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Further, we did not detect a correlation of GSH status and levels of MDA or total cysteine, suggesting that the GSH buffer capacity is not a limiting factor for protection from oxidative stress in this cohort of healthy older adults
Another potential mechanism for age-dependent loss of antioxidant genes was provided by one of the studies showing that the presence of transcription repressor BACH1 along with the absence of coactivator CREB-binding protein (CBP) in the aged mice may convert NRF2 binding from an active ARE to an alternative ARE [114]
