[Deamination of nitrogenous compounds in mitochondrial membranes under stimulation of lipid peroxidation].

Fragments of mitochondrial membranes, obtained by freezing-thawing of mitochondrial fraction from rat liver homogenate, were treated with Fe2+ ions under conditions, which were optimal for accumulation of a product of lipid peroxidation--malondialdehyde (MDA). The accumulation of MDA in the mitochondrial membranes was accompanied by a decrease in deamination of monoamines (tyramine or, especially, tryptamine) and by appearance of qualitatively new properties to deaminate histamine or cadaverine as well as adenylic acid. Appearance of these properties was prevented by blocking with trans-2-phenylcyclopropylamine or N-methyl-N-benzylpropynylamine of the mitochondrial monoamine oxidase activity. Inhibitors of initiated by free radicals lipid peroxidation (propylgallate, butyl hydroxytoluene) did not bind Fe2+ ions but prevented the alterations in deamination of nitrogenous compounds induced by the treatment of the fragments of mitochondrial membranes with Fe2+ ions. Stimulation of lipid peroxidation in mitochondrial membranes was, thus, accompanied not only by partial inactivation of the structure-bound monoamine oxidase but also by apparent qualitative alteration (transformation) in its catalytic properties.