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It is certain that while B1 cells from the spleen did not die of iron during GPX4 deficiency, B1 cells taken from the abdominal cavity of mice experienced a higher degree of ferroptosis at the time of GPX4 defect (166) ( Figure 3 )

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Combined research protocols allow investigators to examine whether modulating NAD+ availability alongside mitochondrial redox activity produces measurable effects on cellular energy metabolism endpoints

ELISA kits have also been developed [480]

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