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Ethanol pathological effects

A very high activity of mitochondrial aldehyde dehydrogenases (together with its low ensures very efficient oxidation in the liver so that the concentration of acetaldehyde in blood remains very low. Nonetheless, it is possible that some of the pathological effects of ethanol are due to acetaldehyde (ethanal). In contrast, a large proportion of the acetate escapes from the liver and is converted to acetyl-CoA by acetyl-CoA synthetase in other tissues ... [Pg.327]

A high rate of ethanol consumption can lead to inhibition of gastric secretion and irritation of the gastric mucosa. Ethanol irritates the entire gastrointestinal tract, which may lead to constipation and diminished absorption of nutrients. Other pathological effects include pancreatitis and peripheral neuropathy. Severe gonadal failure is often found in both men and women, accompanied by low blood levels of sex hormones. [Pg.415]

Pathologic effects of ethanol on hematopoietic tissue can result directly from alcohol ingestion or from secondary nutritional deficiencies or hepatic disease. The clinician will often confront an array of overlapping syndromes in the alcoholic patient, which involves abnormalities of immune system cells. Hemodialysis efficiently clears ethanol from the... [Pg.1076]

Ethanol, an experimental mimic of hjrperthermia, potentiates the cytotoxicity of DNA damaging agents (1-3). Ethanol and hyperthermia have been suggested to act via similar or related mechanisms. Hiis potentiation is an early event and occurs within the Erst few minutes of the DNA damage response, precisely the time when one expects to see the substantial but transient increase in poly(ADP-ribose) synthesis and accumulation (4). It has been reported that hyperthermia elicits an increase in poly(ADP-ribose) levels in cells which is potentiated by ethanol (5). We report here the first comprehensive study of the mechanism by which ethanol exerts its effect on poly(ADP-ribose) metabolism in vivo and in vitro. The data defines a mechanism by which ethanol has a net effect on polymer levels similar to that of hyperthermia, but via a uniquely different mechanism. This mechanism unifies some of the diverse effects attributed to ethanol treatment of cells via a common effect on poly(ADP-ribose) metabolism, explains die synergistic effects ethanol and hyperthermia, and implies that polymer metabolism may be intimately tied to ethanol pathology. [Pg.105]

In the present work, a combination of three chemiluminescence (CL) methods is used, based on lumino 1-dependent CL for registering antioxidant properties of ethanol extract of Crataegus oxycantha leaves and flowers. Sources of the most reactive ROS - hypochlorite and hydroxyl radical were used, as well as a HRP/H2O2 system. There is information that this plant favourably influences cardiovascular diseases and other conditions related to free-radical pathology.3 5 Regarding some other Crataegus species, information has been obtained that they show antioxidant activity in some model systems, which is one of the possible explanations of the curative effect of these herbs.6... [Pg.193]

Watts, MT. McDonald, O.L. (1987) The effect of biologic specimen type on the gas chromatograpic headspace analysis of ethanol and other volatile compounds. American Journal of clinical Pathology. 87, 79-85... [Pg.224]

Thiamine deficiency leads to beriberi, which has a cardiac and peripheral nerve involvement. Why some patients develop beriberi without cerebral pathology and others develop Wernicke-Korsakoff syndrome without cardiac involvement is not clear. Presumably, undefined nutritional or metabolic factors play a role in both, as may the toxic effects of ethanol. [Pg.85]


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See also in sourсe #XX -- [ Pg.9 , Pg.328 ]




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