The ability of mitochondria to oxidize substrates and generate energy
is integral to normal homeostasis and to the ability of cells to survi
ve in the face of impending energy failure. Lactic acidosis is a commo
n and readily apparent biochemical marker for mitochondrial dysfunctio
n. However, lactic acidosis represents only the most obvious example i
n which acquired or congenital abnormalities of mitochondrial oxidativ
e phosphorylating capacity contribute to the pathobiology and phenotyp
ic expression of a broad spectrum of clinical disorders. Consequently,
interventions that improve mitochondrial function or prevent mitochon
drial energy failure may have widespread therapeutic implications. Cop
yright (C) 1997 by W.B. Saunders Company.