In:
Alcoholism: Clinical and Experimental Research, Wiley, Vol. 24, No. S4 ( 2000-04)
Abstract:
Background: We examined the effects of glutathione depletion on the level of superoxide anion released into hepatic sinusoids after lipopolysaccharide challenge. Methods: Rats were given 1 mg/kg of maleic acid diethyl ester to deplete glutathione in vivo and then 0.5 mg/kg body weight of lipopolysaccharide. Results: This treatment significantly depleted serum reduced glutathione (32.7 ±1.7 vs. 23.0 ± 3.2 mM, p = 0.002). However, it did not affect the serum oxidized glutathione concentration (2.88 ± 0.56 vs. 3.10 ± 0.78 mM, not significant). The lipopolysaccharide challenge caused significant superoxide anion formation as compared with controls (0.12 ± 0.04 vs. 0.22 ± 0.05 o.d., p 〈 0.001), and it was enhanced significantly by glutathione depletion (0.28 ± 0.04 o.d., p 〈 0.05). There were no significant differences in levels of lipopolysaccharide (2142 ± 452 vs. 2503 ± 612 pg/ml) and tumor necrosis factor α (277 ± 186 vs. 252 ± 88 pg/ml) after the lipopolysaccharide challenge between the glutathione‐depleted and nondepleted rats. Moreover, the purine nucleoside phosphorylase/glutamic‐pyruvic transaminase ratio in liver perfusates, a marker of damage to endothelial cells in hepatic sinusoids, was significantly higher in the glutathione‐depleted rats than in the nondepleted rats. Conclusions: The reduced form of glutathione can decrease levels of the superoxide anion released into hepatic sinusoids and can decrease subsequent damage to endothelial cells in these sinusoids caused by lipopolysaccharide; that is, it can reduce lipopolysaccharide‐induced liver injury.
Type of Medium:
Online Resource
ISSN:
0145-6008
,
1530-0277
DOI:
10.1111/acer.2000.24.issue-S4
DOI:
10.1111/j.1530-0277.2000.tb00014.x
Language:
English
Publisher:
Wiley
Publication Date:
2000
detail.hit.zdb_id:
2046886-6
detail.hit.zdb_id:
3167872-5
SSG:
15,3
