GALACTOSAMINE-INDUCED SENSITIZATION TO THE LETHAL EFFECTS OF ENDOTOXIN
GALACTOSAMINE-INDUCED SENSITIZATION TO THE LETHAL EFFECTS OF ENDOTOXIN
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DOI：
10.1073/pnas.76.11.5939
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发表时间：
1979-01-01
影响因子：
11.1
通讯作者：
REUTTER, W
中科院分区：
文献类型：
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作者：
GALANOS, C;FREUDENBERG, MA;REUTTER, W
用 D-半乳糖胺治疗兔子、大鼠和小鼠，它们对脂多糖（来自马流产沙门氏菌）致死作用的敏感性增加了数千倍。脂多糖与半乳糖胺同时注射时动物的敏感性最高，注射1、2、3 h后敏感性依次降低。当在半乳糖胺之前1小时或之后4小时给予脂多糖时，不存在致敏作用。使用半乳糖胺和脂多糖处理后的致死发生比单独使用脂多糖更快；通常所有动物都会在 5-9 小时后死亡。半乳糖胺诱导的脂多糖敏感性可以被尿苷逆转，尿苷抑制肝细胞中氨基糖诱导的早期生化改变。尽管半乳糖胺表现出肝毒性活性，诱导肝细胞最终坏死，但数据表明对脂多糖的敏感性仅与己糖胺的早期代谢作用有关。
Treatment of rabbits, rats and mice with D-galactosamine increased their sensitivity to the lethal effects of lipopolysaccharide [from Salmonella abortus equi] several thousand-fold. The susceptibility of the animals was highest when the lipopolysaccharide was injected together with galactosamine and decreased successively when injection was carried out 1, 2 and 3 h later. Sensitization was absent when the lipopolysaccharide was administered 1 h before or 4 h after galactosamine. The onset of lethality after treatment with galactosamine and lipopolysaccharide occurred faster than with lipopolysaccharide alone; usually all animals died 5-9 h later. The galactosamine-induced sensitization to lipopolysaccharide could be reversed by uridine, which inhibits the early biochemical alterations induced by the amino sugar in the hepatocytes. Although galactosamine exhibits hepatotoxic activity, inducing ultimate necrosis of the hepatocytes, the data suggest that the sensitization to lipopolysaccharide is related only to the early metabolic effects of the hexosamine.