Short term toxicity tests using mitochondrial and microsomal metabolism were developed and applied to a series of eight quinones In the mitochondrial assay, the degree to which test compounds inhibited mitochondrial respiration varied from an effective concentration (EC50) of 9 to 125 μM In the microsomal assay, the maximum percentage of increase over control oxygen consumption rates elicited by the quinones ranged from 8 to 837% The ability of the compounds to stimulate microsomal oxygen uptake reflects their capability to redox cycle and form reactive oxygen species Results of the mitochondrial and microsomal assay were statistically correlated with several quinone physicochemical parameters and qualitatively compared to reduction potential The biological response observed in both test systems appeared to be most strongly influenced by the re duction potential of the quinone Biomechanisms of action were suggested on the basis of this relationship To assess the abil lty of the mitochondrial and microsomal assays to indicate toxicity of the quinonoid compounds, results were statistically correlated with literature derived toxicity data It was concluded that the mitochondrial assay appears to be a valid indicator of acute tox lcity, whereas the microsomal assay better portends the potential for chronic toxicity