Galanos C, Freudenberg M A, Reutter W
Proc Natl Acad Sci U S A. 1979 Nov;76(11):5939-43. doi: 10.1073/pnas.76.11.5939.
Treatment of rabbits, rats, and mice with D-galactosamine increased their sensitivity to the lethal effects of lipopolysaccharide 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 hr later. Sensitization was absent when the lipopolysaccharide was administered 1 hr before or 4 hr after galactosamine. The onset of lethality after treatment with galactosamine and lipopolysaccharide occurred faster than with lipopolysaccharide alone; usually all animals died 5-9 hr later. The galactosamine-induced sensitization to lipopolysaccharide could be reversed by uridine which is known to inhibit the early biochemical alterations induced by the amino sugar in the hepatocytes. Although galactosamine is known to exhibit hepatotoxic activity inducing ultimate necrosis of the hepatocytes, the data so far suggests that the sensitization to lipopolysaccharide is related only to the early metabolic effects of the hexosamine.
用D - 半乳糖胺处理兔子、大鼠和小鼠，可使其对脂多糖致死效应的敏感性提高数千倍。当脂多糖与半乳糖胺一起注射时，动物的易感性最高，而在1、2和3小时后注射时，易感性则依次降低。当脂多糖在半乳糖胺之前1小时或之后4小时给药时，未出现致敏现象。用半乳糖胺和脂多糖处理后致死的发生比单独用脂多糖更快；通常所有动物在5 - 9小时后死亡。尿苷可逆转半乳糖胺诱导的对脂多糖的致敏作用，已知尿苷可抑制氨基糖在肝细胞中诱导的早期生化改变。虽然已知半乳糖胺具有肝毒性活性，可导致肝细胞最终坏死，但目前的数据表明，对半乳糖胺的致敏作用仅与己糖胺的早期代谢效应有关。
