he ability of mitochondria to oxidize substrates and
generate energy is integral to normal homeostasis and to
the ability of cells to survive in the face of impending
energy failure. Lactic acidosis is a common and readily
apparent biochemical marker for mitochondrial
dysfunction. However, lactic acidosis represents only the
most obvious example in which acquired or congenital
abnormalities of mitochondrial oxidative phosphorylating
capacity contribute to the pathobiology and phenotypic
expression of a broad spectrum of clinical disorders.
Consequently, interventions that improve mitochondrial
function or prevent mitochondrial energy failure may have
widespread therapeutic implications.
PW Stacpoole, Metabolism 1997;46/3:306-321
Copyright © 2003 Anamol Laboratories Ltd.
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