A study of the temporal effect of alcohol on human erythrocyte sodium-lithium countertransport in relation to membrane cholesterol and phospholipids

被引:2
|
作者
Adebayo, GI
Gaffney, P
Feely, J
机构
[1] ST JAMES HOSP,TRINITY CTR HLTH SCI,DEPT THERAPEUT,DUBLIN 8,IRELAND
[2] ST JAMES HOSP,DEPT BIOCHEM,CENT PATHOL LAB,DUBLIN 8,IRELAND
关键词
SLC V(m)ax; alcohol; membrane cholesterol; phospholipids;
D O I
10.1016/S0741-8329(96)00074-2
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
The effect of a single dose of alcohol (0.8 g/kg), given with ''diet coke,'' on erythrocyte sodium-lithium countertransport (SLC) in relation to membrane cholesterol and phospholipids was assessed over 24 h in 10 healthy volunteers. Baseline passive lithium efflux (0.168 +/- 0.008 mmol l(-1) cell h(-1)) was increased 1 h (0.202 +/- 0.014 mmol l(-1) cell h(-1); p < 0.030), and 4 h (0.200 +/- 0.014 mmol l(-1) cell h(-1); p < 0.020), but similar to that at 24 h postalcohol (0.173 +/- 0.011 mmol l(-1) cell h(-1)). These changes were not associated with any change in intracellular lithium. Control SLC V-max of 0.387 +/- 0.054 mmol l(-1) cell h(-1) fell at 1 h (0.328 +/- 0.050 mmol l(-1) cell h(-1); p = 0.0012) and 4 h (0.312 +/- 0.048 mmol l(-1) cell h(-1); p < 0.0005). Its value 24 h postalcohol (0.371 +/- 0.047 mmol l(-1) cell h(-1)) was comparable to that at baseline. There was no significant change in the affinity of the transporter for external sodium throughout the experimental period, suggesting that the reduction in V-max 1 and 4 h after alcohol ingestion resulted from a noncompetitive inhibition. Intracellular sodium 4 h after alcohol was lower than at baseline, but returned to the control value within 24 h. In a control group (n = 5), pretreatment with ''diet coke'' alone did not alter any of the measured parameters. It is concluded that alcohol pretreatment increases passive lithium efflux and decreases SLC V-max. Both effects are evident up to at least 4 h postdosing, but recover within 24 h in the absence of further alcohol intake. Copyright (C) 1996 Elsevier Science Inc.
引用
收藏
页码:597 / 602
页数:6
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