ABSTRACT
The biochemical organism state markers were studied in the rat serum and brain cortex at short-term (28 days) and long-term (16 month) chronic ethanol consumption (15%, v/v). In the first case the increase of alanine aminotransferase activity in the serum and hypertriglyceridemia have been revealed on the background of the stable main biochemical characteristics. The statistically significant decrease of cholinesterase activity and increase of alkaline phosphatase, aminotransferases, lactate dehydrogenase and alpha-amylase activities in the serum, the reduction of the serum triglycerides, total and lipoprotein cholesterol, increased atherogenic index and serum urea concentration were revealed at long-term alcoholization. Total sulphydryl groups/protein level ratio decreased in the brain cortex. It is concluded, that ethanol-induced long-term metabolic stress is accompanied by certain organism state impairment at rat aging, determined by interdependence of pathological and adaptive processes.
Subject(s)
Central Nervous System Depressants/adverse effects , Cerebral Cortex/drug effects , Enzymes/blood , Ethanol/adverse effects , Lipids/blood , Aging/drug effects , Aging/metabolism , Animals , Bilirubin/blood , Blood Glucose/analysis , Blood Proteins/analysis , Blood Urea Nitrogen , Female , Rats , Time FactorsABSTRACT
The range of the Na+, K(+)-ATPase functional stability in microsomal fraction of rat brain cortex under long-term chronic ethanol (15%, v/v) consumption was ascertained. The enzyme activity decreased only after 15 months of alcoholisation on the background of the stable structural membrane characteristics (on the basis of the intrinsic and 1-anilinonaphthalene-8-sulfonate fluorescence parameters) and SH-content in postmitochondrial supernatant. The cellular homeostatic mechanisms under ethanol effect are discussed.
Subject(s)
Alcoholism/physiopathology , Cell Membrane/physiology , Cerebral Cortex/physiology , Microsomes/physiology , Sodium-Potassium-Exchanging ATPase/metabolism , Administration, Oral , Alcoholism/enzymology , Anilino Naphthalenesulfonates/pharmacology , Animals , Cell Membrane/enzymology , Cerebral Cortex/enzymology , Disease Models, Animal , Ethanol/administration & dosage , Female , Microsomes/enzymology , Rats , Spectrometry, FluorescenceABSTRACT
When finding the mechanism of the in vitro ethanol membrane action it was established that alcohol in moderate concentrations enhanced the inactivation of the rat brain cortex Na+, K(+)-ATPase after modification of the microsomal fraction by phospholipase A2 from cobra venom. It is supposed that ethanol sensitivity is determined by the structural state of the functional protein-lipid enzyme complexes in membrane. The decrease of the intrinsic tryptophan fluorescence of the membrane proteins and fluorescence of the probe 1-anilinonaphthalene-8-sulfonate (both without and under membrane surface charge shielding) in the presence of ethanol was revealed. It is concluded, that conformational changes of the membrane polar surface area coincide with the enzyme inactivation by ethanol.
Subject(s)
Cell Membrane/metabolism , Cerebral Cortex/metabolism , Ethanol/pharmacology , Anilino Naphthalenesulfonates/pharmacology , Animals , Cell Membrane/drug effects , Cell Membrane/enzymology , Cells, Cultured , Cerebral Cortex/cytology , Cerebral Cortex/enzymology , Fluorescent Dyes/pharmacology , Membrane Lipids/metabolism , Microsomes/drug effects , Microsomes/enzymology , Phospholipases/pharmacology , Rats , Sodium-Potassium-Exchanging ATPase/metabolism , Spectrometry, FluorescenceABSTRACT
To investigate the role of rat brain cortex Na+, K(+)-ATPase plasma membrane microenvironment in ethanol effect in vitro on membrane the sensitivity of enzyme activity to alcohol was studied under membrane perturbation induced by sodium dodecyl sulfate. The increase of enzyme sensitivity to detergent inactivation in the presence of high ethanol concentrations and to alcohol inhibition after modification by Ds-Na was revealed. It is supposed that Na+, K(+)-ATPase sensitivity to ethanol is dependent on structural state of protein microenvironment in accordance with assumed differences in structural organization of the boundary lipids of the neuronal enzyme isoforms.
Subject(s)
Cell Membrane/drug effects , Cell Membrane/enzymology , Cerebral Cortex/enzymology , Ethanol/toxicity , Sodium-Potassium-Exchanging ATPase/drug effects , Animals , Cerebral Cortex/drug effects , Detergents/pharmacology , Enzyme Inhibitors/pharmacology , Isoenzymes/drug effects , Isoenzymes/metabolism , Microsomes/drug effects , Microsomes/enzymology , Neurons/drug effects , Neurons/enzymology , Rats , Sodium Dodecyl Sulfate/pharmacology , Sodium-Potassium-Exchanging ATPase/metabolismABSTRACT
The ontogenetic development of the rat brain cortex Na+, K(+)-ATPase and Mg(2+)-ATPase activities under female ethanol (20% v/v) consumption in the third trimester of gestation or in postpartum period was studied. The weight characteristics (body, whole brain and cortex weight) of viable rats on the first day after birth were not affected critically by prenatal alcohol exposure. It is revealed that the delay of postnatal rat growth 10 days after birth under translactational ethanol consumption is accompanied by reliable decrease of plasma membrane Na+, K(+)-ATPase activity in comparison with control animals. The comparable decrease in activities was observed for the ouabain-sensitive and ouabain-resistant Na+, K(+)-ATPase components (isoform species). From the 20th day the differences in enzyme activity were not revealed. Mg(2+)-ATPase increases in postnatal period independent of Na+, K(+)-ATPase activity and it remains insensitive to postnatal maternal alcohol intake. It is suggested, the first ten day period of lactation is critical for ethanol effect on the developmental control of the brain Na+, K(+)-ATPase functional expression and the course of adaptive processes in the rat organism.
Subject(s)
Alcohol Drinking/adverse effects , Brain/drug effects , Cerebral Cortex/drug effects , Ethanol/toxicity , Lactation/drug effects , Pregnancy , Sodium-Potassium-Exchanging ATPase/metabolism , Adaptation, Physiological , Adenosine Triphosphatases/metabolism , Age Factors , Animals , Animals, Newborn , Body Weight/drug effects , Brain/enzymology , Brain/growth & development , Cerebral Cortex/enzymology , Cerebral Cortex/growth & development , Female , Maternal-Fetal Exchange , Organ Size/drug effects , Protein Isoforms/metabolism , Rats , Sodium-Potassium-Exchanging ATPase/drug effectsABSTRACT
The current state of the researches related to the Na+, K(+)-ATPase isoenzyme complexes in nervous and muscle tissues affected by some experimental pathologies (hypokalemia, diabetes, hypertension, ischemia) has been reviewed. The mechanisms of the isoenzymes pathophysiological disorders, their tissue-specific adaptive relevance for the cellular homeostasis regulation are considered.