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PubMedDate not supplied

[Deamination of nitrogenous compounds in mitochondrial membranes under stimulation of lipid peroxidation].

Fragments of mitochondrial membranes, obtained by freezing-thawing of mitochondrial fraction from rat liver homogenate, were treated with Fe2+ ions under conditions, which were optimal for accumulation of a product of lipid peroxidation--malondialdehyde (MDA). The accumulation of MDA in the mitochondrial membranes was accompanied by a decrease in deamination of monoamines (tyramine or, especially, tryptamine) and by appearance of qualitatively new properties to deaminate histamine or cadaverine as well as adenylic acid. Appearance of these properties was prevented by blocking with trans-2-phenylcyclopropylamine or N-methyl-N-benzylpropynylamine of the mitochondrial monoamine oxidase activity. Inhibitors of initiated by free radicals lipid peroxidation (propylgallate, butyl hydroxytoluene) did not bind Fe2+ ions but prevented the alterations in deamination of nitrogenous compounds induced by the treatment of the fragments of mitochondrial membranes with Fe2+ ions. Stimulation of lipid peroxidation in mitochondrial membranes was, thus, accompanied not only by partial inactivation of the structure-bound monoamine oxidase but also by apparent qualitative alteration (transformation) in its catalytic properties.

Animals↗
PubMedDate not supplied

[Mechanism of disturbances in the deamination of nitrogenous compounds in experimental hypercholesterolemia and atherosclerosis].

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.

Aged↗
PubMed2000

Modulation of growth performance in disease: reactive nitrogen compounds and their impact on cell proteins.

During life, all animals encounter situations that challenge their capability for optimal growth. In reacting to immune challenges in the form of disease, homeostatic mechanisms attempt to overcome disharmony of the body's internal environment, or simply put, stress. The overall impact of stress revolves around a dynamic relationship between the level of challenge imparted on physiological systems and the degree of host response that is mounted in the process of detecting and reacting to the stress. In growing animals, the majority of milder stress encounters are manifest in terms of energetic inefficiencies and periods of reduced anabolism. In contrast, severe stress is often characterized by frank catabolism and tissue wasting. In some instances a level of stress (that might be termed a "stress breakpoint") is reached at which time the host response itself contributes to the cascade of negative effectors that further cause illness. These "breakpoint" responses are characterized by more intense acute responses to stress or a much more protracted duration of the response than would be expected given the nature of the stress. Key to understanding how growth in the young animal responds to infectious stresses is the recognition that (a) when immune responses that normally maintain health go awry, the reporters and effectors of the immune system (cytokines and the nitric oxide cascade) can contribute to stress disease processes and (b) reactive nitrogen compounds derived from the nitric oxide, as well as super oxide anion can modify intracellular proteins and block otherwise normal biochemical processes that regulate cell function. A key example of this is the loss of regulation of IGF-I by GH. As animals react more severely to disease stress, IGF-I concentrations in plasma decline progressively. Recent data derived from (LPS) challenges performed on young calves suggest that the prolonged decline in IGF-I is associated with the development of hepatic cytotoxicity localized to regions of protein nitration as identified by immunohistochemistry. Identifying biochemical criteria for disease processes provides needed guidance for the further development of intervention strategies to limit the impact of disease on growth.

Animals↗
PubMed1962

Utilization of nitrogen compounds by unicellular algae.

Eight Chlorophyta employ urea as a sole nitrogen source; five utilize uric acid and xanthine. The Cyanophyta, Rhodophyta, and Euglenophyta studied do not grow on these three nitrogen sources, although Anacystis nidulans decomposes uric acid to allantoin. None of the algae tested utilized either allantoin or creatinine.

Allantoin↗
PubMedDate not supplied

[Metabolism of organic nitrogen compounds by carboxydobacteria].

The capability to hydrolyze and assimilate creatinine, uric and hippuric acids as sources of nitrogen, carbon and energy was studied in Comamonas compransoris Z-1155, Seliberia carboxydohydrogena Z-1062 and Pseudomonas gazotropha Z-1156. The organisms effectively hydrolyzed these compounds and assimilated their nitrogen under the conditions of autotrophic growth. The carboxydobacteria were also capable of growing in media containing creatinine, uric and hippuric acids and assimilated these compounds as carbon sources. In the absence of extraneous energy sources, none of the organisms grew in media with organic nitrogen compounds though the latter were hydrolyzed.

Bacteria↗
PubMed2001

Changes in nitrogen compounds in must and wine during fermentation and biological aging by flor yeasts.

Urea, ammonium, and free amino acid contents were quantified in a must from Vitis vinifera cv. Pedro Ximenez grapes and in fermented wine and after a short aging of this wine by Saccharomyces cerevisiae race capensis yeast under variable oxygen availability conditions. The previous compounds were also determined in a wine in which the nitrogen source was depleted by the same race of flor yeast (old wine) and also following the addition of ammonium ion, L-glutamic acid, and L-proline. Under specific conditions such as low oxygen level and the absence of some nutrients, the yeasts release some amino acids including L-threonine, L-tryptophan, L-cysteine, and L-methionine to the medium. These amino acids must originate primarily in a de novo synthesis from ethanol that regenerates NAD(P)+. On the basis of these results, the yeasts may be able to use amino acids not only as nitrogen sources but also as redox agents to balance the oxidation-reduction potential under conditions of restricted oxygen, when electron transport along the respiratory chain may be hindered or limited.

Aging↗