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Sodium nitroprusside alleviates nanoplastics-induced developmental toxicity by suppressing apoptosis, ferroptosis and inflammation
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Researchers discovered that sodium nitroprusside, a compound that releases nitric oxide, could protect zebrafish larvae from the toxic effects of nanoplastics by reducing oxidative stress, cell death, and inflammation. The treatment worked by activating a signaling pathway that neutralized the harmful reactive oxygen species triggered by nanoplastic exposure. This is one of the first studies to identify a potential treatment that could counteract nanoplastic toxicity, offering hope for developing protective strategies against plastic particle exposure.
The health damage caused by nanoplastics (NPs) pollution has become one of the global scientific problems to be solved urgently. However, the toxicological mechanism of NPs is complex, and the research progress of anti-toxicity is limited. Thus, it has potential application value to explore or develop drugs that can effectively alleviate or remove NPs with biological toxicity. In this research, 8 μM sodium nitroprusside (SNP) solution was used to treat zebrafish larvae with 20 mg/L NPs for up to 12 days, and the results showed that SNP treatments were effective in alleviating NPs-caused developmental toxicity in zebrafish larvae. Further examination of its signaling pathway revealed that NPs-induced oxidative stress was mitigated by activating the NO-sGC-cGMP signaling pathway and reduced most of the reactive oxygen species (ROS). Subsequently, we detected the key substances and the key enzymes involved in apoptosis and ferroptosis, and found that oxidative stress-induced mitochondria-dependent apoptosis and lipid peroxidation-caused ferroptosis were alleviated. Finally, observed the accumulation of NPs and ROS in the liver of zebrafish larvae, which is the target organ of immunotoxicity, and we found that SNP could alleviate NPs-caused inflammation by analyzing the fluorescence intensity of neutrophils and macrophages in transgenic zebrafish and detecting the expression of key immune genes. In conclusion, this research has shown for the first time that SNP treatment can significantly inhibit NPs-induced developmental toxicity, resulting from oxidative stress-induced apoptosis, ferroptosis and inflammation in zebrafish larvae.
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This review examines how nano- and micro-sized plastic particles cause toxic effects in zebrafish, focusing on the link between oxidative stress and neurodevelopmental damage. Researchers found that plastic particle exposure disrupts the balance of reactive oxygen species in cells, which can impair brain development and nervous system function. The study suggests these oxidative stress responses may serve as early warning signals of plastic particle toxicity in aquatic organisms.
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Adult female zebrafish were exposed to polystyrene nanoplastics for 28 days. The particles passed to their embryos and larvae, which had lower hatching rates, more malformations, reduced movement and fewer neurons in part of the brain. The damage was driven by oxidative stress and two cell-death pathways, and antioxidant treatment partly reversed it.
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Researchers showed that polystyrene nanoplastics accumulate in zebrafish larvae and trigger excessive reactive oxygen species production via NADPH oxidase upregulation, causing mitochondrial dysfunction, apoptosis, and NF-κB-driven inflammation — with inhibiting ROS generation effectively blocking downstream cell death and inflammatory responses.
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Exposure to 20-nanometer plastic particles caused developmental problems in zebrafish embryos, including shorter body length, heart defects, and lower survival rates. The nanoplastics specifically damaged the development of motor neurons and triggered oxidative stress, a harmful chemical imbalance in cells. These results suggest that very small plastic particles could interfere with early brain and nerve development.
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