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Subchronic exposure of tire wear particles leachate induces oxidative stress and DNA damage in zebrafish (Danio rerio) brain
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Researchers exposed zebrafish to tire wear particle leachate for up to 28 days and found progressive oxidative damage, DNA strand breaks 19-fold above controls, neuroinflammation, and elevated acetylcholinesterase activity in brain tissue, with molecular docking analysis implicating leachate compounds 3-BHA and 4-tert-butylphenol as likely drivers of antioxidant enzyme disruption.
In recent years, microplastic pollution has garnered widespread attention, with tire wear particles (TWPs) being the largest source of microplastic pollution. These particles are frequently detected in aquatic environments and release various organic pollutants (such as 4-tert-Butylphenol and 3-tert-Butyl-4-hydroxyanisole(3-BHA)), potentially threatening aquatic organisms. This study hypothesized that exposure to TWPs leachate would induce brain tissue injury in zebrafish. Accordingly, after 7, 14, 21, and 28 days of continuous exposure, we investigated the ecological toxicity and mechanisms of TWPs leachate on the zebrafish brain from physiological, biochemical, and molecular perspectives. The results indicated that exposure to TWPs leachate induced varying degrees of oxidative damage and lipid peroxidation in the zebrafish brain. After 14 days of exposure, the content of 8-OHdG in the 8.5% was 19.30 times higher than the control group, signifying severe DNA damage. Moreover, significant inflammatory cell infiltration and enlarged tissue gaps were observed in the brain tissue. Acetylcholinesterase (AChE) activity increased notably, suggesting potential neurotoxic effects of TWPs leachate in zebrafish. Exposure to TWPs leachate altered the expression of antioxidant- and apoptosis-related genes in the zebrafish brain. QSAR toxicity prediction results indicated that 3-BHA and 4-tert-Butylphenol may exhibit developmental toxicity, with predicted scores of 0.88 and 0.79, respectively. Furthermore, molecular docking analyses suggested that these two compounds may interact with antioxidant enzymes (SOD), providing supportive evidence for their potential involvement in oxidative stress. These results are important for assessing the toxicological effects of TWPs leachate and exploring its mechanisms of toxicity in aquatic organisms.
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Zebrafish exposed to tire wear particle leachates at three concentrations over 28 days showed dose- and time-dependent increases in oxidative stress markers (SOD, MDA) and liver cell apoptosis, confirming significant hepatotoxic effects from tire-derived pollution.
Oxidative Stress and Apoptosis of Adult Zebrafish ( Danio rerio ) Liver Exposed to Tire Wear Particle (TWP) Leachates
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Zebrafish exposed to tire wear particle leachates at three concentrations over 28 days showed dose- and time-dependent increases in oxidative stress markers and liver cell apoptosis, confirming hepatotoxicity from tire-derived microplastic pollution.
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Researchers studied how chemicals that leach from tire wear particles affect developing zebrafish, a common lab organism. The tire particle chemicals damaged eye development and impaired swimming behavior, even at concentrations found in the real environment. Since tire wear is one of the largest sources of microplastic pollution, these findings raise concerns about the ecological impact of road runoff on aquatic life.
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Researchers tested the toxicity of micro- and nano-sized tire particles and their chemical leachates on zebrafish embryos and water fleas, two commonly used model organisms. They found that nano-sized tire particles were more toxic than micro-sized ones, and that the chemical leachate alone also caused significant developmental harm to zebrafish. The study demonstrates that tire debris poses a meaningful environmental risk to freshwater organisms through both direct particle exposure and the release of harmful chemicals.
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