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New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
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Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.
Microplastics biological toxicity, environmental persistence and biological chemicals have been paid widespread attention. Microplastics exposed to chicken spleen injury of the specific mechanism is unclear. Thus, we randomly assigned chickens to 4 groups: C (normal diet), L-MPs (1 mg/L), M-MPs (10 mg/L), and H-MPs (100 mg/L), and assessed spleen damage after 42 d of exposure. Morphologically, the boundary between the red and white pulp of the spleen was blurred, along with the expansion of the white pulp. It was further speculated that microplastics induced mitochondrial dynamic homeostasis (Drp1 upgraded, Mfn1, Mfn2, and OPA1 reduced), and provoked the mitochondrial apoptotic pathway (Bcl-2/Bax decreased, cytc, caspase3, and caspase9 raised), resulting in redox imbalance and lipid peroxide accumulation (MDA increased, CAT, GSH, and T-AOC plummeted), and further stimulated ferroptosis (FTH1, GPX4, and SLC7A11 decreased). Here we explored the impact of polystyrene microplastics on the spleen, as well as the programmed death (apoptosis and ferroptosis) involved, and the regulative role of mitochondria in this process. This could be of significant importance in bridging the gap in laboratory research on microplastics-induced spleen injury in chicken.
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Scientists found that tiny plastic particles (microplastics) can damage the liver in fish by triggering inflammation and a type of cell death linked to iron and fat breakdown, essentially causing cells to self-destruct in a harmful way. While this study was done in tilapia, not humans, it adds to growing evidence that the microplastics we're increasingly exposed to through food, water, and air may cause similar organ damage in other animals—including potentially us—making this an important area for future human health research.
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In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
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Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
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