کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1316868 | 976489 | 2009 | 7 صفحه PDF | دانلود رایگان |

The Fenton reaction was investigated, in a medium approximating to that of the extracellular fluid (ECF), by rapid-mixing stopped flow experiments and HPLC analysis using sodium terephthalate (TA2−). The reactive intermediate of the Fenton reaction hydroxylates the essentially nonfluorescent, TA2− to the brilliant fluorophor 2-hydroxy-terephthalate (OH-TA), which allows the Fenton reaction to be monitored in stopped-flow experiments. There was no artefactual quenching of the fluorescence by substances present in the Fenton-reaction mixture or in the artificial cerebrospinal fluid (aCSF) that might have influenced OH-TA quantification. A mathematical model based on kinetic considerations was developed. This explains the observed independence of the OH-TA concentration on the amount of TA2− present in aCSF as well as its dependence on TA2− concentration in potassium acetate buffer. A mechanism based on this model, involving complex formation between Fe(II), TA2− and H2O2, followed by an intra-molecular hydroxylation accompanied by an intra-molecular electron transfer was developed. The results are consistent with a reactive intermediate, which causes oxidative stress in vivo, not being a free hydroxyl radical, but a ferryl species or a “crypto” radical. The biological implications of these results are discussed.
Journal: Journal of Inorganic Biochemistry - Volume 103, Issue 1, January 2009, Pages 28–34