0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Environmental Sources Human Health Effects Marine & Wildlife Reproductive & Development Sign in to save

Hepatotoxicity, developmental toxicity, and neurotoxicity risks associated with co-exposure of zebrafish to fluoroquinolone antibiotics and tire microplastics: An in silico study

Journal of Hazardous Materials 2024 13 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Jingya Wen, Yajing Liu, Bingjia Xiao, Zuning Zhang, Zuning Zhang, Qikun Pu, Xixi Li, Xiaowen Ding, Xiaowen Ding, Feng Qian, Yu Li

Summary

Using computer modeling, this study found that tire microplastics combined with common antibiotics caused significantly more liver damage in zebrafish than brain or developmental harm. The two pollutants worked together to amplify toxicity, meaning the combination was worse than either one alone. This highlights how microplastics in waterways can interact with other contaminants to create greater health risks for aquatic life and potentially for humans who consume seafood.

This study aimed to investigate the differences in the mechanisms of microscopic hepatotoxicity, developmental toxicity, and neurotoxicity in aquatic organisms co-exposed to styrene-butadiene rubber tire microplastics (SBR TMPs) and fluoroquinolone antibiotics (FQs). We found that hepatotoxicity in zebrafish induced by SBR TMPs and FQs was significantly higher than developmental toxicity and neurotoxicity. Furthermore, the main effects of the FQs primarily manifested as synergistic toxicity, whereas the low- and high-order interactions of the FQs mainly exhibited synergistic and antagonistic effects, respectively. Factorial analysis and the mixture toxicity index revealed that the synergistic effects of lomefloxacin × moxifloxacin and ciprofloxacin × lomefloxacin × enrofloxacin interactions significantly contributed to hepatotoxicity in zebrafish exposed to SBR TMP. SBR TMPs and antibiotics primarily induced hepatotoxicity, developmental toxicity, and neurotoxicity in zebrafish by affecting the activities of Cyp1a, Acox1, TRα, and mAChR. The observed toxicities were closely linked to the hydrophilic/hydrophobic groups, electronegativity, group mass, and structural complexity of the FQ molecules. This study provides new insights regarding the toxicological risks to aquatic organisms from co-exposure to SBR TMPs and FQs from a microscopic perspective. Future studies should include a broader range of antibiotics and tire microplastics and consider their long-term adverse effects on aquatic life.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Toxicological mechanisms and molecular impacts of tire particles and antibiotics on zebrafish

Researchers investigated the combined toxic effects of tire microplastics and antibiotics on zebrafish, finding that co-exposure caused more severe damage than either pollutant alone. The combination disrupted liver function, triggered oxidative stress, and altered the expression of genes involved in immune response and metabolism. The study suggests that the widespread co-occurrence of tire particles and antibiotics in waterways may pose compounding risks to aquatic life.

Article Tier 2

Co-exposure of TMPs and antibiotics in zebrafish: The influence of additives on the risk of hepatotoxicity

Researchers investigated how tire microplastics combined with antibiotics cause liver damage in zebrafish, focusing specifically on the role of chemical additives in the tire particles. They found that different antibiotic-tire microplastic combinations produced varying levels of liver toxicity, with certain additive chemicals playing a key role. The study suggests that the additives leaching from tire microplastics may be an underappreciated contributor to their environmental toxicity.

Article Tier 2

Enhanced hepatotoxicity in zebrafish due to co-exposure of microplastics and sulfamethoxazole: Insights into ROS-mediated MAPK signaling pathway regulation

Zebrafish exposed to both microplastics and the antibiotic sulfamethoxazole (commonly found in waterways) suffered significantly worse liver damage than exposure to either pollutant alone. The combined exposure triggered a cascade of oxidative stress, inflammation, and cell death in liver tissue, showing how microplastics can amplify the harmful effects of other environmental contaminants.

Article Tier 2

Microplastic-contaminated antibiotics as an emerging threat to mammalian liver: enhanced oxidative and inflammatory damages

Researchers used a mouse model to study what happens when microplastics contaminated with antibiotics are ingested together, simulating real-world food chain exposure. The study found that the combination caused enhanced oxidative stress and inflammatory damage in the liver compared to either pollutant alone. The findings suggest that microplastics carrying adsorbed antibiotics may pose a greater threat to liver health than microplastics or antibiotics individually.

Article Tier 2

Co-exposure to microplastics and tire particles exacerbates oxidative stress and gut microbiome dysbiosis in zebrafish (Danio rerio)

Researchers exposed zebrafish for 21 days to environmentally relevant mixtures of microplastics and tire particles and found that combined exposure caused more severe oxidative stress and gut microbiome disruption than either pollutant alone. Particle accumulation occurred mainly in the gut with secondary deposition in the liver, and the most pronounced tissue damage was observed under the highest combined exposure. Gut microbiota analysis revealed significant shifts in community structure, including reduced beneficial bacteria and increased pollutant-tolerant species.

Share this paper