Abstract
The norepinephrine analogue meta-iodo-benzylguanidine (MIBG), a substrate for mono(ADP-ribosylation) and inhibitor of eukaryotic ADP-ribosyltransferases, inhibits the prooxidant-induced and spontaneous calcium release from intact rat liver mitochondria without affecting pyridine nucleotide oxidation and hydrolysis. This finding strongly suggests regulation of calcium release by ADP-ribosylation in mitochondria, and may be relevant for the cellular and pharmacological effects of MIBG.