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Impact of Polyethylene Terephthalate Microplastics on Drosophila melanogaster Biological Profiles and Heat Shock Protein Levels
Summary
Scientists exposed fruit flies to PET microplastics and found severe cell damage in the gut, reproductive organs, and reduced fertility. The microplastics caused oxidative stress and triggered stress-response genes, with one gene (hsp83) identified as an early warning biomarker for microplastic toxicity. These findings in a well-studied model organism suggest that PET microplastics, commonly found in food and water, could pose risks to both gut health and reproductive function.
Microplastics and nanoplastics are abundant in the environment. Further research is necessary to examine the consequences of microplastic contamination on living species, given its widespread presence. In our research, we determined the toxic effects of PET microplastics on <i>Drosophila melanogaster</i> at the cellular and genetic levels. Our study revealed severe cytotoxicity in the midgut of larvae and the induction of oxidative stress after 24 and 48 h of treatment, as indicated by the total protein, <i>Cu-Zn SOD</i>, <i>CAT</i>, and MDA contents. For the first time, cell damage in the reproductive parts of the ovaries of female flies, as well as in the accessory glands and testes of male flies, has been observed. Furthermore, a decline in reproductive health was noted, resulting in decreased fertility among the flies. By analyzing stress-related genes such as <i>hsp</i>83, <i>hsp</i>70, <i>hsp</i>60, and <i>hsp</i>26, we detected elevated expression of <i>hsp83</i> and <i>hsp70</i>. Our study identified <i>hsp83</i> as a specific biomarker for detecting early redox changes in cells caused by PET microplastics in all the treated groups, helping to elucidate the primary defense mechanism against PET microplastic toxicity. This study offers foundational insights into the emerging environmental threats posed by microplastics, revealing discernible alterations at the genetic level.
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