Adaptive changes in rat liver plasma membranes after chronic alcohol administration and its subsequent withdrawal

Lee, Hung; Hosein, E. A.

doi:10.1139/y86-013

Cited by 7 publications

(7 citation statements)

References 10 publications

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“…[55][56][57][58] Ethanol feeding has also been reported to alter membrane composition by inducing lipid peroxidation, 59,60 decreasing the biosynthesis of polyunsaturated fatty acids and changing membrane cholesterol and phospholipids. 61,62 However, how ethanol abuse may exert a nephrotoxic effect remains poorly understood. The presence of multiple abnormalities of renal tubules involving different segments indicates that exposure to ethanol may cause generalized tubular dysfunction.…”

Section: Biochemical and Molecular Basis Of Alcohol-induced Injury Tomentioning

confidence: 99%

Alcohol misuse and renal damage

Cecchin¹,

Marchi²

1996

Addiction Biology

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Recent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid-base disturbances commonly observed in these patients, and possibly in alcohol-induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti-inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol-induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.

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Section: Biochemical and Molecular Basis Of Alcohol-induced Injury Tomentioning

confidence: 99%

Alcohol misuse and renal damage

Cecchin¹,

Marchi²

1996

Addiction Biology

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“…The importance of phospholipids for structure and integrity of cellular membranes suggests that many functional distur bances in alcoholism may be related to changes in phospholipid content and composition (3). Some stud ies showed that chronic alcohol intake resulted in the change of phospholipid content (11,25) but several studies have reported minor changes in phospholipid distribution (6,26,27). Resolution of the mechanisms underlying this change is complicated by changes of amount and duration of alcohol abuse.…”

Section: Methodsmentioning

confidence: 99%

Effects of Different Quantities of Fat on Serum and Liver Lipids, Phospholipid Class Distribution and Fatty Acid Composition in Alcohol-Treated Rats

Ristić‐Medić¹,

Ristic²,

Tepšić³

2003

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe present study investigated the quantitative effect of dietary fats and inges tion of alcohol on serum and liver lipids, fatty acid bound to phospholipids and their class distribution of male Wistar rats. The rats in C (control) and A (alcohol) groups were fed a standard laboratory diet, HFC (high fat-control) and HFA (high fat-alcohol) groups were fed a high fat diet (standard diet supplemented with 20g%w/w, sunflower oil: lard mixture 1: 1) for 6wk. Alcohol-treated rats consumed alcohol at the rate of 9g/kgbw/d (15-20% energy). Liver phospholipid (PL) content was decreased, and phospholipid/cholesterol liver molar ratio increased in the alcohol treated rats. The proportion of serum sphingophospho lipid (Sph) was significantly lower and proportion of phosphatidylcholin (PC) significantly higher in serum PL in alcohol-treated rats. Phospholipid class distribution was unaffected by alcohol feeding in liver. Significantly lower levels of 16:1n-7 and higher levels of 20:5n-3 and 22:4n-6 in the serum PL were observed in the alcohol-treated rats. The groups on the HF diet increased levels of 20:4n-6, 22:4n-6 and total n-6, polyunsaturated fatty acid (PUFA)and decreased levels of 18:1n-9 and total monounsaturated fatty acids (MUFA)in both liver and serum PL, but n-3 fatty acid increased in serum PL and decreased in liver PL compared to groups on the standard diet. Alcohol fat interaction was evident in MUFA and PUFA/SFA in serum PL and n-6, MUFA, PUPA and polyunsaturated/saturated fatty acid ratios (PUFA/SFA) in liver PL. This study showed that the high fat intake in alcohol-treated rats increased levels of 20:4n-6, 22:4n-6 and 20:4/18:2 ratio, and decreased level of 18:1n -9 in liver and serum phospholipids.

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“…One mechanism for cells to adapt to changing environmental conditions and/or membrane-active agents is to alter the lipid composition of their membranes [2,21,22], thereby altering membrane £uidity [6]. The membrane po-larization patterns of R. eutropha H850 cells grown on biphenyl suggested these cells adapted to the £uidizing e¡ect of biphenyl (Fig.…”

Section: Fatty Acid Composition Analysismentioning

confidence: 99%

Effects of 2,2′,5,5′-tetrachlorobiphenyl and biphenyl on cell membranes of Ralstonia eutropha H850

Kim¹

2001

FEMS Microbiology Letters

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The effects of 2,2P,5,5P-tetrachlorobiphenyl (TeCB), a PCB congener, and biphenyl on the cytoplasmic membranes of Ralstonia eutropha H850 were investigated by measuring fluorescence polarization using 1,6-diphenyl-1,3,5-hexatriene (DPH) as the probe, and determining the cellular fatty acid compositions. TeCB significantly affected the membrane of R. eutropha H850 cells grown on fructose by decreasing DPH fluorescence polarization. In contrast, the membrane of cells grown on biphenyl showed a considerably less significant effect of TeCB on membrane polarization than in fructose-grown cells. An increase in the ratio of total saturated to unsaturated fatty acids in cells grown on biphenyl suggested less of a fluidizing effect of TeCB on membranes in those cells. When biphenyl-grown cells were transferred back to a fructose medium, they required 25 generations for the membrane polarization and fatty acid compositions of these cells to revert back to those of the initial fructose-grown cells. The re-adaptation to a change in temperature required only five generations to return to normal. These results show that biphenyl affects cells in more ways than simply fluidizing the cytoplasmic membrane. ß : S 0 3 7 8 -1 0 9 7 ( 0 1 ) 0 0 1 9 5 -1

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Adaptive changes in rat liver plasma membranes after chronic alcohol administration and its subsequent withdrawal

Cited by 7 publications

References 10 publications

Alcohol misuse and renal damage

Alcohol misuse and renal damage

Effects of Different Quantities of Fat on Serum and Liver Lipids, Phospholipid Class Distribution and Fatty Acid Composition in Alcohol-Treated Rats

Effects of 2,2′,5,5′-tetrachlorobiphenyl and biphenyl on cell membranes of Ralstonia eutropha H850

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