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Unravelling the Potential Role of Nanoplastics and Microplastics‐Induced Toxicity in Freshwater Fish: Emerging Role of Programmed Cell Death Mechanisms
Summary
This review examines how micro- and nanoplastics trigger various forms of programmed cell death in freshwater fish, including apoptosis, autophagy, ferroptosis, and pyroptosis. The study highlights that exposure to these plastic particles generates oxidative stress, inflammation, and DNA damage, with the resulting cell death mechanisms potentially compromising fish health and raising concerns about contamination reaching humans through seafood consumption.
Microplastics (MPs) and nanoplastics (NPs) have emerged as pollutants in aquatic ecosystems, resulting in several detrimental consequences for aquatic animals, particularly fish. Fish is a fundamental and economical food source, abundant in animal protein as well as micronutrients. Exposure of fish to MPs and NPs generates reactive oxygen species and induces oxidative stress, inflammation, and DNA damage, while also altering gut microbiota, thus diminishing fish development and quality. Additionally, the accumulation of MPs and NPs in aquatic habitats may reach the human body through the consumption of polluted fish, potentially leading to significant health consequences. Programmed cell death (PCD) is a genetically controlled process of autonomous and controlled cell death that maintains homeostasis and facilitates development. PCD is crucial in the pathological mechanisms of toxicity generated by MPs and NPs. Although research on PCD in MPs and NPs toxicity is limited, it is crucial to discover key molecules and understand their regulatory roles for better disease prevention and management. This comprehensive review aims to delineate and elaborate on the emerging role of different PCD mechanisms, including pyroptosis, apoptosis, necroptosis, autophagy, ferroptosis, cuproptosis, oxeiptosis, and PANoptosis, in the pathogenesis of toxicity generated by MPs and NPs in freshwater fish.
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