Novelli E L, Rodrigues N L, Ribas B O, Curi P R
Departamento de Química, Universidade Estadual Paulista, UNESP, Botucatu, São Paulo, Brasil.
Can J Physiol Pharmacol. 1992 May;70(5):709-11. doi: 10.1139/y92-091.
Superoxide radical (O2-) is a free radical that may be involved in various toxic processes. Cu--Zn superoxide dismutase catalyses the dismutation of the superoxide free radical and protects cells from oxidative damage, and it has been used clinically. The concentration of Ni2+ and Cu--Zn superoxide dismutase activity were measured in lungs of rats at time intervals of 5, 12, 19, 26, 33, and 40 days following an intratracheal injection of 127 nmol of NiCl2. Nickel chloride increased nickel content and resulted in a significant increase of Cu--Zn superoxide dismutase activity in lungs. This elevation of Cu--Zn superoxide dismutase activity was highest on the 12th day (approximately threefold) and is at levels comparable to controls rats on day 40 onwards. Since Cu--Zn superoxide dismutase activity was increased in lung throughout our experimental period without corresponding increases of Cu2+ and Zn2+, we speculate that the elevation of Cu--Zn superoxide dismutase activity might be due to an increased half-life of the enzyme, induced by nickel.
超氧阴离子自由基(O2-)是一种可能参与各种毒性过程的自由基。铜锌超氧化物歧化酶催化超氧自由基的歧化反应,保护细胞免受氧化损伤,并且已在临床上得到应用。在气管内注射127 nmol氯化镍后的5、12、19、26、33和40天时间间隔,测量大鼠肺组织中Ni2+的浓度和铜锌超氧化物歧化酶的活性。氯化镍增加了镍含量,并导致肺组织中铜锌超氧化物歧化酶活性显著增加。铜锌超氧化物歧化酶活性的升高在第12天最高(约为三倍),并且从第40天起与对照大鼠的水平相当。由于在我们的整个实验期间肺组织中铜锌超氧化物歧化酶活性增加,而Cu2+和Zn2+没有相应增加,我们推测铜锌超氧化物歧化酶活性的升高可能是由于镍诱导的该酶半衰期延长所致。