Endogenous stimulation of lipid peroxidation in brain increases proteolytic inactivation of mitochondrial monoamine oxidases.

Stimulation of lipid peroxidation in vivo (in experimental epilepsy and closed cranio-cerebral injury, as models for endogenous stimulation of lipid peroxidation) affects catalytic activity, substrate specificity of mitochondrial monoamine oxidases and increases their susceptibility to trypsinolysis. It is suggested that increased susceptibility to trypsinolysis reflects an appearance of new hydrophilic site(s) in monoamine oxidase molecules which may be responsible for an involvement of the modified enzymes in the deamination of other important nitrogenous compounds (such as gamma-aminobutyric acid) with subsequent impairment of a ratio between inhibition and excitation processes in the brain.