Daryani R, LaLonde C, Zhu D, Demling R H
Longwood Area Trauma Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Circ Shock. 1990 Dec;32(4):273-80.
Endotoxemia in the sheep produces oxidant-induced cardiopulmonary dysfunction and lung and liver lipid peroxidation, which can be prevented with exogenous catalase, indicating a role for hydrogen peroxide. We determined whether endotoxin-induced oxidant release altered endogenous catalase activity to help explain the lipid peroxidation. Unanesthetized sheep were given 2 micrograms/kg Escherichia coli endotoxin and killed at 5 hr or 24 hr. Lung and liver lipid peroxidation, measured as malondialdehyde, and catalase activity were determined after endotoxin and compared with controls. Lung tissue MDA increased by 100% at 5 hr and was still elevated by 50% at 24 hr, while catalase activity decreased by 50% at 5 hr and remained decreased, suggesting irreversible inactivation. Liver MDA was also doubled at both 5 and 24 hr, but catalase activity remained unchanged. We conclude that endotoxemia results in a significant inactivation of endogenous catalase activity in lung, but not in liver. The lung may be more prone to a subsequent H2O2 injury before restoration of catalase activity.
绵羊内毒素血症会引发氧化应激诱导的心肺功能障碍以及肺和肝的脂质过氧化,而外源性过氧化氢酶可预防这种情况,这表明过氧化氢发挥了作用。我们研究内毒素诱导的氧化剂释放是否会改变内源性过氧化氢酶活性,以助于解释脂质过氧化现象。对未麻醉的绵羊给予2微克/千克大肠杆菌内毒素,并于5小时或24小时后处死。测定内毒素处理后肺和肝的脂质过氧化(以丙二醛衡量)及过氧化氢酶活性,并与对照组进行比较。肺组织丙二醛在5小时时增加了100%,在24小时时仍升高了50%,而过氧化氢酶活性在5小时时降低了50%且持续降低,提示不可逆失活。肝丙二醛在5小时和24小时时也增加了一倍,但过氧化氢酶活性保持不变。我们得出结论,内毒素血症导致肺内源性过氧化氢酶活性显著失活,但肝中未出现这种情况。在过氧化氢酶活性恢复之前,肺可能更容易受到随后的过氧化氢损伤。