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An alternate possibility is that cytosolic NADPH manipulation ultimately affects matrix NADPH status through metabolite shuttles, which are used to convey reducing equivalents across the mitochondrial membranes by coupling mitochondrial redox reactions with their cytosolic counterparts (for example, using the transport of citrate to couple IDH2 and IDH1) (Taylor, 2017)

Metabolomic studies in the preclinical ischemic AKI model have shed substantial light on this issue and demonstrated widespread changes in energy metabolism in the kidney as well as remote organs including the heart and lung 6,15, 16

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Both forms are generally safe when taken as directed