ACETALDEHYDE-SERUM PROTEIN ADDUCTS INHIBIT INTERLEUKIN-2 SECRETION INCONCANAVALIN A-STIMULATED MURINE SPLENOCYTES - A POTENTIAL COMMON PATHWAY FOR ETHANOL-INDUCED IMMUNOMODULATION

Citation
Kp. Braun et al., ACETALDEHYDE-SERUM PROTEIN ADDUCTS INHIBIT INTERLEUKIN-2 SECRETION INCONCANAVALIN A-STIMULATED MURINE SPLENOCYTES - A POTENTIAL COMMON PATHWAY FOR ETHANOL-INDUCED IMMUNOMODULATION, Alcoholism, clinical and experimental research, 19(2), 1995, pp. 345-349
Citations number
37
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
19
Issue
2
Year of publication
1995
Pages
345 - 349
Database
ISI
SICI code
0145-6008(1995)19:2<345:APAIIS>2.0.ZU;2-D
Abstract
Variable immunobiological changes occur with alcohol consumption. Prev ious studies have shown that acetaldehyde forms stable adducts with se rum proteins, including albumin. These adducts are elevated in persons and animals consuming ethanol. We examined the effect of serum protei n-acetaldehyde adducts formed with fetal bovine serum (FBS) on concana valin A-stimulated murine splenocytes. Interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R) expression were determined as a function of the effect of the acetaldehyde-protein adduct(s), FBS was incubated wi th acetaldehyde (500, 100, 50, 25, 10, and 0 mu M) for 1 hr at 37 degr ees C. Excess acetaldehyde was removed by ultrafiltration using a 500 molecular weight cut-off membrane in 3 volumes. Free as well as bound acetaldehyde was quantified using fluorigenic HPLC before and after in cubation. Recovered acetaldehyde correlated with the amount added (r(2 ) = 0.996). Splenocytes were cultured for 48 hr in complete medium con taining 5% acetaldehyde-treated and 5% untreated FBS with 4 mu g/ml co ncanavalin A. Although cell viability was unchanged, acetaldehyde-trea ted FBS mixed with native FBS decreased IL-2 secretion in a dose-depen dent manner. The percentage of cells expressing IL-2R was reduced only at the highest acetaldehyde-fas dose. Therefore, immunological effect s ascribed to ethanol may result in part from the toxic properties of acetaldehyde-protein adducts on IL-2 secretion.