Abstract
The cytotoxicity of 1-methyl-4-phenylpyridinium (MPP +) is believed to arise as a consequence of its time- and energy-dependent accumulation inside mitochondria, followed by inhibition of electron transport at Complex I of the respiratory chain. Consistent with our proposal that the accumulation of MPP + represents a passive Nernstian transport into mitochondria in response to the transmebrane electrochemical potential gradient, tetraphenylborate (TPB −) was found to accelerate the onset of the respiratory inhibition by MPP + on intact mitochondria. Moreover, the ultimate level of inhibition reached was unexpectedly also increased. The latter is now explained by our finding that TPB − elicits a 12-fold enhancement of MPP + inhibition of respiration in electron transport particles. It is suggested that TPB − facilitates access of MPP + to its intramembrane site of inhibitory action in Complex I.
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