The role of lipid peroxidation in the possible involvement of membrane-Bound monoamine oxidases in gamma-aminobutyric acid and glucosamine deamination in rat brain

Abstract

Incubation of rat brain synaptosomes and mitochondria with LPO inducers (Fe2+ and ascorbate) was accompanied by a decrease of deamination of serotonin (substrate of MAO-A) in mitochondria, but not in synaptosomes, with simultaneous stimulation of GABA and GLCA deamination, apparently owing to modification of catalytic properties of brain membrane-bound MAO. Oxidation of PEA (substrate of MAO-B) was insignificantly altered in both fractions. Reactions of deamination of serotonin, GABA, and GLCA (but not PEA), were highly sensitive to a selective inhibitor of MAO-A pyrazidol (pyrlindole). Isoniazid and hydrazides of quinoline carbonic acids (inhibitors of both modified MAO and copper-containing amine oxidases) strongly inhibited deamination of GABA and GLCA. During epileptiformic seizures in rats, genetically selected for high incidence of audiogenic epilepsia, stimulation in brain synaptosomes and mitochondria of LPO was observed. This was accompanied by a marked decrease in serotonin and PEA deamination, with a simultaneous increase in GABA and GLCA deamination in both fractions. The data obtained suggest that appearance of GABA-deaminating activity owing to modification of catalytic properties of MAO, might be an essential pathogenetic component in the development of epileptic seizures.

The Krushinsky-Molodkina rat strain: The study of audiogenic epilepsy for 65 years

“…The latter was apparently due to modification of catalytic properties of brain membrane-bound MAO [61]. The similar parameters of the KM rat brain taken at the height of AS demonstrated the stimulation of lipid peroxidation in brain synaptosomes and mitochondria.…”

“…These data suggested that appearance of GABA-deaminating activity might be the important component in the development of epileptic seizures. It was also demonstrated that this deamination was due to modification of catalytic properties of MAO [61][62][63]. The parallel data were obtained in a mouse audiogenic seizure-prone strain [DBA/2] in which the inhibition of serotonin uptake and of oxidative deamination attenuated audiogenic seizures.…”

Redox Processes in Neurodegenerative Disease Involving Reactive Oxygen Species

“…A study indicates the anticonvulsant and AO effects of curcumin and Nigella saliva oil in reducing OS, excitability and induction of seizures [41]. The role of lipid peroxidation was examined in the possible involvement of monamine oxidase in the epileptic rat brain [42].…”

Audiogenic Epilepsy -- The Pathological Neural Net and Genetic Predisposition

“…At the same time noradrenergic, dopaminergic, serotoninergic, purinergic and several other brain systems function in the aberrant way in AE prone rats. This could signify that the brain anomaly of genetic origin exists in these animals and this abnormal genetic system is expressed in the brain at the early stage of ontogeny so that the widespread pleyotropic effects of this genetic anomaly are present in many neurotransmitter systems [15][16][17][18][19][20]. In particular, the significant interstrain differences (between KM and "0" strain in the number of D1-D2 and glutamate in striatum they being less numerous in KM rats [21].…”