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Based on the implication of redox imbalance and ferroptosis in DON pathology 22 , and GAs profile as an Nrf2 activator 27 with anti-ferroptotic potential 28 , we hypothesized that GA protects against DON toxicity by enhancing cellular antioxidant defenses via the Nrf2 pathway, thereby suppressing ferroptosis

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Naturally or synthetic chemotherapeutic agents exert their effects through oxidation or modification of cysteine thiol groups present in the cellular signal molecules mediated by phosphatases and kinases

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