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In addition, exposure to exogenous glutathione promoted the potential for virulence through accelerated and increased zoospore release
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However, in resistant patients, oxidative stress causes a conformational change in Keap1, leading to the release of NRF2, which translocates to the nucleus and binds to antioxidant response element (ARE), activating the expression of downstream antioxidant genes, including GPX4, NQO1, HO-1 and SOD1 [33], and promoting the synthesis of GSH, as illustrated in Fig
Br J Cancer 1995
Thiol-disulphide balance and total oxidant-antioxidant status in patients with chronic hepatitis C
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