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New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
Tiantian Guo1, Xiren Geng1, Yue Zhang1
1College of Wildlife and Protected Area, Northeast Forestry University, Harbin, Heilongjiang 150040, PR China.
Abstract:
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.
Insights
Polystyrene microplastics harm chicken spleen by disrupting mitochondrial function, leading to cell death via apoptosis and ferroptosis. This research clarifies the mechanisms behind microplastic-induced spleen injury in poultry.
Area of Science:
- Environmental Science
- Toxicology
- Cell Biology
Background:
- Microplastic contamination is a growing global concern due to its persistence and potential biological toxicity.
- The specific mechanisms by which microplastics induce spleen injury in chickens remain largely unknown.
- Understanding these mechanisms is crucial for assessing the risks to poultry health and food safety.
Purpose of the Study:
- To investigate the impact of polystyrene microplastics on chicken spleen morphology and cellular pathways.
- To elucidate the roles of mitochondrial dysfunction, apoptosis, and ferroptosis in microplastic-induced spleen damage.
- To provide insights into the regulative role of mitochondria in the programmed death of spleen cells exposed to microplastics.
Main Methods:
- Chickens were randomly assigned to four groups and exposed to varying concentrations of microplastics (0, 1, 10, 100 mg/L) for 42 days.
- Spleen damage was assessed morphologically and at the molecular level, analyzing mitochondrial dynamics, apoptosis, ferroptosis, and redox balance.
- Key proteins and markers related to mitochondrial function (Drp1, Mfn1/2, OPA1), apoptosis (Bcl-2/Bax, cytc, caspases), ferroptosis (FTH1, GPX4, SLC7A11), and oxidative stress (MDA, CAT, GSH, T-AOC) were quantified.
Main Results:
- Microplastic exposure caused morphological changes in the spleen, including blurred red-white pulp boundaries and white pulp expansion.
- Microplastics disrupted mitochondrial homeostasis by upregulating Drp1 and downregulating Mfn1, Mfn2, and OPA1.
- The study observed increased apoptosis (decreased Bcl-2/Bax, increased cytc, caspase3/9) and ferroptosis (decreased FTH1, GPX4, SLC7A11), alongside redox imbalance (increased MDA, decreased CAT, GSH, T-AOC).
Conclusions:
- Polystyrene microplastics induce significant spleen injury in chickens through the disruption of mitochondrial dynamics.
- Microplastic exposure triggers programmed cell death pathways, including apoptosis and ferroptosis, in chicken spleen cells.
- This study highlights the critical role of mitochondria in mediating microplastic-induced spleen toxicity and provides a foundation for further research in this area.
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