[Features of the biochemical action of paraquat on oxidative deamination of biogenic amines and other nitrogen compounds].

Intoxication of rats with the herbicide paraquat (1,1-dimethyl-4,4-bipyridilium dichloride) was accompanied by accumulation in lungs, brain, heart, liver or kidney of malonic dialdehyde (MDA) (the compounds reacting with 2-thiobarbituric acid), indicating that the intoxication stimulated lipid peroxidation (LPO) in biomembranes. Treatment of the intoxicated rats with the antioxidant diludin (2,6-dimethyl-3,5-diethoxycarbonyl-1,4-dihydropyridine) or with the nucleophilic reagents sodium ascorbate or thiosulphate normalized the content of MDA in lungs, brain, heart, liver or kidney demonstrating the reversibility of the LPO stimulation caused by paraquat. On incubation of mitochondrial fractions of homogenates of lungs, brain, heart, liver or kidney of the intoxicated rats (as compared with the corresponding fractions from the intact animals) a decrease was noted in deamination of the substrates of monoamine oxidases serotonin, tryptamine, benzylamine, tyramine; at the same time, deamination of glucosamine and gamma-aminobutyric acid was increased and deamination of putrescine and L-lysine appeared. These impairments in deamination of nitrogenous compounds caused by paraquat were reversible. All the impairments were normalized by the treatment of the experimental animals with the antioxidative and nucleophilic reagents; a decrease was noted in the rate of development of the lethal paraquat intoxication and appearance of morphological manifestations of normalization. The data obtained suggest that the reversible, qualitative modification ("transformation") of the monoamine oxidases of the type A might explain the peculiarities of the alterations in deamination of nitrogenous compounds in paraquat intoxication.