These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Mechanism of disturbances in the deamination of nitrogenous compounds in experimental hypercholesterolemia and atherosclerosis].
    Author: Khuzhamberdiev M, Mamadiev M, Gorkin VZ.
    Journal: Vopr Med Khim; 1981; 27(6):829-35. PubMed ID: 7336659.
    Abstract:
    Experimental alimentary hypercholesterolaemia in rabbits caused not only a decrease in deamination of monoamines (serotonin, benzylamine, tyramine) in liver, brain, kidney and heart mitochondrial fractions but also an appearance in these fractions of a qualitatively new reactions, namely that of cadaverine deamination, which was occasionally accompanied by stimulation of AMP deamination. In mitochondrial fractions from liver tissue obtained by autopsy in cases of ischemic heart disease accompanied by atherosclerosis, as compared with the corresponding fractions from the liver of persons who died in accidents and in whom no distinct morphological manifestations of atherosclerosis could be noted, there was observed a decrease in deamination of serotonin or tyramine (by 52% and 63%), appearance of cadaverine deamination (Vmax constitutes 35% of the Vmax value for serotonin deamination in the same fraction (and stimulation) 2-fold) of AMP deamination. The impairments in deamination of the nitrogenous compounds in experimental hypercholesterolaemia and in atherosclerosis are apparently due to qualitative alteration (transformation) in catalytic properties of mitochondrial monoamine oxidases. Implications of this hypothesis for future research on treatment of atherosclerosis are discussed.
    [Abstract] [Full Text] [Related] [New Search]