ABSTRACT
The relationship between lipid peroxidation and rat heart mitochondrial monoamine oxidase activity was studied in experimental myocardial necrosis induced by adrenaline injection. It has been established that both the intensity of peroxidation and the activity of monoamine oxidase in mitochondria from adrenaline-injured rat myocardium were essentially increased. The preliminary administration of antioxidants (vitamin E and ionol) was shown to decrease both the intensity of lipid peroxidation and the activity of monoamine oxidase. It is suggested that intensification of lipid peroxidation which is considered to be the main pathogenic factor in ischemic myocardial injury depends on mitochondrial monoamine oxidase activity. Protective effects of antioxidants are realized by the action on two subsequent chains during the formation of active oxygen forms and destruction of lipid peroxidation products.
Subject(s)
Lipid Peroxides/biosynthesis , Mitochondria, Heart/metabolism , Monoamine Oxidase/physiology , Myocardium/pathology , Animals , Male , Myocardium/metabolism , Necrosis , Rats , Rats, Inbred StrainsABSTRACT
Chronic experiments on rabbits have shown that visual cortex stimulation resulted in intensified lipid peroxidation in the retina with the parallel decrease of electroretinogram amplitude parameters. The transsection of the optic nerve resulting in the elimination of retinal corticofugal inputs diminished the accumulation of lipid peroxidation products in the rabbit retina during light adaptation. Preliminary insertion of antioxidants to animals (vitamin E and ionol) prevents the inhibitory effect of the cortex on the function of the retina. The data obtained are discussed in view of possible involvement of lipid peroxidation in the retina into the realization of the regulating influence of the cortex on the function of the retina.
Subject(s)
Lipid Peroxides/metabolism , Retina/metabolism , Visual Cortex/physiology , alpha-Tocopherol/analogs & derivatives , Animals , Butylated Hydroxytoluene/pharmacology , Dark Adaptation , Electroretinography , Malondialdehyde/metabolism , Optic Nerve/physiology , Oxidation-Reduction/drug effects , Physical Stimulation/methods , Rabbits , Retina/drug effects , Tocopherols , Vitamin E/analogs & derivatives , Vitamin E/pharmacologyABSTRACT
The influence of lipid peroxidation (LPO) in isolated frog retina on dark adaptation of photoreceptors was studied. Stimulus-response functions, late receptor potential (LRP) as function of the stimulus light intensity were measured before bleach and in a steady state after dark adaptation. It was shown that accumulation of LPO products influenced dark adaptation in photoreceptors. Based on the displacements of the stimulus-response curves and experimental measurement data on the rate of LRP collapse after retina treatment with strophanthin it is concluded that the most probable mechanism of such an influence lies in a change of photoreceptor plasma membrane permeability.
