Impact of Polyethylene Terephthalate Microplastics on IDrosophila melanogaster/I Biological Profiles and Heat Shock Protein Levels

The threat posed by microplastic toxicity to organisms is growing substantially, and the ramifications of daily microplastic usage cannot be disregarded. The extent of toxicological research pertaining to microplastics has increased due to the grave and alarming nature of microplastic pollution. We have, therefore, conducted research in an effort to determine the toxicological impact of microplastics on the cellular and genetic levels. The toxicity of accumulated polyethylene terephthalate microplastics on Drosophila melanogaster has been determined by our research. At higher concentrations of microplastics, cellular and reproductive toxicities have been observed, which correspond to elevated oxidative stress, identified through the analyses of various oxidative stress markers’ activities. Furthermore, the levels of heat shock proteins have been identified, contributing to the understanding of the primary defense mechanism against the toxicity of microplastics. The study has provided significant and concerning insights into the escalating health risks posed by microplastics. It appears that microplastics are inducing genetic alterations; therefore, further investigation should be undertaken at the genetic level to clarify the potential transgenerational consequences that pose a significant risk to future generations. 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 Drosophila melanogaster 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, Cu-Zn SOD, CAT, 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 hsp83, hsp70, hsp60, and hsp26, we detected elevated expression of hsp83 and hsp70. Our study identified hsp83 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 microplas