ABSTRACT
O T3 sérico, assim como a razäo T3/T4, säo sensíveis a comprometimento do sistema do citocromo P-450 microssomal, que desempenha importante papel no metabolismo de xenobióticos. Neste trabalho, confirmamos a diminuiçäo dos dois parâmetros em doentes portadores de cirrose e verificamos sua normalidade em portadores da forma hepatoesplênica e compensada da esquistossomose (estes últimos näo alcoólatras, nem portadores de AgHBs); por outro, em 53% dos esquistossomóticos, detectamos diminuiçäo na albuminemia e/ou transtiretinemia. Estes resultados sugerem que nesta forma de parasitose: 1) o comprometimento da síntese hepática de proteínas precede o da conversäo hepática de T4 em T3; 2) a capacidade de metabolizar xenobióticos está preservada
Subject(s)
Liver Diseases, Parasitic , Microsomes, Liver/physiopathology , Schistosomiasis , Thyroxine/blood , Triiodothyronine/bloodABSTRACT
Liver tissues were isolated from rats acutely intoxicated with carbon tetrachloride, and Na-23 NMR signals were analyzed to investigate the T1 relaxation times of intracellular sodium ions under pathological conditions in presence of the paramagnetic shift reagent (dysprosium tripolyphosphate). We studied the significant increase of T1 found in CCl4 treated rats with respect to controls, which was elsewhere demonstrated as being independent of cell necrosis. Evidence is given that neither fat accumulation nor proliferative processes affect the observed T1 lengthening. When T1 relaxation times were measured in the liver of vitamin E treated rats subsequently intoxicated with carbon tetrachloride, a significative shortening of T1 with respect to CCl4-intoxicated rats was observed. These results were discussed in terms of the antioxidant action exerted by vitamin E, taking into account that peroxidation of microsomal lipids is the key factor in the process of carbon tetrachloride induced liver injury. Furthermore, the observed T1 changes were discussed in terms of the interactions of Na+ with cell membranes and/or the occurrence of viscosity changes.
Subject(s)
Carbon Tetrachloride Poisoning/physiopathology , Liver/physiopathology , Sodium/physiology , Hepatectomy , Lipid Peroxides/metabolism , Magnetic Resonance Spectroscopy , Microsomes, Liver/physiopathology , Time Factors , Vitamin E/pharmacologyABSTRACT
The presence of ethanol disorders (fluidizes) biological membranes, but its chronic administration confers resistance to this perturbation (membrane tolerance). The latter effect has been invoked as an explanation for behavioral tolerance in alcoholics, but the molecular basis for membrane tolerance is obscure. To study the molecular mechanisms of this acquired resistance to disordering, we fed rats ethanol (36% of total calories) for 35 days, after which we quantitatively separated the phospholipids of hepatic microsomal membranes by high-performance liquid chromatography. Multilamellar vesicles were prepared from the recombined phospholipid classes, and their physical properties were examined by electron spin resonance. Vesicles composed of phospholipids from untreated rats were disordered (fluidized) in the presence of ethanol, whereas those made from phospholipids of ethanol-fed rats were resistant to this effect. When phosphatidylcholine (66.5 mol %), phosphatidylethanolamine (21 mol %), or phosphatidylserine (4.0 mol %) from ethanol-fed rats replaced their corresponding phospholipids in vesicles prepared from microsomal phospholipids from untreated rats, the membranes were still disordered by ethanol. In contrast, when 2.5-8.5 mol % phosphatidylinositol from ethanol-fed rats replaced phosphatidylinositol from untreated rats, the reconstituted membranes were rendered resistant to ethanol-induced disordering. Liver microsomal phosphatidylinositol (2.5-8.5 mol %) from ethanol-fed rats also conferred membrane tolerance to vesicles composed of bovine liver and brain phospholipids, an effect which demonstrates that the ability of phosphatidylinositol to confer membrane tolerance is not restricted to the microsomal membrane.
