Yamada M, Okigaki T, Awai M
Department of Pathology, Okayama University Medical School, Japan.
Cell Struct Funct. 1987 Oct;12(5):407-20. doi: 10.1247/csf.12.407.
We studied the cytotoxic effects of ferric nitrilotriacetate (Fe-NTA) on normal rat liver epithelial cells (RL34) cultured in medium containing 10% fetal calf serum. Marked cytolysis was present in cells exposed to greater than or equal to 25 micrograms/ml iron of Fe-NTA, but not all the cells exposed to 50 micrograms/ml iron were lethally injured. The remaining cells showed anomalous growth, namely cell pile-up and aggregation. Superoxide dismutase inhibited this iron-induced cytotoxicity, whereas catalase, mannitol, dimethyl sulfoxide, and 1,4-diazabicyclo-[2.2.2.] octane did not. RL34 cells exposed to Fe-NTA actually produced a large amount of superoxide radicals (O2-.), whereas unexposed control cells produced none. Allopurinol inhibited O2-. production and prevented cell injury by Fe-NTA. These results show that the injury to cells produced by Fe-NTA depends on the generation of O2-., the source of which may be xanthine oxidase.
我们研究了次氮基三乙酸铁（Fe-NTA）对在含10%胎牛血清的培养基中培养的正常大鼠肝上皮细胞（RL34）的细胞毒性作用。暴露于大于或等于25微克/毫升Fe-NTA铁的细胞出现明显的细胞溶解，但并非所有暴露于50微克/毫升铁的细胞都受到致命损伤。其余细胞表现出异常生长，即细胞堆积和聚集。超氧化物歧化酶抑制这种铁诱导的细胞毒性，而过氧化氢酶、甘露醇、二甲基亚砜和1,4-二氮杂双环-[2.2.2.]辛烷则没有。暴露于Fe-NTA的RL34细胞实际上产生了大量超氧阴离子自由基（O2-.），而未暴露的对照细胞则没有产生。别嘌呤醇抑制O2-.的产生并防止Fe-NTA对细胞的损伤。这些结果表明，Fe-NTA对细胞的损伤取决于O2-.的产生，其来源可能是黄嘌呤氧化酶。
