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Increased expression of iNOS and nNOS, excessive production of superoxide, mitochondrial membrane depolarization, the release of cytochrome c, and activation of caspase 3 leading to apoptosis of myenteric and submucosal neurons are prominent after oxaliplatin treatment (McQuade et al., 2016c)
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TKT has been identified as a driver of HCC development by counteracting oxidative stress through the NRF2/KEAP1/BTB and CNC homolog 1 (BACH1) pathway [60]
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