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These findings suggest that manoeuvres designed to increase mucosal GSH content may be useful to withstand the lethal consequences of oxidative stress that may contribute to attenuate the activation and recruitment of related factors that participate in the development of IBD, including VCAM-1 and ICAM-1 (Sans et al, 1999)
It has been shown that p53 can activate ALOX12 transcription under conditions of DNA damage or oxidative stress and increase the production of lipid peroxides, thereby promoting ferroptosis (75)
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