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NADPH contributes to recycling in oxidized antioxidant systems involving glutathione, thioredoxins, glutaredoxins, and peroxiredoxins and maintains another reactive oxygen species (ROS)-detoxifying enzyme, catalase, in its active form, suggesting that the homeostatic level of G6PD-derived NADPH determines the rate of oxidative damage [8]

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Urinary 8-OHdG as a biomarker for oxidative stress: a systematic literature review and meta-analysis

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The major pathogenetic mechanism of GD is the stimulation of the thyroid stimulating hormone receptor (TSH-R) by autoantibodies that bind to it and promote thyrocyte proliferation and activity, resulting in thyroid hyperfunction (13)