Koster J F, van Berkel T J
Biochem Pharmacol. 1983 Nov 15;32(22):3307-10. doi: 10.1016/0006-2952(83)90355-6.
The role of the oxygen radicals in lipid peroxidation, induced by ADP/Fe3+ or cumene hydroperoxide was investigated by administering diethyldithiocarbamate, an inhibitor of superoxide dismutase, to hepatocytes or rats. Intact rat-liver hepatocytes perform a delayed ADP/Fe3+-induced lipid peroxidation after pretreatment with diethyldithiocarbamate. The cumene hydroperoxide-induced lipid peroxidation is unchanged. Hepatocytes, isolated from a rat administered with diethyldithiocarbamate in vivo, exhibit the same pattern, a delayed iron-induced lipid peroxidation and an unchanged cumene hydroperoxide-induced lipid peroxidation. Liver microsomes isolated from liver of a rat administered with diethyldithiocarbamate do not perform lipid peroxidation with NADPH/ADP/Fe3+, but do undergo lipid peroxidation with cumene hydroperoxide. It can be concluded that besides the inhibition of superoxide dismutase, diethyldithiocarbamate inhibits directly the microsomal lipid peroxidation. Although this inhibition hampers the conclusion, evidence is obtained that superoxide dismutase is probably involved in the protection against lipid peroxidation of the mitochondria, but not of the microsomes.
通过向肝细胞或大鼠施用超氧化物歧化酶抑制剂二乙二硫代氨基甲酸盐，研究了氧自由基在由ADP/Fe3+或氢过氧化异丙苯诱导的脂质过氧化中的作用。完整的大鼠肝脏肝细胞在用二乙二硫代氨基甲酸盐预处理后，对ADP/Fe3+诱导的脂质过氧化有延迟作用。氢过氧化异丙苯诱导的脂质过氧化没有变化。从体内施用二乙二硫代氨基甲酸盐的大鼠分离出的肝细胞表现出相同的模式，即铁诱导的脂质过氧化延迟，而氢过氧化异丙苯诱导的脂质过氧化不变。从施用二乙二硫代氨基甲酸盐的大鼠肝脏分离出的肝微粒体，在NADPH/ADP/Fe3+存在下不会发生脂质过氧化，但在氢过氧化异丙苯存在下会发生脂质过氧化。可以得出结论，除了抑制超氧化物歧化酶外，二乙二硫代氨基甲酸盐还直接抑制微粒体脂质过氧化。尽管这种抑制妨碍了得出结论，但有证据表明超氧化物歧化酶可能参与了对线粒体脂质过氧化的保护，但不参与对微粒体脂质过氧化的保护。
