Indexed on: 06 Apr '05Published on: 06 Apr '05Published in: Reproductive Toxicology
Polychlorinated biphenyls (PCBs) are global pollutants of major concern to human and animal reproductive health. The present study has examined the impact of Aroclor 1254 exposure on oxidative stress and testicular Leydig cell function. Adult albino male rats of the Wistar strain were dosed for 30 days with daily intraperitoneal injections of 2 mg/kg Aroclor 1254 or vehicle (corn oil). One day after the last treatment, animals were euthanized and blood collected for the assay of serum testosterone and estradiol. Testes were removed and Leydig cells were isolated for the assay of luteinizing hormone (LH) receptors, steroidogenic enzymes cytochrome P450 side chain cleavage enzyme (P450 scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD). Cellular antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione-S-transferase (GST) were also assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were quantified. Results showed that Aroclor 1254 exposure lowered serum testosterone and estradiol levels. Leydig cell LH receptor density, activities of the steroidogenic enzymes P450 scc, 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPX, GR, and GST were significantly diminished whereas, LPO and ROS significantly elevated. Taken together, these results suggest that inefficient LH receptors, steroidogenic enzymes and antioxidant enzymes are possible mechanisms by which Aroclor 1254 treatment disrupts Leydig cell steroidogenesis.