ABSTRACT
The paper is dedicated to the study of peculiarities of ubiquinone and ubichromenol distribution and metabolism in subcellular fractions of rats' liver under A,E-hypovitaminosis. It is shown, that dietary deprivation of vitamins A and E leads to a sharp decrease in intensity of CoQ biosynthesis in rats' liver tissue and to its intracellular redistribution. Under these circumstances the observed decrease in the inclusion of labelled tyrosine in rats' liver CoQ under A,E-hypovitaminosis may be really caused by dietary deprivation of vitamin E.
Subject(s)
Chromans/metabolism , Liver/metabolism , Ubiquinone/metabolism , Vitamin A Deficiency/metabolism , Vitamin E Deficiency/metabolism , Animals , Rats , Tocopherols/administration & dosage , Tritium , Tyrosine/chemistry , Ubiquinone/biosynthesis , Vitamin A/administration & dosage , Vitamin A Deficiency/complications , Vitamin E Deficiency/complicationsABSTRACT
The character of some lipids level change--cholesterol and phospholipids--as basic lipid components of cell membranes in the guinea-pig brain and liver tissue, and in serum in conditions of development of experimental autoimmune encephalomyelitis (EAE) have been investigated on the 11th, 21st, 27th day after inoculation. It has been detected, that the level of the investigated lipids changes wavely and indifferent-direction in the brain tissue on the 21st day of EAE. Similar variability observed in the activity of proteolytic ferment calpain, which is authentically reduced in the brain tissue by the 11th hour and increases up to the test objective level in the subsequent periods of EAE development. In the liver the level of alpha-tocopherol is reduced, while the content of studied lipids does not change. The investigated parameters can be attributed to the factors, which play an essential role in structural stability of cell membranes and their variability in conditions of EAE development is related to the processes of nervous cells demyelinisation and, hence to occurrence of such pathology as multiple sclerosis in people.
Subject(s)
Autoimmune Diseases of the Nervous System/metabolism , Calpain/metabolism , Cholesterol/metabolism , Encephalomyelitis/metabolism , Phospholipids/metabolism , Animals , Autoimmune Diseases of the Nervous System/immunology , Brain/immunology , Brain/metabolism , Disease Models, Animal , Encephalomyelitis/immunology , Guinea Pigs , Liver/immunology , Liver/metabolismABSTRACT
Concentration of lipid peroxidation products and antioxidant enzyme activities in rat brain and erythrocytes and the effects of nicotinamide and nicotinoyl-GABA administration on these parameters were estimated on 21st day of streptozotocin-induced diabetes. It was demonstrated more then two-fold diabetes-induced accumulation of conjugated dienes and malondialdehyde in tissues studied. Superoxide dismutase and glutathione reductase activities of both brain homogenate and erythrocytes as well as catalase and glutathione peroxidase activities of brain homogenate were shown to decrease significantly in diabetic rats, meanwhile, catalase activity of erythrocytes was increased and glutathione peroxidase unchanged. So the correlation between changes in enzymatic antioxidant system in brain and erythocytes failed to be found. Alterations observed were virtually prevented by the course of nicotinamide and nicotinoyl-GABA treatment. The results suggested that the suppression of antioxidant system could be primary biochemical disturbance in diabetic neuropathy progression. It was shown that the antioxidant efficacy of nicotinoyl-GABA is lower than that of nicotinamide. It was suggested that the mechanism of antioxidant action of nicotinamide and its structural analogue consists of both scavenging of lipid peroxides and NAD biosynthesis that leads to activation and normalization of altered energy and lipid metabolism.
Subject(s)
Diabetes Mellitus, Experimental/metabolism , Diabetic Neuropathies/drug therapy , Niacinamide/therapeutic use , Oxidative Stress/drug effects , gamma-Aminobutyric Acid/therapeutic use , Animals , Antioxidants/metabolism , Brain/drug effects , Brain/enzymology , Brain/metabolism , Catalase/metabolism , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Experimental/enzymology , Diabetic Neuropathies/enzymology , Diabetic Neuropathies/metabolism , Erythrocytes/drug effects , Erythrocytes/enzymology , Erythrocytes/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Lipid Peroxidation/drug effects , Malondialdehyde/blood , Rats , Rats, Wistar , Superoxide Dismutase/metabolismABSTRACT
It is shown that alpha-tocopherol in vitro stimulates respiration of the liver mitochondria in E-hypovitaminosis rats only in the presence of the specific protein factor isolated from the liver cytosol. The action of alpha-tocopherol on mitochondria in the presence of NAD and a protein factor is not accompanied by an increase in the NADH level, that evidences for the absence of the direct redox interaction between NAD and tocopherol.
