Burkitt M J, Mason R P
Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8440-4. doi: 10.1073/pnas.88.19.8440.
Although the hydroxyl radical is often implicated as the species responsible for the initiation of oxidative damage in iron-overload conditions, no ESR evidence for the formation of the radical in vivo has been reported. We have employed a secondary radical-trapping technique in which the hydroxyl radical reacts with dimethyl sulfoxide to form the methyl radical, which is then detected as its adduct of the spin trap N-t-butyl-alpha-phenylnitrone in the bile of animals given an intragastric dose of ferrous sulfate. The identity of this adduct was verified by isotope-substitution techniques. We show that unless measures are taken to inactivate the iron excreted in the bile of treated animals, reactions between iron, oxygen, dimethyl sulfoxide, N-t-butyl-alpha-phenylnitrone, and bile components lead to the formation of artifacts during sample collection.
尽管羟自由基常被认为是铁过载条件下引发氧化损伤的物质,但尚无体内形成该自由基的电子自旋共振(ESR)证据报道。我们采用了一种二级自由基捕获技术,即羟自由基与二甲基亚砜反应形成甲基自由基,然后在给动物灌胃硫酸亚铁后,在其胆汁中作为自旋捕获剂N-叔丁基-α-苯基硝酮的加合物进行检测。通过同位素取代技术验证了该加合物的身份。我们发现,除非采取措施使处理动物胆汁中排出的铁失活,否则铁、氧、二甲基亚砜、N-叔丁基-α-苯基硝酮和胆汁成分之间的反应会在样品采集过程中导致假象的形成。