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Microplastic Exposure Disrupts Energy Homeostasis and Welfare in Goldfish
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Researchers exposed goldfish to polystyrene microplastics for 14 days and found that the particles suppressed appetite through neuroendocrine disruption — downregulating hunger-signaling neuropeptides and elevating cortisol — while simultaneously increasing metabolic demand, resulting in impaired growth and anxiety-like behavior.
The accumulation of microplastics in aquatic ecosystems poses a significant threat to fish physiology and welfare. This study investigated the impact of exposure to virgin polystyrene microplastics (15 µm) on energy balance and welfare in goldfish (Carassius auratus). Fish were exposed for 14 days, and the effects were assessed through an integrated analysis of behavioral, metabolic, neuroendocrine, and physiological parameters. Microplastic exposure significantly reduces feed intake and feed anticipatory activity, indicating a potent anorexigenic effect. This effect was driven by neuroendocrine disruption, characterized by the downregulation of orexigenic neuropeptides (npy, agrp, hcrt) and the upregulation of anorexigenic signaling (pomca, cartpt, lepa). Simultaneously, exposed fish exhibited increased oxygen consumption, suggesting elevated metabolic demands. These factors converged to impaired growth and reduced hepatosomatic index, suggesting altered energy allocation. Furthermore, microplastic exposure induced anxiety-like responses and increased plasma cortisol levels, confirming the activation of the physiological stress response. Overall, these findings demonstrate that microplastics disrupt energy homeostasis and trigger behavioral shifts that ultimately compromise fish welfare and the biological resilience of aquatic species.
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Micro/nanoplastics impair the feeding of goldfish by disrupting the complicated peripheral and central regulation of appetite
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Goldfish exposed to environmentally realistic levels of polystyrene micro and nanoplastics for 28 days ate significantly less food due to disruption of both gut-based and brain-based appetite signals. Smaller nanoplastics caused more severe effects than larger microplastics, damaging internal organs and altering hormones that regulate hunger. The findings suggest that plastic particle pollution in waterways could impair feeding and survival in fish populations.
Polystyrene nanoplastics disrupt glucose metabolism and cortisol levels with a possible link to behavioural changes in larval zebrafish
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Researchers exposed larval zebrafish to polystyrene nanoplastics and found the particles accumulated in the pancreas, lowering blood glucose and triggering a stress hormone (cortisol) spike that caused the fish to swim hyperactively. The study identifies a specific biological pathway — disrupted glucose regulation leading to stress hormone activation — through which nanoplastics may alter behavior in aquatic animals.
Some Behavioural and Physiological Effects of Plastics (Polyethylene) on Fish
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Researchers examined behavioral and physiological effects of polyethylene microplastics on fish, finding that plastic exposure disrupted endocrine function, altered behavior, and impaired normal development and reproduction.
Microplastics Induced Dysfunctions in Physiology and Behavior of Fish: A Comprehensive Review.
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Researchers comprehensively review how microplastics disrupt fish physiology, documenting effects on growth, blood chemistry, reproduction, oxidative stress, immune function, and behavior — tracing mechanisms from gastrointestinal damage and endocrine disruption to neurotoxicity and transgenerational harm — to inform ecological risk assessment in aquatic and fisheries contexts.
Micro-polystyrene plastic and benzo[α]pyrene exposure affects the endocrine system and causes physiological stress in Carassius auratus
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Researchers found that combined exposure to polystyrene microplastics and benzo[a]pyrene caused significantly greater endocrine disruption, oxidative stress, and DNA damage in goldfish than either pollutant alone, with effects intensifying through the hypothalamus-pituitary-interrenal axis.
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