Overview
In addition, the transmembrane transfer of calcium ions is disrupted, the excitability of the membranes is reduced.
Metabolism and Ethanol
The mechanisms of biotransformation of ethyl alcohol lead to the formation of toxic acetaldehyde, as well as to the accumulation of the reduced form of NAD.
Ethanol, enzymes
The mechanism of metabolic disorders in acute fact that intoxication is associated with the development of stress and the release into the blood of adenocorticotropic hormones (ACTH), glucocorticoids and adrenaline.
With prolonged exposure of https://zentherapycenter.com/let-i/imrest.php to the body, the direct effect of ethyl alcohol on the metabolism of proteins, fats and carbohydrates comes to the fore. Ethyl alcohol and acetaldehyde delay and change the direction of many energy metabolism reactions. The cause of these violations is considered to be a shift in the NAD.N / NAD ratio towards a reduced coenzyme.
No less important is the damaging effect of ethyl alcohol on subcellular membranes with an increase in their permeability, inhibition of the activity of Na + - K + -ATPases and the ability to capture calcium ions.
Ethyl alcohol in the liver, heart and skeletal muscles reduces oxygen tension, the activity of glutamate and malate dehydrogenases, NAD.N-cytochrome C oxidoreductases, switches the respiratory chain to the predominant oxidation of succinic acid, removing oxalacetic inhibition of succinate dehydrogenase.
Ethanol and lipid metabolism
Ethyl alcohol, disrupting lipid metabolism, causes the accumulation of fat in the liver - steatosis. It is manifested by hepatomegaly, fatty infiltration, breakdown of proteins of subcellular structures and hydropic degeneration of preparations. In the organ parenchyma, the content of triglycerides increases 20-25 times, as well as phospholipids, cholesterol and its esters.
The content of triglycerides increases the more, the heavier the alcohol intoxication. The defeat progresses according to the scheme: fatty degeneration → alcoholic hepatitis element cirrhosis. It is believed that in the development of such effects of the influence of ethanol effectiveness hepatitis, cirrhosis, cardiomyopathy, functional and structural disorders in the central nervous system, Ca ++ metabolic disturbances due to damage to cell membranes play an important role. Its massive entry into the cell against the background of a decrease can utilized the activity of Na + and Ka + -ATPases leads to structural and functional changes, up to the development of necrosis.
Ethanol and Vitamin Exchange
The metabolic effects of ethyl alcohol include polyhypovitaminosis, resulting from a slowdown in absorption and metabolic disorders of many vitamins. Ethyl alcohol inhibits the absorption of thiamine and reduces the intestinal-hepatic circulation of folic acid.
Acetaldehyde enhances the decomposition of pyridoxal-5-phosphate, because it is displaced from communication with proteins, as a result of which it becomes more accessible to the hydrolytic action of basic phosphatase. In addition, ethyl alcohol reduces the concentration of vitamin A in the liver and inhibits its conversion to active retinol.
Ethanol and water-salt metabolism
Alcohol is one of the adverse factors affecting the water-salt metabolism. In chronic alcohol intoxication, the balance of ions and water in the tissues changes, which leads to disorders of the cardiovascular, endocrine and nervous systems. Violations of water and electrolyte metabolism do not occur in isolation, out of touch with each other.
Significant changes in the content of water, sodium and potassium in the body threaten the life of the cell. Molar concentration of blood plasma is the most important pill of water-salt homeostasis. Molar concentrations of intravascular interstitial and intracellular fluids are considered the same, despite the fact that intracellular fluid contains more anions. This is due to the formation of the so-called polyvalent ions and anions during the preparation of anions to proteins. Such polyvalent anions act as osmotically active units, reducing the number of osmotically active anions.
The gradient of molar concentrations between the body’s fluid spaces is one of the mechanisms responsible for the flow of water between them — water will move toward the body of water with a higher molar concentration. Urea and Na + ions cannot be used great channels passable for water, although the radius of the water molecule is larger than the radius of Na + (0.15 nm and 0.1 nm, respectively).
The intake of water in the body is regulated by thirst, and the excretion of water by the kidneys is regulated by the neurohumoral route with the participation of the neuropeptide hormone - vasopressin, which is formed in the neurons of the supraoptic nucleus of the hypothalamus. It was found that the hormonal effect of vasopressin is carried out through the adenylcyclase system. With a decrease in the molar concentration of blood plasma, vasopressin secretion stops and water diuresis develops, with hydration and an increase in molar concentration of blood plasma, vasopressin secretion increases and water is another in the body.
Ethanol and Hormones
It was also found that ethanol leads to a significant decrease in luteinizing hormone (LH) in serum [17]. This suggests that ethanol reduces the level of LH in serum by reducing the release of luliberin from the hypothalamus. At present, the concept that the decrease in LH by alcohol is mediated by endogenous opiates, enkephalins, endorphins seems attractive. According to available data, endogenous opiates are involved in the functioning of feedback that supports LH production, since it was found that naloxone, for example, eliminates the inhibitory testosterone on LH production. Thus, it is suggested that endogenous opiates released under the influence of alcohol enhance inhibition of More secretion.
The introduction of alcohol leads to increased activity of hepatic testosterone A-reductase. This increase in enzyme activity contributes to enhanced metabolic clearance of testosterone. It was also established that the production of testosterone is reduced, resulting in a decrease in its concentration in blood plasma. Moreover, a higher level of peripheral conversion of testosterone to estradiol with liver cirrhosis was found.
It is obvious that look acceleration of the conversion of testosterone to estradiol is associated with the appearance of a portal shunt with cirrhosis, which increases the delivery of testosterone to peripheral tissues that can interconvert steroids. There is a reasoned opinion that ethanol has a pronounced ability to modify the activity of the hormonal system of the Betadine
Ethanol and endocrine glands
There is practically no single endocrine gland whose function would not change with the development of alcoholism. The levels of ethanol exposure to endocrine complexes are extremely diverse; this includes the effect on the secretion of releasing factors, a change in the hormone-producing activity of the pituitary cells, lesions of the peripheral endocrine gland cell contain systems, quantitative and qualitative changes in hormone metabolism in the liver, as well as impaired complexation of hormones with specific receptors and with transport proteins.
Naturally, such a polyglandular effect on the endocrine system and a wide range of ethanol-affected hormone action mechanisms creates a specific picture of alcoholic endocrinopathies, the multiplicity and interaction of which often does not allow us to establish primary and biologically more significant endocrine disorders, which can be etiopathogenetic in the syndrome of alcoholism.
Among the characteristic hormonal disorders that occur during chronic use of ethanol in men, in particular, effective with symptoms of hypogonadism, impotence, infertility, feminization, Betadine a number of other changes.
In addition to the central effect on the systems regulating and carrying out the synthesis of Betadine, the preparation effect of ethanol on sex steroids is realized through a direct effect on steroidogenesis. At least several possible mechanisms of inhibition of androgen synthesis by ethanol or acetal guide in testicles have been shown.
First, alcohol or its metabolites can directly inhibit the biosynthesis of testosterone, reducing the activity of enzymes there in this process. Secondly, the oxidation of ethanol and its metabolites in testicles can cause an increase in the NAD.H / NAD ratio in testis cells. Finally, ethanol and its metabolites can interact with hormonal receptors both indirectly and independently affect the synthesis of cAMP in testicles
Ethanol significantly inhibits the activity of alcohol dehydrogenase, increases the formation of acetaldehyde, which does not have time to oxidize to acetate, and, accumulating in the body, determines many toxic effects of alcohol, leading to significant changes in the metabolism of various organs and tissues
