Novelli E L, Sforcin J M, Rodrigues N L, Ribas B O
Department of Chemistry, Universidade Estadual Paulista, UNESP, Botucatu, São Paulo, Brasil.
Bol Estud Med Biol. 1990 Jul-Dec;38(3-4):54-8.
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.
在气管内给予大鼠氯化镍（8.4微摩尔/千克）后，研究了其胰腺中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.）的活性变化，以及铜、总蛋白、甘油三酯、磷脂和总脂质的水平。氯化镍诱导胰腺和红细胞中的SOD活性增加。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，动物耐受氯化镍诱导损伤的能力取决于细胞毒性剂的产生与胰腺各种防御能力之间的微妙平衡。
