Andersen H R, Andersen O
Department of Environmental Medicine, Odense University, Denmark.
Biol Trace Elem Res. 1989 Jul-Sep;21:255-61. doi: 10.1007/BF02917261.
Intraperitoneal administration of nickel chloride enhanced hepatic lipid peroxidation (HLP) in 6-wk-old and 8-12-wk-old male CBA-mice but not in 3-wk-old mice. Nickel chloride administration depleted hepatic GSH in 8-12-wk-old mice but not in the younger age groups. After 300 mumol NiCl2/kg mortality occurred among 8-12-wk-old mice but not among the younger mice. Stimulation of GSH synthesis by administration of L-2-oxothiazolidine-4-carboxylate reduced nickel chloride induced mortality and HLP. Reduction of GSH synthesis by administration of buthionine sulfoximine (BSO) did not, however, enhance the toxicity of nickel chloride. This might be owing to chelation of the Ni(II)-ion by BSO. The results demonstrate age dependency and a protective effect of enhanced GSH synthesis in nickel chloride stimulated HLP.
腹腔注射氯化镍可增强6周龄和8 - 12周龄雄性CBA小鼠的肝脏脂质过氧化（HLP），但对3周龄小鼠无此作用。给予氯化镍会使8 - 12周龄小鼠肝脏中的谷胱甘肽（GSH）减少，但在较年轻的年龄组中则不会。在给予300 μmol NiCl₂/kg后，8 - 12周龄小鼠出现死亡，而较年轻的小鼠未出现死亡。通过给予L - 2 - 氧代噻唑烷 - 4 - 羧酸刺激GSH合成可降低氯化镍诱导的死亡率和HLP。然而，通过给予丁硫氨酸亚砜胺（BSO）减少GSH合成并没有增强氯化镍的毒性。这可能是由于BSO对Ni(II)离子的螯合作用。结果表明了年龄依赖性以及增强GSH合成在氯化镍刺激的HLP中的保护作用。
