We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polylactic acid microplastics and fish species intestinal inflammation risk: Associated with mitochondrial function mediated by Sesn2/Nrf2 pathway
AI summary Read the abstract
Researchers exposed rare minnow fish to polylactic acid microplastics and found that even low concentrations caused intestinal inflammation and disrupted mitochondrial function. The study identified a specific molecular pathway involving the proteins Sesn2 and Nrf2 that mediated the damage. The findings suggest that microplastics from biodegradable plastics may still pose meaningful risks to the gut health of aquatic organisms.
The polylactic acid (PLA), a kind of biodegradable plastic (BP), is widely used in various industries due to its environmental friendliness. Microplastics (MPs) derived from incomplete degradation of PLA presents significant ecological and health risks to aquatic organisms. However, the potential toxic mechanism of PLA MPs on intestines is still unclear. In the present study, rare minnows (Gobiocypris rarus) were exposed to 0 µg/L, 4.5 µg/L and 18 µg/L PLA MPs for 15 d. The results showed that PLA MPs exerted slight influence on intestinal growth in rare minnows, but caused intestinal damage as evidenced by intestinal villous epithelial cells eroded and necrotic, gap of edematous mucosal layer increased and fibrosis, and significantly increased inflammatory related genes expression. Moreover, the incidence and severity of intestinal damage escalated in a concentration-dependent manner, accompanied with the severe deterioration at distal intestines. Additionally, PLA MPs exposure caused intestinal mitochondrial dysfunction, as evidenced by significantly increased mitochondrial reactive oxygen species (ROS) and markedly decreased adenosine triphosphate (ATP) contents and mitochondrial respiratory enzymes activities (p < 0.05). The further studies found that PLA MPs exposure activated intestinal oxidative stress, as evidenced by significantly increased intestinal ROS and malondialdehyde (MDA), markedly decreased antioxidative stress enzyme activities and decreased antioxidative related genes expression. And then, the expression of pro-apoptotic related genes was significantly increased in PLA MPs exposure groups compared with the control levels, but decreased in the anti-apoptotic gene. Moreover, inhibited Sesn2/Nrf2 pathway may promote mitochondrial dysfunction by amplifying oxidant responses and apoptosis under PLA MPs exposure. Taken together, environmental PLA MPs aggravated intestinal damage through Sesn2/Nrf2 pathway-mediated mitochondrial dysfunction. These findings reveal a specific molecular pathway for PLA MPs to induce intestinal damage, which will contribute to assessing the ecological risks of BMPs to aquatic organisms.
More Papers Like This
Assessment on intestinal health from polylactic acid microplastics degradation on rare minnow (Gobiocypris rarus): Inflammation regulation by mitochondrial dysfunction
AI summary Read the abstract
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.
Mechanisms underlying mitochondrial dysfunction and intestinal damage induced by ingestion of microplastics in Leuciscus waleckii: The role of the NF-κB/Nrf2 signaling pathway
AI summary Read the abstract
This study found that polystyrene microplastics harmed juvenile fish by triggering immune dysfunction, oxidative stress, and mitochondrial damage in their intestines. The microplastics activated inflammatory pathways, damaged the intestinal barrier, and shifted the gut microbiome toward harmful bacteria. These findings suggest that microplastic ingestion could have cascading effects on fish health through multiple biological pathways.
Investigating the toxicity of polylactic acid microplastics on the health and physiology of freshwater fish, Cirrhinus mrigala
AI summary Read the abstract
Researchers fed freshwater fish polylactic acid (PLA) microplastics, often considered a more eco-friendly plastic alternative, for 90 days at various concentrations. They found that PLA microplastics negatively affected the fish's growth, nutrient digestibility, blood chemistry, and caused tissue damage to the liver and intestines. The findings suggest that even biodegradable plastics can be harmful to aquatic organisms when ingested over time.
Microplastics accumulation in gut and revealing their impacts on nutritional quality and health of freshwater carp, Catla catla
AI summary Read the abstract
Researchers fed common carp (Catla catla) diets containing increasing concentrations of polylactic acid microplastics (PLA-MPs) — a type of biodegradable plastic — for 90 days, finding that at higher levels the fish experienced stunted growth, reduced nutrient absorption, altered blood cell counts, and intestinal tissue damage. The study demonstrates that even "biodegradable" microplastics can accumulate in fish and significantly harm their health.
Long-term exposure to microplastics induces intestinal function dysbiosis in rare minnow (Gobiocypris rarus)
AI summary Read the abstract
Researchers exposed rare minnow fish to polystyrene microplastics for up to 28 days and found progressive intestinal dysfunction including structural damage, increased oxidative stress enzyme activity, and disruption of gut microbiota. The study suggests that long-term microplastic exposure can cause cumulative intestinal damage, with inflammation and barrier function impairment worsening over extended exposure periods.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.