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Microsomal Oxidation of Hydroxyl Radical Scavenging Agents
Published in Robert A. Greenwald, CRC Handbook of Methods for Oxygen Radical Research, 2018
Arthur I. Cederbaum, Gerald Cohen
Experiment B shows that the addition of ferric-EDTA to the microsomes results in a large increase in the oxidation of the scavengers. Experiment C shows that the addition of EDTA itself also stimulates the oxidation of the scavengers. The stimulation by EDTA may reflect chelation of iron present in the microsomes or the reaction mixture (although attempts to remove iron in the buffers by chelex treatment were made). An important function of microsomal electron transfer, besides the production of H2O2, is probably to reduce the ferric-EDTA. This reduction may be mediated via superoxide produced from autoxidation of the reductase or oxy-cytochrome P-450, or directly via microsomal enzymes such as the reductase. Recent experiments have shown that the reductase can reduce ferric EDTA in the presence of superoxide dismutase,22 and it would appear that the reductase may represent an important locus for the oxidation of hydroxyl radical scavengers by microsomes. The oxidation of alcohols may involve interaction with ·OH, as well as a second pathway, involving cytochrome P-450, and independent of ·OH.18-20 The oxidation of aminopyrine, a typical substrate for the mixed-function oxidase activity of cytochrome P-450, is not affected by the addition of azide, EDTA, or iron-EDTA. Thus, the mixed-function oxidase pathway can be dissociated from the pathway that oxidizes hydroxyl radical scavengers.
Antioxidant and antihyperlipidemic activities of catechol derivatives and biflavonoid isolated from Semecarpus anacardium seeds
Published in Toxicology Mechanisms and Methods, 2022
Ramalingam Sundaram, Karuppiah Muthu, Palanivelu Shanthi, Panchanatham Sachdanandam
Hydroxyl radical is the principal contributor for tissue injury. The formation of Hydroxyl radical from Fenton reaction was quantified using 2, deoxy-D-ribose degradation. Hydroxyl radicals are considered to be one of the rapid initiators of lipid peroxidation process, abstracting hydrogen atoms from polyunsaturated fatty acids which brings about peroxidic reactions of membrane lipids and also from the sugar moiety of DNA causing oxidative damage to DNA (Halliwell and Gutteridge 1999). These effects have been implicated in mutagenesis, carcinogenesis and aging (Halliwell et al. 1987). Ferric-EDTA incubated with H2O2 and BHT at pH 7.4, produces hydroxyl radicals and was detected by their ability to degrade 2-deoxyribose into fragments, on heating with TBA at low pH forming a pink chromogen (Aruoma et al. 1989). The highest inhibition activity was observed in biflavonoid followed by catechol derivatives I–IV. Biflavonoid might have caused the removal of hydroxyl radical and prevented the degradation of 2-deoxyribose. From this result, it can be concluded that Biflavonoid is powerful scavengers of OH radical and therefore prevent OH radical related pathophysiological events.
Dietary iron variably modulates assembly of the intestinal microbiota in colitis-resistant and colitis-susceptible mice
Published in Gut Microbes, 2020
Melissa Ellermann, Raad Z. Gharaibeh, Nitsan Maharshak, Ernesto Peréz-Chanona, Christian Jobin, Ian M. Carroll, Janelle C. Arthur, Scott E Plevy, Anthony A. Fodor, Cory R. Brouwer, R. Balfour Sartor
Intestinal inflammation is associated with compositional changes to the intestinal microbiota, including an expansion of Enterobacteriaceae.38,39,54–56 Because dietary iron restriction induced similar perturbations to the fecal microbiota, we investigated the impact of dietary iron on the development of colitis in ex-GF Il10−/- mice. Interestingly, dietary iron supplementation modestly limited the development of inflammation. However, an important limitation of our study is that iron supplementation was provided to iron replete hosts rather than iron-deficient hosts, as often occurs in IBD patients. However, many IBD patients with anemia of chronic disease are encouraged to take supplemental iron despite normal iron stores, and IBD patients are routinely encouraged to take multi-vitamins that contain iron, regardless of their iron status. Nonetheless, in agreement with our observations, Dostal and colleagues reported higher baseline inflammation in the ilea and ceca of rats on a control diet compared to iron-deficient rats receiving iron supplementation.48 Similarly, dietary iron restriction has also been reported to minimize intestinal inflammation.11,48 In chemically induced models of colitis, increased dietary iron exacerbated colitis.10,12 However, in many of these studies, dietary iron was administered at doses approximately 100 times higher than what is present in normal mouse chow and may therefore not reflect amounts consumed with iron fortification or oral iron supplements. Indeed, similar to our study, oral iron supplementation ranging from 2 to 10 fold higher than iron levels in the control diets protected against TNBS-induced and DSS-induced colitis.57,58 Administration of an iron-fortified diet in infants with high initial pathogen burden also resulted in increased fecal markers of inflammation.7 However, two other studies demonstrated no impact of dietary iron supplementation on inflammation markers in infants or children with low pathogen burden.49,59 Interestingly, dietary iron restriction has been reported to minimize intestinal inflammation,11,48 consistent with our statistically insignificant trends. Finally, it should also be noted that a recent study demonstrated that the formulation of iron also impacts the effect of oral iron supplementation on colitis severity, where ferrous iron and ferrous bisglycinate both ameliorated DSS-induced colitis and ferric-EDTA had the opposite effect.58 Together, these studies provide evidence that dietary iron influences colitis development, albeit in a complex manner that depends on the iron formulation as well as microbial and host factors that remain to be fully defined.