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- W2029080626 abstract "One of the common explanations for oxidative stress in the physiological milieu is based on the Fenton reaction, i.e. the assumption that radical chain reactions are initiated by metal-catalyzed electron transfer to hydrogen peroxide yielding hydroxyl radicals. On the other hand - especially in the context of so-called iron switches - it is postulated that cellular signaling pathways originate from the interaction of reduced iron with hydrogen peroxide. Using fluorescence detection and EPR for identification of radical intermediates, we determined the rate of iron complexation by physiological buffer together with the reaction rate of concomitant hydroxylations of aromatic compounds under aerobic and anaerobic conditions. With the obtained overall reaction rate of 1,700 M(-1)s(-1) for the buffer-dependent reactions and the known rates for Fenton reactions, we derive estimates for the relative reaction probabilities of both processes. As a consequence we suggest that under in vivo conditions initiation of chain reactions by hydroxyl radicals generated by the Fenton reaction is of minor importance and hence metal-dependent oxidative stress must be rather independent of the so-called peroxide tone. Furthermore, it is proposed that - in the low (subtoxic) concentration range - hydroxylated compounds derived from reactions of non-free (crypto) OH radicals are better candidates for iron-dependent sensing of redox-states and for explaining the origin of cellular signals than the generation of free hydroxyl radicals." @default.
- W2029080626 created "2016-06-24" @default.
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- W2029080626 date "2000-01-01" @default.
- W2029080626 modified "2023-09-25" @default.
- W2029080626 title "Arguments against the significance of the Fenton reaction contributing to signal pathways under<i>in vivo</i>conditions" @default.
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- W2029080626 doi "https://doi.org/10.1080/10715760000301101" @default.
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