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<div><p>Reactive oxygen species (ROS) are essential modulators of epigenetic modifications under abiotic stress. However, the mutual regulation mechanism of the two under cadmium (Cd) stress is unclear. In this work, we investigated this issue using Cd-stressed pakchoi seedlings treated with six epi-modification inhibitors (5-AC, RG108, TSA, CUDC101, AT13148, and H89) as experimental materials. The experimental data showed that Cd stress caused ROS accumulation and chromatin decondensation. Addition of low concentrations of epi-modification inhibitors increased histone acetylation modification levels, and effectively attenuated cell cycle arrest and DNA damage caused by Cd-induced ROS accumulation, where histone acetylation modification levels were co-regulated by histone acetyltransferase and deacetyltransferase gene transcription. Moreover, the addition of the antioxidant Thi enhanced this mitigating effect. Also, TSA addition at high concentrations could also increase Cd-induced ROS accumulation. Based on this, we propose that the ROS molecular pathway may be related to epigenetic regulation, and chromatin modification may affect ROS accumulation by regulating gene expression, providing a new perspective for studying the regulatory mechanism of epigenetic modification under abiotic stress.</p></div>