Al toxicity is the main limiting factor for crop production in acidic soil, so this study is aimed to improve understanding of the effects of curcumin on the aluminum (Al) tolerance of grapes, Al-tolerant cultivation and the epigenetic mechanism of grapes exposed to Al. Vitis vinifera x V labrusca `Shuifing' cuttings were cultivated in greenhouse, which were exposed to 20 mmol L-1 aluminum sulfate and then treated with curcumin in different concentrations. Then, indicators of physiological resistance and the DNA methylation level of the grape leaves were measured. The results demonstrated that Al stress led to a series of physiological and biochemical changes in grape leaves and significantly increased DNA methylation levels. Specifically, the chlorophyll, protein, phosphorus (P) and potassium (K) content decreased, activity of superoxide dismutase (SOD) and peroxidase (POD) also decreased, while the proline, malonaldehyde and Al content increased drastically, resulting in damage to grape plants. However, treatment by 100 and 200 mu cool L-1 of curcumin led to significantly reduced DNA methylation levels and Al accumulation in grape leaves, reduced accumulation of malonaldehyde and proline, increased chlorophyll and protein content, enhanced SOD and POD activity, and improved intake of P and K. In summary, treatment by 100 and 200 mu mot Li curcumin had a significant effect on the Al tolerance of grapes, indicating that toxicity for grape cultivation in acidic soil.

Atrazine (ATR), a water-soluble herbicide commonly used to control broad-leaf and monocotyledonous weeds, presents a significant risk to environmental soil and water quality. Exposure to ATR adversely affects human and animal health, frequently resulting in cardiac impairment. Curcumin (Cur), an acidic polyphenol derivative from plants acclaimed for its pronounced anti-inflammatory and antioxidant properties, has garnered interest as a potential therapeutic agent. However, whether it has the potential to ameliorate ATR-induced cardiac toxicity via modulation of endoplasmic reticulum stress (ERS) and apoptosis pathways in mice remains unclear. Our results showed that Cur supplementation attenuates ATR-induced cardiotoxicity, evidenced by decrease in creatine kinase and lactate dehydrogenase, key biochemical markers of myocardial injury, which have a more significant protecting effect in high-dose ATR induced injury. Histopathological and electron microscopy examinations further solidified these findings, demonstrating an amelioration in organellar damage, particularly in endoplasmic reticulum swelling and subsequent mitochondrial impairment. Additionally, ATR exposure augments ERS and triggers apoptotic pathways, as indicated by the upregulation of ERS-related gene expression (ATF6, CHOP, IRE1, GRP78) and pro-apoptotic markers (BAX, BAK1, Caspase3, Caspase. Intriguingly, Cur counteracts this detrimental response, significantly reducing ERS and pro-apoptotic signals at both transcriptional and translational levels. Collectively, our findings illuminate Cur's cardioprotective effect against ATRinduced injury, primarily through its anti-ERS and anti-apoptotic activities, underscoring Cur's potential as a therapeutic for ATR-induced cardiotoxicity.