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doi: 10.1016/j.tips.2019.04.014

These findings suggest that pathological cardiac pressure overload induces NNT reverse functional mode to generate NADH at the expense of NADPH resulting in a high NADH/NAD + and reductive stress, further promoting ROS at complex I leading to oxidative injury and cell death (Fig

Maritim and colleagues reviewed in detail that diabetes has multiple effects on the protein levels and activity of these enzymes, which further augment OS by causing a suppressed defense response

Clinicians: circulating LPS, advanced glycation end-products, and xenobiotics promote oxidative stress and tubular injury

Nat Rev Cancer 3 (9): 639-49, 2003

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