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Melatonin mitigates polystyrene nanoplastics-induced impairment of oocyte maturation in mice
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Mice were exposed to polystyrene nanoplastics for 35 days, and their egg cells were then matured in culture. Exposure impaired maturation and fertilization. Adding melatonin to the culture medium restored mitochondrial function, lowered oxidative stress and eased the defects.
The widespread contamination of polystyrene nanoparticles (PS-NPs) has emerged as a significant global concern due to its potential threats to human and animal health. Although the toxicity of PS-NPs to ovarian function has been established, how to relieve the damage of PS-NPs to oocyte maturation remains elusive. Since melatonin (MLT) plays an essential role in regulating ovarian function. This study is the first attempt to explore the protective roles of melatonin in counteracting the maturation defects of oocytes caused by PS-NPs exposure. In this investigation, the reproductive toxicity of PS-NPs was evaluated after continued exposure for 35 days. After exposure, cumulus oocyte complexes (COCs) obtained from PS-NPs exposed-mice were cultured in vitro, meanwhile the various concentration MLT were supplemented into the culture medium to determine the beneficial roles. The results revealed that PS-NPs exposure could impede the meiotic progression, fertilization competence and subsequent embryonic development of oocytes. These impairments are likely mediated through multiple mechanisms, including excessive ROS generation, reduced ATP contents, mitochondrial dysfunction and subsequent induction of early apoptosis. Besides, PS-NPs exposure was found to compromise the architecture of spindle and the alignment of chromosome via altering the key epigenetic markers (tubulin-ace and H4K12ac). Notably, these adverse effects could be alleviated after MLT administration. Further analysis demonstrated that MLT supplementation significantly enhanced antioxidant capacity and mitochondrial dynamics, which indicated by enlarged the mRNA expression levels of anti-oxidative enzyme and mitochondrial dynamics-related genes. In conclusion, MLT could rescue PS-NPs-induced oocyte quality decline by ameliorating oxidative stress, restoring mitochondrial function, and normalizing epigenetic modifications.
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Melatonin Alleviates the Damage of Polystyrene Microplastics to Porcine Oocytes by Reducing Oxidative Stress and Mitochondrial Damage, and Regulating Autophagy and Apoptosis Levels
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Researchers investigated whether the antioxidant melatonin could protect porcine oocytes from damage caused by polystyrene microplastics. The study found that microplastics at 30 micrograms per milliliter significantly impaired oocyte maturation, but melatonin treatment helped alleviate this damage by reducing oxidative stress, protecting mitochondrial function, and regulating autophagy and cell death pathways.
Melatonin prevents the transgenerational toxicity of nanoplastics in zebrafish (Danio rerio)
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Adult zebrafish were exposed to polystyrene nanoplastics for 14 days, with or without melatonin, and their embryos were studied. Parental exposure at 1 mg/L lowered fertilization and survival rates in the offspring and raised deformity rates and oxidative stress. Offspring of fish that also received melatonin showed fewer of these effects.
Exploring Oxidative Stress and Metabolic Dysregulation in Lung Tissues of Offspring Rats Exposed to Prenatal Polystyrene Microplastics: Effects of Melatonin Treatment
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Researchers found that rat pups exposed to polystyrene microplastics before birth showed significant oxidative stress and metabolic disruption in their lung tissues. The prenatal exposure altered nucleic acid metabolism and amino acid profiles in the lungs of newborn pups. Encouragingly, treatment with melatonin significantly improved lung function and reduced tissue damage in the affected offspring.
Polystyrene nanoplastic exposure induces excessive mitophagy by activating AMPK/ULK1 pathway in differentiated SH-SY5Y cells and dopaminergic neurons in vivo
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Researchers found that 50-nanometer polystyrene nanoplastics accumulate in brain cells and their mitochondria, causing Parkinson's disease-like damage in both lab-grown nerve cells and mice. The nanoplastics triggered excessive mitophagy, a process where the cell destroys too many of its own mitochondria, leading to energy loss and nerve cell death. Melatonin treatment helped protect against this damage, suggesting a potential preventive strategy.
Polystyrene Nanoparticles Cause Sex‐Specific Toxicity in Male Zebrafish, Which Can Be Mitigated by Melatonin
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Adult zebrafish were exposed to polystyrene nanoparticles for 14 days, with or without melatonin. At 1 mg/L the particles shrank gonad and brain size relative to body weight, disrupted reproductive hormone signaling and caused oxidative stress, with differences between males and females. These effects were largely reduced in fish that also received melatonin.
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