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Effects of Microplastics and Nanoplastics Exposure on Neurogenesis. Are Thymidine Analogues a Good Option to Study Such Effects?
Summary
This review covers the neurotoxic effects of microplastics and nanoplastics, examining how these particles enter the nervous system through inhalation, ingestion, and skin contact, and discusses whether thymidine analogues used to track cell division are appropriate tools for studying plastic-induced neurogenesis disruption.
An important disadvantage of plastics is their fragmentation into smaller particles, classi-fied 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 gen-esis 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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