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. 2022 Jun 19;15(6):764. doi: 10.3390/ph15060764

Figure 7.

Figure 7

Antioxidant therapies against A-T. The defective ATM gene leads to the disruption of DNA damage response and repair, excessive production of ROS, and impairment of mitochondria. Antioxidant therapies can modulate ATM, NRF2, TERT, serine-1981, serine-824, KAP1 and γ-H2A.X expressions, and mitochondrial impairment, resulting in the restoration of DNA damage response and repair, antioxidant enzyme and gene levels, mitochondrial function, and telomere activity and elongation. This also leads to the attenuation of ROS production and pro-apoptotic activities. ATM, Ataxia-telangiectasia mutated; ATP, adenosine triphosphate; DNA, deoxyribonucleic acid; GCLC, glutamyl-cysteine ligase catalytic subunit; GCLM, glutamyl-cysteine ligase modifier subunit; GSEs, genetic suppressor elements; GSH, glutathione; GSR, glutathione reductase; GSS, glutathione synthetase; IL, interleukin; KAP1, KRAB-associated protein 1; KEAP1, Kelch-like ECH-associated protein 1; MMP, mitochondrial membrane potential; NQO1, NAD(P)H quinone oxidoreductase 1; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; NRF2, nuclear factor erythroid 2–related factor 2; OGG1, 8-oxoguanine DNA glycosylase-1; ROS, reactive oxygen species; SOD1, superoxide dismutase 1; TERT, telomerase reverse transcriptase; γ-H2A.X, gamma-H2A histone family member X; 8-oxoG, 8-oxoguanine.