The Fenton reaction of FeII(citrate) in the presence and absence of bicarbonate (HCO3-) is studied. It is found that the rate constant of the Fenton reaction (kobs) increases with increasing [citrate]. kobs also increase with increasing [HCO3-]; this effect is most significant at biological citrate concentrations. Methane and ethane gases are formed from (CH3)2SO when the Fenton reaction is carried out in the presence of large [citrate] due to the reaction of the citrate radical, (-2OC)CH2C(OH)(CO2-)CH(CO2-)/(-2OC)CH2C(O)(CO2-)CH2(CO2-) with (CH3)2SO. In the absence of citrate (CH3)2SO2 is the main product of the Fenton reaction. However, in the presence of 0.10 mM citrate, no (CH3)2SO2 is formed, some (CH3)SOOH is formed, along with a low yield of beta-ketoglutaric acid. Formation of (CH3)SOOH and beta-ketoglutaric acid are due to the citrate radical and FeIV(citrate). In the presence of bicarbonate formation of abundant beta-ketoglutaric acid confirms the formation of carbonate radical anion (CO3-). Thus, bicarbonate affects the mechanism and kinetics of the reaction dramatically. Hydroxyl radicals (OH) are not formed in the presence of bicarbonate and probably also not in its absence. These results point out that hydroxyl radicals, formed by the Fenton reaction, do not initiate oxidative stress in biological systems.

中文翻译：

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生理条件下的FeII（柠檬酸盐）Fenton反应。

研究了在有和没有碳酸氢盐（HCO3-）存在下，FeII（柠檬酸盐）的芬顿反应。发现芬顿反应的速率常数（kobs）随[柠檬酸盐]的增加而增加。穗轴也随着[HCO3-]的增加而增加；这种作用在生物柠檬酸盐浓度下最为显着。当Fenton反应在大柠檬酸盐存在下进行时，由于柠檬酸盐自由基（-2OC）CH2C（OH）（CO2-）CH（CO2）的反应，甲烷和乙烷气体由（CH3）2SO形成-）/（-2OC）CH2C（O）（CO2-）CH2（CO2-）与（CH3）2SO。在不存在柠檬酸盐的情况下，（CH3）2SO2是芬顿反应的主要产物。但是，在存在0.10 mM柠檬酸盐的情况下，没有形成（CH3）2SO2，形成了一些（CH3）SOOH，并且β-酮戊二酸的产率低。（CH3）SOOH和β-酮戊二酸的形成是由于柠檬酸根和FeIV（柠檬酸根）。在碳酸氢盐的存在下，丰富的β-酮戊二酸的形成证实了碳酸根自由基阴离子（CO3-）的形成。因此，碳酸氢盐显着影响反应的机理和动力学。在碳酸氢根存在下不会形成羟基自由基（OH），并且在不存在碳酸氢根的情况下也不会形成羟基自由基。这些结果指出，由芬顿反应形成的羟基自由基不会在生物系统中引发氧化应激。在碳酸氢根存在下不会形成羟基自由基（OH），并且在不存在碳酸氢根的情况下也不会形成羟基自由基。这些结果指出，由芬顿反应形成的羟基自由基不会在生物系统中引发氧化应激。在碳酸氢根存在下不会形成羟基自由基（OH），并且在不存在碳酸氢根的情况下也不会形成羟基自由基。这些结果指出，由芬顿反应形成的羟基自由基不会在生物系统中引发氧化应激。