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Abstract
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Plastic pollution is one of the widespread environmental and health issues of the 21st century. Of the many plastics, polystyrene (PS) is a major source of microplastic (MP) contamination due to its extensive application in packaging, disposable food containers, and insulation. Microplastics (diameter < 5 mm) are also referred to increasingly as persistent emerging pollutants that persist in the environment and aggregate in ecosystems. Microplastics have the potential to adsorb toxic chemicals and traverse the body by ingestion, inhalation, or dermal uptake [1, 2].
In the body, PS microplastics can cross epithelial barriers, enter the bloodstream, and accumulate in vital organs like the liver, kidneys, and brain. The liver, the detoxifying and metabolic central organ, is especially vulnerable to the toxicity of such contaminants. Experimental studies have shown that PS microplastics are capable of causing oxidative stress—a disturbance in the equilibrium between the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms—and inflammatory responses that lead to tissue damage [3, 4].
Exposure to microplastics was demonstrated in studies involving mouse models to enhance lipid peroxidation, decrease antioxidant enzyme activities (e.g., superoxide dismutase (SOD) and catalase (CAT)), and increase pro-inflammatory cytokines (IL-6, TNF-α). For example, Zou et al. found exposure of mice to PS microplastics to induce hepatocellular damage, oxidative stress, and inflammatory cell infiltration [5]. Xie et al. likewise reported significant increases in serum cytokines and impaired hepatic antioxidant defenses with long-term PS-MP exposure [6].
Nevertheless, while the issue has been on the rise, the mechanism by which oxidative stress is linked with inflammatory cascades in liver injury caused by microplastics remains unidentified. Specifically, no appropriate understanding of whether oxidative stress is an initial or secondary event following immune acti
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