Aluminum exposure impairs oocyte quality via subcellular structure disruption and DNA damage-related apoptosis in mice.

J Environ Sci (China)

The Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi 533000, China; School of Medical Laboratory, Youjiang Medical University for Nationalities, Guangxi 533000, China; Industrial College of Biomedicine and Health Industry, Youjiang Medical University for Nationalities, Guangxi 533000, China; Reproductive Medicine, Guangxi Medical and Health Key Discipline Construction Project, The Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi 533000, China. Electronic address:

Published: May 2024

Aluminum (Al) can lead to an exposure of creature in varieties ways for its universality, and it could disturb normal physiological metabolism, with the damage to multisystem including reproduction. Since the oocyte quality is critical for female reproduction, we inspected the toxicity of Al on mouse oocyte maturation. We constructed in vitro exposure mouse model, and we found that 5 mmol/L Al had adverse effects on oocyte maturation by impairing organelle and cytoskeleton. Aberrant spindle and misaligned chromosomes which might be considered to be caused by elevated levels of acetylation, as well as abnormal distribution of actin dynamics could hinder normal meiosis of oocytes. Organelle dysfunction indicated that Al affected proteins synthesis, transport and digestion, which would further damage oocyte maturation. In order to explore the mechanism of Al toxicity, our further investigation demonstrated that Al caused mitochondrial dysfunction and imbalance calcium homeostasis, resulting in limited energy supply. Moreover, high level of reactive oxygen species, DNA damage and apoptosis caused by oxidative stress were also the manifestation of Al toxicity on oocytes. In conclusion, our study provided the evidence that Al exposure affected oocyte quality through its effects on spindle organization, actin dynamics, organelle function and the induction of DNA damage-related apoptosis with mouse model.

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Source
http://dx.doi.org/10.1016/j.jes.2023.04.007DOI Listing

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