exposure and hyperglycemia on testicular function in male Wistar rats. Objectives: To assess the independent and synergistic effects of hyperglycemia and dioxin (TCDD) exposure on testicular function, spermatogenesis, and oxidative balance. Methodology: Twenty male Wistar rats were divided into four groups: normal control, diabetes only (STZ-induced), dioxin only, and diabetes combined with dioxin. Fasting blood glucose, body weight, serum testosterone, sperm parameters, oxidative stress markers (MDA and SOD), and testicular histology were assessed. Histological sections were analyzed using hematoxylin-eosin and Masson’s trichrome staining. Results: Diabetic and diabetic+dioxin groups exhibited elevated blood glucose, though differences were not statistically significant. Body weight increased significantly in the diabetic group but decreased markedly with dioxin exposure. Testosterone levels rose in diabetes alone but were significantly suppressed by dioxin, especially in the combined exposure group. Sperm motility, count, and viability were significantly reduced in diabetic and diabetic+dioxin groups, while dioxin alone paradoxically increased motility and viability. MDA levels were lowest, and SOD activity was severely reduced in dioxin-exposed groups, indicating heightened oxidative stress. Histological analyses revealed pronounced degeneration, germinal epithelium thinning, and extensive interstitial fibrosis in the diabetic+dioxin group, confirming synergistic testicular toxicity. Conclusion/Recommendations: Combined exposure to hyperglycemia and dioxin has a synergistic, deleterious effect on male reproductive health, exacerbating oxidative stress, impairing spermatogenesis, and promoting fibrotic remodeling. These findings underscore the heightened reproductive risks posed by concurrent metabolic and environmental insults.