Dose-dependent hepatorenal genotoxicity induced by polyethylene microplastics: Evidence from comet assay and apoptotic pathway activation.

Polyethylene microplastics (PE-MPs) have recently emerged as ubiquitous environmental contaminants capable of penetrating biological systems and exerting toxic effects on vital organs. Experimental evidence indicates that oral exposure to PE-MPs induces biochemical, hepatic, and renal dysfunctions; however, dose-dependent metabolic and histopathological alterations following sub-acute exposure and subsequent recovery remain insufficiently characterized. Sixty male C57BL/6 mice were randomly allocated into four groups (n = 15/group): control, 6 µg/mL, 60 µg/mL, and 600 µg/mL PE-MPs. Animals received daily oral gavage of PE-MPs suspended in distilled water for 15 days. After treatment, eight animals from each group were sacrificed, while the remaining animals were allowed 15 days recovery period. Liver and kidney tissues were examined histologically using hematoxylin and eosin (H&E) and histochemical by periodic acid-Schiff (PAS) staining. Meanwhile, detection of apoptosis stained with acridine orange and DNA damage by comet assay in blood tissue. Many histopathological alternations, apoptosis, and genotoxicity were prominent in both liver and kidney tissue. The severity of harmful alternation increased progressively with escalating polyethylene microplastics exposure. Sub-acute oral exposure to polyethylene microplastics induces dose-dependent in hepatic, renal, blood tissues toxicity in mice. Although partial recovery occurs after exposure cessation, the findings highlight the cumulative and potentially irreversible toxic effects of PE-MPs.