胰腺损伤和气管内NiCl2给药。氯化镍的影响。

E L Novelli, J M Sforcin, N L Rodrigues, B O Ribas
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引用次数: 0

摘要

研究了气管内给药(8.4 μ mol/kg) NiCl2后大鼠胰腺铜锌超氧化物歧化酶(SOD- e.c 1.15.1.1.)和乳酸脱氢酶(LDH- e.c 1.1.1.27.)活性及铜、总蛋白、甘油三酯、磷脂和总脂含量的变化。氯化镍诱导胰腺和红细胞SOD活性升高。这种升高与这些动物胰腺中铜含量增加和磷脂含量降低有关。总之,动物耐受氯化镍引起的损伤的能力是由细胞毒性物质的产生和各种胰腺防御能力之间的微妙平衡所控制的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pancreas damage and intratracheal NiCl2 administration. Effects of nickel chloride.

Changes in activities of Cu-Zn superoxide dismutase (SOD- E.C.1.15.1.1.) and lactate dehydrogenase (LDH- E.C.1.1.1.27.) and levels of copper, total protein, triglycerides, phospholipids and total lipids were investigated in pancreas of rats after intratracheal administration of NiCl2 (8.4 mumol/kg). Nickel chloride induced increased SOD activity in pancreas and erythrocytes. This elevation was related to increased copper and decreased phospholipid content in pancreas of these animals. In conclusion, the ability of an animal to tolerate nickel chloride induced damage was governed by a delicate balance between the generation of cytotoxic agents and the various pancreas defense capabilities.

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