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Assessment on intestinal health from polylactic acid microplastics degradation on rare minnow (Gobiocypris rarus): Inflammation regulation by mitochondrial dysfunction
Summary
Researchers exposed rare minnow fish to photodegraded polylactic acid microplastics to assess intestinal health effects. The study found that these biodegradable plastic particles induced visible intestinal damage, triggered inflammation through mitochondrial dysfunction, and caused oxidative stress, suggesting that even biodegradable plastics may pose ecological risks after environmental degradation.
Biodegradable plastics (BPs), a class of polymers designed to break down under natural environmental conditions, are currently effective measures to deal with the crisis of "white pollution" (the persistent accumulation of non-degradable plastic waste in the environment). Despite their environmental promise, growing concerns have emerged regarding the potential ecological risks of BPs. However, the health risks and its underlying mechanism of natural degradable BPs on intestinal tissues remain unclear. Herein, rare minnows (Gobiocypris rarus) were exposed to different concentrations of photodegraded polylactic acid microplastics (PDPLA-MPs) for 14 days, and the PDPLA-MPs was obtained via visible light and ultraviolet light for 5 days. The results revealed that PDPLA-MPs exposure induced villi fusion and beheading, shortened intestinal villi length, and upregulated the expression of IL-6, IL-8, IL-1β, and TNFα. Histological results found that 50 % postal intestine of rare minnow showed severe (score 4) structural alteration in 30 μg/L exposure group. Molecular toxicological results revealed that PDPLA-MPs exposure aggravated intestinal redox status and apoptosis in rare minnow, characterized by markedly increased ROS production and upregulated expressions of pro-apoptosis genes. The further study demonstrated that ROS-triggered mitochondrial structural damage and lower activities of mitochondrial complexes I-V in the intestines were identified as crucial mechanisms the intestinal toxicity induced by PDPLA-MPs, which may be regulated by Sesn2/Nrf2 pathway. These findings highlighted the potential mechanisms of intestinal inflammation of PDPLA-MPs exposure, which provided important references for further research on the impact of BPs on ecosystems health.