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KMID : 0377519920170020123
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Chung-Ang Journal of Medicine
1992 Volume.17 No. 2 p.123 ~ p.136
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In Vitro Effects of Cadmium on Superoxide Radical Productions, Lipid Peroxidation, and Activities of Cu, Zn-Superoxide Dismutase, Catalase and Total ATPase in Rat Lungs
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Chung Kyou-Chull
Choi Dae-Hwa
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Abstract
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In order to understand the role of free radical and lipid peroxidation in the mechanism of Cdinduced lung toxicity, the effects of Cd in vitro on the levels of superoxide radical, Cu,ZnSOD, catalase, lipid peroxidation and total ATPase in rat lung were studied.
Superoxide radical production in normal lung homogenate was 3.30 1.43 nmols/mg protein/min. Superoxide radical production was increased to 146, 150, 160, 268, 386 and 534 %o at 0.01, 0.05, 01, 0.3, 0.5 and 0.8 MM CdCIZ concentrations, respectively. Further increase in concentration of CdCIZ resulted in a greater increase superoxide radical production and at 1.0 mM superoxide radical production was increased by 676% to 22.30 0.80 nmols/mg protein/min.
Cu,Zn-superoxide dismutase activity in normal rung homogenate was 21.641.73 units/mg protein. Cu,Zn ,SOD activity was decreased to 84, 53 and 217% at 0.01, 0.05 and 0.1 mM CdCIZ concentrations, respectively. Further increase in concentration of CdC1Z resulted in a greater inhibition of Cu, ZnSOD activity, and at 0.15 mM, C.i,ZnSOD activity showed a 92% inhibition to 1.770.23 units/mg protein.
Catalase activity in normal lung homogenate was 13.150.50 units/mg protein. Catalase activity was decreased- to 80, 56,
38, 28 and 22% at 0.01, 0.03, 0.05 and 0.08 mM CdCIZ concentrations, respectively. Further increase in concentration of CdCIZ resulted in ´a greater inhibition of catalase activity, and at 0.1 mM, catalase activity showed a 78 % inhibition to 2.89 0.38 units /mg protein.
Lipid peroxidation in normal lung homogenate was 0.090.01 nmols/mg protein/ hr. Lipid peroxidation was increased to 133, 189 and 222% at 0.01, 0.05 and 0.08 mM CdCIZ concentrations, respectively. And at 0.1 mM, lipid peroxidation was increased by 266% to 0.2,50.02 nmols/mg protein/hr. But further increase in concentration of CdCIZ did not bring about the increase of´ the peroxidation and showed the plateau eff ects.
Total ATPase activity in normal lung homogenate was 6.850.03 umols/mg protein/hr. Total ATPase activity was inhibited with increasing concentration of CdCl, to 1.0 mM in dosedependent manner and at 1.0 mM, was decreased by 50% to 3.40.O. 18 umol/mg protein/hr.
These results suggest that elevation in lipid peroxidation may not be solely due to the possibility of higher level of superoxide radicals resulting from inhibited superoxide dismutase but partly due to the direct act-ion of Cd` on the peroxidation reaction, and may play a role in Cd-induced lung toxicity. But lipid peroxidation may not be responsible for cell damage at the higher Cd concentrations. And another mechanism ap
pears to be responsible for cellular injury in
duced by Cd
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