Coumarin and hesperidin lessen oxidative damage by regulating metal sequestration, redox homeostasis, and ionomics in castor bean (Ricinus communis L.) under chromium, copper, and nickel stress

• Coumarin and hesperidin diminished metal phytotoxic effects. • Castor bean plants are highly sensitive to Ni toxicity. • Metals caused higher O 2 •‒ , H 2 O 2 , and •OH production. • Higher LOX activity triggered malondialdehyde production. • Coumarin and hesperidin regulated NO and H 2 S production. The present study was performed to examine the potential of coumarin and hesperidin to subside the phytotoxic effects of copper (Cu), nickel (Ni), and chromium (Cr) in castor bean plants. Metal toxicity diminished growth, chlorophyll, and antioxidant pigments, alongside a profound diminution in relative water content. Conversely, metal toxicity initiates a surge in the accumulation of amino acids, soluble sugars, proline, and glycine betaine, which indicates osmotic adjustment in plants. Metal toxicity diminished nitrate reductase activity, elevated reactive oxygen species (ROS) generation, and heightened oxidative injury. In stressed plants, enhanced lipoxygenase (LOX) activity exacerbated membrane lipid peroxidation. Antioxidant enzyme activities decreased while the levels of flavonoids, phenolics, reduced glutathione (GSH) and oxidized glutathione (GSSG) increased, accompanied by a reduction in the GSH:GSSG ratio. Plants experienced impaired nutrient acquisition under metal toxicity. Coumarin and hesperidin increased nitric oxide and hydrogen sulfide levels, which might have restored the redox balance. Consequently, plants administered coumarin and hesperidin manifested more profound levels of chlorophyll, strengthened antioxidant system, efficient ROS detoxification, and diminished oxidative damage that, in turn, restored cellular homeostasis. Coumarin and hesperidin remarkably ebbed aerial translocation of metals, thereby preventing colossal metal accumulation in leaves.