📖 ABSTRACT/OVERVIEW
Heavy metal contamination from oil industry activities in the Niger Delta poses significant reproductive health risks to resident animal and human populations, and cadmium is a particularly potent testicular toxicant whose molecular mechanisms of action have not been characterised in locally relevant experimental models. This doctoral study mechanistically investigated cadmium-induced testicular biochemical toxicity in Wistar rats as a model for understanding heavy metal reproductive health impacts in Niger Delta communities of Bayelsa, Delta, and Rivers States, South South Nigeria. Sixty male Wistar rats were exposed to cadmium chloride at 0, 1, 2, and 5 mg/kg body weight daily by oral gavage for eight weeks. Testicular testosterone biosynthesis enzyme activities including steroidogenic acute regulatory protein, 3-beta-hydroxysteroid dehydrogenase, and 17-beta-hydroxysteroid dehydrogenase were quantified. Oxidative stress markers, sperm parameters, blood-testis barrier integrity proteins including occludin and claudin-11, and caspase-mediated apoptotic markers were assessed. Cadmium significantly inhibited steroidogenic enzyme activities in a dose-dependent manner, with the 5 mg/kg group showing 78% reduction in 3-beta-hydroxysteroid dehydrogenase activity. Blood-testis barrier protein expression declined significantly, indicating barrier disruption as a primary toxicity mechanism. Oxidative stress markers were significantly elevated, and mitochondria-mediated caspase-9 activation confirmed apoptosis as a downstream outcome. These mechanistic findings provide original molecular evidence for cadmium testicular toxicology relevant to Niger Delta communities and support urgent environmental remediation and occupational health interventions. Keywords: cadmium toxicity, testicular biochemistry, steroidogenesis, blood-testis barrier, Niger Delta.
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