Issues   /  ISSUES 12 VOLUME 30 2025 (OCTOBER- DECEMBER)   /  Article

Study of Quantitative Toxicogenomics How and Why Environmental Pollutants Became Toxic Throughout Their Life Cycle

Research Paper

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Keyword :-
Oxidative degradation, intermediates, genotoxicity, membrane stress, protein stress, oxidative stress, Toxicogenomics, toxicity evolution.

Author 1 :- Kriti Maheswari ( Research Scholar )
Author 2 :- Dr. Neelam Kumari ( Associate Professor )

The partial mineralization of contaminants of emerging concern (CECs) during advanced oxidation processes may produce transformation products that possess toxicity equivalent to or exceeding that of the original pollutant. In this study, we demonstrated the application of a novel, rapid, and cost-effective quantitative toxicogenomics-based approach for evaluating the evolution and nature of toxicity during the electro-Fenton oxidative degradation of three representative CECs—bisphenol A, triclosan, and ibuprofen—whose oxidative degradation pathways have been relatively well characterized. The progression of toxicity due to the transformation of parent chemicals and the generation of intermediates during degradation is observed, with quantitative toxicogenomics assay results elucidating the dynamic changes in toxicity and their mechanisms, alongside their correlation with identified intermediates during the electro-Fenton oxidation of the selected CECs. For the three CECs, more than 75% of the parent compounds were gone after 15 minutes of reaction time. However, it took at least 30 minutes for the toxicity to almost completely go away, and this seems to be related to the disappearance of certain aromatic intermediates. Bisphenol A caused a wide range of stress responses. Some of the transformation products that were found, such as 1,4-benzoquinone and hydroquinone, likely caused the DNA stress (genotoxicity) and membrane stress that happened during the degradation. from primarily inducing membrane stress to causing persistent membrane stress, with protein stress and DNA damage.