A phenomenon associated with the aging process is a general age-dependent d
ecline in cellular bioenergetic capacity that varies from tissue to tissue
and even from cell to cell within the same tissue. This variation eventuall
y forms a tissue bioenergy mosaic. Recent evidence by our group suggests th
at the accumulation of mitochondrial DNA mutations, in conjunction with a c
oncurrent decrease in full-length mtDNA in tissues such as skeletal and car
diac muscle, strongly correlates with decreased mitochondrial function and
accounts for the bioenergy mosaic. Evidence is also presented suggesting th
at amelioration with coenzyme Q(10) may restore some of the age-associated
decline in bioenergy function, in effect providing the potential for a "red
ox therapy". Coenzyme Q is a naturally occurring material that is present i
n the membranes of all animal cells. Its primary function is to act as an e
lectron carrier in the mitochondrial electron transport chain enabling the
energy from substrates such as fats and sugars (in the form of reducing equ
ivalents) to be ultimately captured in the form of ATP. which in turn may b
e utilised as a source of cellular bioenergy. Coenzyme Q(10) has no known t
oxic effects and has been used in a limited number of animal studies and hu
man clinical trials: however, the mechanism of action of coenzyme Q(10) rem
ains unclear. A series of experiments by this group aimed at determining th
e efficacy of coenzyme Q(10) treatment on ameliorating the bioenergy capaci
ty at the organ and cellular level will also be reviewed.