Hussain T, Shukla G S, Chandra S V
Pharmacol Toxicol. 1987 May;60(5):355-8. doi: 10.1111/j.1600-0773.1987.tb01526.x.
Intraperitoneal administration of cadmium acetate (Cd2+, 0.4 mg/kg) to rats daily for 30 days was found to inhibit the activity of superoxide dismutase (SOD), to increase the endogenous levels of lipid peroxides and lipid peroxidation in the liver and the kidney tissues. Addition of varying concentrations of Cd2+ (10-100 microM) in vitro also inhibited SOD in both the tissues. It appears that the inhibition of SOD could be due to direct interaction of Cd2+ with the enzyme molecule. Lipid peroxidation reaction was also increased after addition of Cd2+ to fresh homogenate of these tissues, however, it did not produce any effect in heated homogenates in in vitro experiments. It indicated that Cd-induced elevation in lipid peroxidation may not be only due to the possibility of higher level of superoxide radicals resulting from inhibited superoxide dismutase but could also be as a result of direct action of Cd2+ on the peroxidation reaction. Thus, the possibility of involvement of free radical damage to the membrane structures in Cd toxicity has been demonstrated in these experiments.
研究发现，连续30天每天给大鼠腹腔注射醋酸镉（Cd2+，0.4毫克/千克）会抑制超氧化物歧化酶（SOD）的活性，增加肝脏和肾脏组织中脂质过氧化物的内源性水平以及脂质过氧化反应。在体外添加不同浓度的Cd2+（10 - 100微摩尔）也会抑制这两种组织中的SOD。似乎SOD的抑制可能是由于Cd2+与酶分子的直接相互作用。向这些组织的新鲜匀浆中添加Cd2+后，脂质过氧化反应也会增加，然而，在体外实验中，加热的匀浆中并未产生任何影响。这表明Cd诱导的脂质过氧化增加可能不仅是由于超氧化物歧化酶受抑制导致超氧自由基水平升高，还可能是Cd2+对过氧化反应直接作用的结果。因此，这些实验证明了自由基损伤参与Cd毒性作用中膜结构破坏的可能性。
