Abstract
AbstractDibutyltin‐3‐hydroxyflavone bromide [Bu2SnBr‐(of)] is a fluorescent inhibitor (excitation max, 395 nm; emission max., 450 nm) of mitochondrial F1F0–ATPase which does not inhibit F1–ATPase. Bu2SnBr(of) binding to mitochondria and submitochondrial particles results in a 10‐fold fluorescence enhancement which correlates with the amount of F1F0–ATPase in the inner membrane. Enhancement is not affected by respiratory‐chain substrates, ATP, uncoupling agents, ionophores or respiratory‐chain inhibitors. It is reversed by tributyltin chloride (Bu3SnCl), indicating competition for a common triorganotin‐binding site on the F0 segment of F1F0–ATPase. Enhancement is not reversed by dialkyltins, monoalkyltins, tributyl‐lead acetate, efrapeptin or oligomycin. Bu2SnBr(of) is thus a new class of fluorescent probe of the F0 segment of F1F0–ATPase which titrates F0.
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