Chronic ethanol consumption upregulates the cytosolic and plasma membrane sialidase genes, but downregulates lysosomal membrane sialidase gene in rat liver

Garige, Mamatha; Azuine, Magnus A.; Lakshman, Raj

doi:10.1016/j.metabol.2006.01.018

Cited by 9 publications

(7 citation statements)

References 52 publications

(57 reference statements)

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“…It is very likely that increased presence of asialoconjugates and free sialic acid after alcohol exposure are promoted by increased transcription rates of cytosolic and plasma membrane sialidase mRNA (CS and PMS, respectively), whereas lysosomal sialidase and its mRNA are downregulated [43]. On the other hand, ethanol treatment inhibits activity of mannosidase II (most likely by acetaldehyde adduct formation), resulting in the synthesis of cell surface glycoproteins with high mannose structures [28].…”

Section: Modification Transport and Secretion Of Glycoconjugatesmentioning

confidence: 99%

Alcohol abuse and glycoconjugate metabolism

Waszkiewicz

Szajda

Zalewska

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The relationship between alcohol consumption and glycoconjugate metabolism is complex and multidimensional. This review summarizes the advances in basic and clinical research on the molecular and cellular events involved in the metabolic effects of alcohol on glycoconjugates (glycoproteins, glycolipids, and proteoglycans). We summarize the action of ethanol, acetaldehyde, reactive oxygen species (ROS), nonoxidative metabolite of alcohol -fatty acid ethyl esters (FAEEs), and the ethanol-water competition mechanism, on glycoconjugate biosynthesis, modification, transport and secretion, as well as on elimination and catabolism processes. As the majority of changes in the cellular metabolism of glycoconjugates are generally ascribed to alterations in synthesis, transport, glycosylation and secretion, the degradation and elimination processes, of which the former occurs also in extracellular matrix, seem to be underappreciated. The pathomechanisms are additionally complicated by the fact that the effect of alcohol intoxication on the glycoconjugate metabolism depends not only on the duration of ethanol exposure, but also demonstrates dose-and regional-sensitivity. Further research is needed to bridge the gap in transdisciplinary research and enhance our understanding of alcohol-and glycoconjugate-related diseases.

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Section: Modification Transport and Secretion Of Glycoconjugatesmentioning

confidence: 99%

Alcohol abuse and glycoconjugate metabolism

Waszkiewicz

Szajda

Zalewska

et al. 2012

Folia Histochem Cytobiol.

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“…Alcohol was also shown to increase cytosolic and plasma membrane sialidase activities [35,36]. Garage et al [37] reported that chronic ethanol consumption upregulates cytosolic and plasma membrane sialidase gene expressions in rat livers. Another study showed that chronic ethanol consumption increases ganglioside sialidase activities in rat leukocytes and brain synaptosomes [38].…”

Section: Resultsmentioning

confidence: 99%

“…The same study also related the increase of free sialic acid and asialoconjugates during chronic ethanol consumption to elevation of sialidase activity in plasma membrane due to an increase in the relative biosynthesis ratio of the enzyme. Sialidases are functionally important because upregulation of sialidases in alcoholics induces the formation of CDT and other asialoconjugates, which can reflect clinical situation of the patient [37].…”

Section: Resultsmentioning

confidence: 99%

Chronic alcohol consumption augments loss of sialic acid residues and alters erythrocyte membrane charge in type II diabetic patients

Değirmenci

Akalın

Kartkaya

et al. 2008

J Biochem & Molecular Tox

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In this study, the effects of alcohol consumption on erythrocyte membrane properties in type 2 diabetic patients were investigated. Therefore, we measured total and lipid-bound sialic acid (LSA) levels, sialidase activities, and erythrocyte membrane negative charge. Three groups, including control group (n = 20), alcohol-consuming diabetic patients group (n = 14), and diabetic patients without alcohol consumption group (n = 42), were created. Plasma total sialic acid (TSA) levels of the alcohol-consuming diabetic group were elevated as compared to the healthy control and diabetic group (p < 0.001 and p < 0.01, respectively). TSA levels of the diabetic group were significantly elevated as compared to the healthy control group (p > 0.001). Plasma LSA levels of the alcohol-consuming diabetic group were higher than that in the healthy control and diabetic group (p < 0.05 and p < 0.05, respectively). LSA levels of the diabetic group were found to be high as compared to the healthy control group (p < 0.05). Plasma sialidase activities of the alcohol-consuming diabetic group and diabetic group were significantly elevated as compared to the healthy control group (p < 0.05 and p < 0.05, respectively). Sialidase activities of the alcohol-consuming diabetic group were elevated as compared to the diabetic group, but this was not statistically significant (p > 0.05). Erythrocyte membrane negativity levels of the alcohol-consuming diabetic group and diabetic group were significantly decreased (p < 0.001 and p < 0.001, respectively) as compared to the healthy control group. Erythrocyte membrane negativity levels of the alcohol-consuming diabetic group were decreased as compared to the diabetic group, but this was not statistically significant (p > 0.05). In conclusion, our results indicate that chronic alcohol consumption may augment membrane alterations in type 2 diabetic patients.

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“…Destabilization of ST (sialyltransferase) mRNA (by accelerating its degradation) and decrease in the hepatic synthetic rate of ST results in a concomitant decrease in the steady-state level of ST mRNA [13]. It is highly likely that increased presence of asialoconjugates and free SA (sialic acid) after alcohol exposure are promoted by increased transcription rates of cytosolic and plasma membrane sialidase mRNA [14]. During abstinence, CDT normalizes with a half-life of 15 days, remaining elevated for several weeks.…”

Section: Glycoconjugate Biomarkersmentioning

confidence: 99%

Glycoconjugates in the detection of alcohol abuse

Waszkiewicz

Szajda

Kępka

et al. 2011

Biochemical Society Transactions

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Up to 30% of all hospital admissions and health-care costs may be attributable to alcohol abuse. Ethanol, its oxidative metabolites, acetaldehyde and ROS (reactive oxygen species), non-oxidative metabolites of alcohol [e.g. FAEEs (fatty acid ethyl esters)] and the ethanol-water competition mechanism are all involved in the deregulation of glycoconjugate (glycoprotein, glycolipid and proteoglycan) metabolic processes including biosynthesis, modification, transport, secretion, elimination and catabolism. An increasing number of new alcohol biomarkers that are the result of alcohol-induced glycoconjugate metabolic errors have appeared in the literature. Glycoconjugate-related alcohol markers are involved in, or are a product of, altered glycoconjugate metabolism, e.g. CDT (carbohydrate-deficient transferrin), SA (sialic acid), plasma SIJ (SA index of apolipoprotein J), CETP (cholesteryl ester transfer protein), β-HEX (β-hexosaminidase), dolichol, EtG (ethyl glucuronide) etc. Laboratory tests based on changes in glycoconjugate metabolism are useful in settings where the co-operativeness of the patient is impaired (e.g. driving while intoxicated) or when a history of alcohol use is not available (e.g. after trauma). In clinical practice, glycoconjugate markers of alcohol use/abuse let us distinguish alcoholic from non-alcoholic tissue damage, having important implications for the treatment and management of diseases.

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Chronic ethanol consumption upregulates the cytosolic and plasma membrane sialidase genes, but downregulates lysosomal membrane sialidase gene in rat liver

Cited by 9 publications

References 52 publications

Alcohol abuse and glycoconjugate metabolism

Alcohol abuse and glycoconjugate metabolism

Chronic alcohol consumption augments loss of sialic acid residues and alters erythrocyte membrane charge in type II diabetic patients

Glycoconjugates in the detection of alcohol abuse

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