Mechanisms of PDC-induced testicular Toxicity: Oxidative stress, steroidogenic suppression, and modulation by ZnO-NP/TEO synergy.

Potassium dichromate (PDC), a potent industrial toxicant, induces severe testicular damage, though its precise mechanisms remain incompletely defined. This study investigated the mechanistic pathways of PDC-induced reproductive toxicity in male Sprague-Dawley rats (n = 108). Rats were allocated into 9 groups: controls (oral, intraperitoneal) (I),(II), PDC-only (10.5 mg/kg bwt, III), Zinc Oxide Nanoparticles, ZnO-NPs-only (5 mg/kg bwt, IV), Thyme Essential Oil, TEO-only (5 mg/kg bwt, V), ZnO-NPs + TEO (VI), PDC + ZnO-NPs (VII), PDC + TEO (VIII), and PDC + ZnO-NPs + TEO (IX), treated for 8 weeks. PDC exposure triggered significant testicular oxidative stress, evidenced by elevated malondialdehyde (MDA) and Nitric oxide (Nox) activity alongside depleted catalase, glutathione, and total antioxidants. This redox imbalance directly correlated with impaired spermatogenesis and steroidogenesis, manifesting as reduced testis weight, decreased serum free testosterone, LH, and FSH levels, compromised sperm quality (motility, count, morphology), and downregulation steroidogenic genes (StAR, CYP11A1, HSD-3β). Histopathological analysis confirmed seminiferous tubule degeneration and germ cell apoptosis. Critically, reversal of these effects by antioxidants (TEO, ZnO-NPs; alone/combined) validated oxidative stress and steroidogenic disruption as primary drivers of PDC testicular toxicity. These findings define the mechanistic basis of PDC-induced reproductive injury, highlighting its disruption of redox balance and endocrine function.