Four different gold compounds and three gold carriers were used to study the toxicity of gold salts on mitochondria isolated from different tissues. Each of the following compounds-aurothiomalate (ATM), thiomalate (TM), aurothiosulfate (ATS), thiosulfate (TS), aurothioglucose (ATG), thioglucose (TG), and gold chloride (GC)-was tested with mitochondria extracted from rabbit (RbLM) or rat liver (RLM), and from rabbit bone marrow (RbMM) or chloroma tumor (CM). The toxicity of these compounds and carriers on mitochondria was evaluated by determining the inhibition of oxidative phosphorylation as measured by oxypolarography. With glutamate as substrate, mitochondria from hematopoietic tissues (e.g. RbMM and CM) showed a very high sensitivity to low concentrations of ATM, while liver mitochondria (RbLM and RLM) were slightly or not at all affected by those concentrations. Such difference of sensitivity was not observed when ATS, ATG or GC was used. Thus, identical concentrations of ATS or GC were needed to inhibit the oxidative phosphorylation in all mitochondria, and concentrations up to 2500 μM ATG were without effect on any of the mitochondria studied. While with glutamate ATM and TM primarily inhibited transition state 4/state 3, suggesting the involvement of site 1 in the respiratory chain, ATS, ATG and GC appeared to have the same effect on mitochondria oxidizing either glutamate or succinate. Furthermore, whereas the inhibitory effect of ATS and GC could be prevented or released by cysteine, inhibition by ATM could not. The interaction of the gold compounds and carriers with the highly reactive thiol groups involved in the energy conservation mechanism is discussed.
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