Chronic Microplastic Exposure Dose‐Dependently Induces Liver Failure via Oxidative Stress, Inflammation, and Apoptosis in Rats

Microplastics (MPs), pervasive environmental contaminants, pose significant health risks due to their persistence and potential toxicity in biological systems. This study evaluated the chronic effects of polyethylene (PE) MPs (1-15 μm) on liver function in rats, focusing on oxidative stress, inflammatory responses, and apoptosis. Twenty-four male Wistar rats were randomized into three groups (n = 8/group): a control group receiving distilled water, a low-dose group receiving 5 mg/kg PE MPs, and a high-dose group receiving 10 mg/kg PE MPs, administered via daily oral gavage for 4 weeks. Results revealed dose-dependent hepatotoxicity, with elevated serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). Oxidative stress marker malondialdehyde (MDA) and pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) increased significantly, while total antioxidant capacity (TAC) and anti-inflammatory interleukin-10 (IL-10) decreased markedly. Furthermore, caspase-3 gene expression was significantly upregulated, indicating enhanced apoptotic activity in the liver. These findings confirm that chronic microplastic exposure induces hepatotoxicity through oxidative stress, inflammation, and apoptosis, highlighting the need for further research into long-term health risks.