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Cytogenotoxic potential of a hazardous material, polystyrene microparticles on Allium cepa L.

Journal of hazardous materials 2020 Score: 30 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Sukhendu Maity, Ankit Chatterjee, Rajkumar Guchhait, Sukanta De, Kousik Pramanick

Summary

This study used the onion root test to assess the genotoxic effects of polystyrene microplastics on plant cells, finding that even at relatively low concentrations the particles caused oxidative stress, reduced root growth, and damaged chromosomes. The results indicate that polystyrene microplastics pose hazards to plant genetics, with implications for agricultural soil contamination.

Polymers

Plastic pollution represents a global concern for the biodiversity conservation, ecosystem and public health. The polystyrene is one of the dominant pollutants in both terrestrial and aquatic ecosystem. This work measured the hazardous nature of 100 nm micropolystyrene (MPS) using 25, 50, 100, 200, and 400 mg/L concentrations in terms of oxidative stress, morphotoxicity and cytogenotoxicity in Allium cepa. The results were compared with the positive control (PC) (400 mg/L chlorpyrifos). MPS significantly (p < 0.05) reduced the root length while induced the production of hydroxyl, superoxide radicals with a concomitant increase in DPPH scavenging activity and lipid peroxidation as compared to the negative control. The significant decrease in mitotic index with respect to the negative control (MI: 23.855 ± 5.336 %; lowest MI: 3.88 ± 1.042 %) showed the cytotoxic nature of MPS. Genotoxicity was assessed by various chromosomal and nuclear aberrations. The highest 3.029 ± 0.403 % (PC: 3.09 ± 0.535 %) chromosomal abnormality index and 2.31 ± 0.338 % (PC: 1.178 ± 0.095 %) nuclear abnormality index were observed. MPS down-regulated the expression of plant CDKA encoding gene: cdc2, an important cell cycle regulator. The overall results indicated that MPS could induce cytogenotoxicity through the exacerbation of ROS production and inhibition of cdc2.

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