Biogenic Selenium Nanoparticles Mitigate Arsenic-Induced Testicular Dysfunction and Steroidogenic Gene Dysregulation in Mice

Abstract

Arsenic poisoning of drinking water is a global environmental health problem, and prolonged exposure has been increasingly linked to male reproductive damage. The present work was aimed to evaluate the protective effects of biogenic selenium nanoparticles (SeNPs) synthesised utilising Moringa oleifera leaf extract against sodium arsenite (NaAsO2)-induced testicular injury and steroidogenic gene dysregulation in adult male Swiss albino mice. The SeNPs were characterised by UV–Vis spectroscopy, TEM, FTIR, XRD and dynamic light scattering (DLS) and confirmed spherical morphology with an average size of 45–65 nm. Forty mice were randomly assigned to five groups (n = 8): control, SeNP control (0.5 mg/kg b.w.), arsenic alone (5 mg/kg b.w.), arsenic + low-dose SeNPs (0.25 mg/kg), and arsenic + high-dose SeNPs (0.5 mg/kg). All therapies were given orally for 35 consecutive days. Arsenic exposure resulted in significant disruption of serum testosterone, luteinizing hormone and follicle-stimulating hormone levels and an increase in oestradiol. Increased morphological defects significantly reduced sperm count, motility and viability. MDA of testicular tissue was markedly increased, while SOD, CAT, GPx and GSH were depleted in concert. RT-qPCR showed significant down-regulation of steroidogenic acute regulatory protein (StAR), CYP11A1, CYP17A1, 3β-HSD, and 17β-HSD mRNA expression, as well as up-regulation of the pro-apoptotic Bax/Bcl-2 ratio in arsenic-treated testes. Co-administration of biogenic SeNPs dose-dependently corrected these aberrations, returning the hormonal balance, sperm quality, antioxidant defences, and steroidogenic gene expression to normal levels. Histopathological study revealed the retention of seminiferous tubular architecture in SeNPs treated groups. These findings suggest that phytochemically capped SeNPs represent a viable chemoprotective strategy against arsenic-mediated male reproductive toxicity.