Mack U, Owens J, Cooksley W G, Powell L W, Halliday J W
Br J Exp Pathol. 1985 Apr;66(2):185-91.
The effects of minimal acute liver injury on circulating ferritin levels have been examined in the rat both in vivo and in the isolated perfused liver. Liver damage produced by 6 mmol/kg of D-galactosamine (GalN) in vivo resulted in a marked rise in plasma ferritin levels 4 h after administration, 2 h before any significant increase in plasma aspartate transaminase. In the isolated perfused liver, damage produced by 5mM GalN introduced into the perfusate also produced an early increase in circulating ferritin before any evidence of release of intracellular enzymes, or alteration in liver histology as assessed by light microscopy was apparent. It is concluded that minimal acute liver damage results in a pronounced increase in circulating ferritin levels before other evidence of liver dysfunction. This is unlikely to be due solely to increased release from damaged cells but may rather result from an alteration in the mechanism responsible for ferritin homeostasis.
在大鼠体内及离体灌注肝脏中,已对轻度急性肝损伤对循环铁蛋白水平的影响进行了研究。体内给予6 mmol/kg D-半乳糖胺(GalN)所产生的肝损伤,在给药后4小时导致血浆铁蛋白水平显著升高,这比血浆天冬氨酸转氨酶出现任何显著升高要早2小时。在离体灌注肝脏中,向灌注液中加入5 mM GalN所造成的损伤,在细胞内酶释放的任何证据出现之前,或通过光学显微镜评估的肝脏组织学改变明显之前,也使循环铁蛋白早期增加。得出的结论是,轻度急性肝损伤在出现肝功能障碍的其他证据之前,会导致循环铁蛋白水平显著升高。这不太可能仅仅是由于受损细胞释放增加所致,而可能是由于负责铁蛋白稳态的机制发生改变所致。