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As an alternative ferroptosis suppressive mechanism, the FSP1/CoQ 10 /NADPH system is independent of the intracellular expression levels of GSH, GPX4 and ACSL4 and can protect cells from GPX4 inhibition-induced ferroptosis[30]

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The clinical effects of these disorders depends on the severity of enzyme deficiency and whether the -glutamyl cycle also is affected in non-erythroid tissues

ROS production is commonly observed during viral infections and modulates the host responses (Table 1)