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Effects of Microplastics and Nanoplastics Exposure on Neurogenesis: Are Thymidine Analogs a Good Option to Study Such Effects?
Summary
This review examines evidence for neurogenesis disruption from microplastic and nanoplastic exposure, investigating whether thymidine analogs used to track cell birth in neural tissue are confounded by plastic-induced proliferation signals and reviewing the broader evidence for MNP effects on neural development.
An important disadvantage of plastics is their fragmentation into smaller particles, classified according to size as microplastics and nanoplastics. These plastic particles persist for extended periods in aerial, terrestrial, and aquatic ecosystems and can be incorporated into animal bodies through various routes, including inhalation, dermal contact, and the food chain. The accumulation of these debris generates toxicity on several organs, including the nervous system. In this review article, I will cover the detrimental consequences of plastic exposure on the nervous system, the impact of microplastics and nanoplastics on the genesis of neurons both in the embryonic period as well as in adulthood, and the reliability of 5-bromo-2'-deoxyuridine (BrdU) labeling as a tool to analyze the effect of microplastic and nanoplastic exposure on the proliferative behavior of neuronal precursors. BrdU is a marker of DNA synthesis. It is widely used to identify proliferating neuroblasts and follow their fate during embryonic, perinatal, and adult neurogenesis. However, the use of BrdU labeling for analyzing neurogenesis may be inaccurate due to pitfalls and limitations. This is because BrdU exposure can induce apoptosis, cellular senescence, and alterations in DNA methylation. Interestingly, these cellular events also occur following exposure to plastic particles.
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