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Chemical Study on Protective Effect Against Hydroxyl-induced DNA Damage and Antioxidant Mechanism of Myricitrin. J. Chin. Chem. Soc., 2014, 61: 383–390.

来源: J. Chin. Chem. Soc.日期: 2015-01-27

Abstract:

Excessive reactive oxygen species (ROS) can oxidatively damage DNA to cause severe biological consequences. In the study, a natural flavonoid, myricitrin (myricetin-3-O-alpha-L-rhamnopyranoside), was found to have a protective effect against hydroxyl-induced DNA damage (IC50 159.86 +/- 54.24 mu g/mL). To investigate the mechanism, it was determined by various antioxidant assays. The results revealed that myricitrin could effectively scavenge center dot OH, center dot O-2(-), DPPH center dot (1,1-diphenyl-2-picrylhydrazyl radical), and ABTS(+)center dot (2,2'-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radicals (IC50 values were respectively 69.71 +/- 5.93, 69.71 +/- 5.93, 25.34 +/- 2.14, and 1.71 +/- 0.09 mu g/mL), and bind Cu2+ (IC50 27.33 +/- 2.36 mu g/mL). Based on the mechanistic analysis, it can be concluded that: (i) myricitrin can effectively protect against hydroxyl-induced DNA oxidative damage via ROS scavenging and deoxynucleotide radicals repairing approaches. Both approaches can be attributed to its antioxidant. From a structure-activity relationship viewpoint, its antioxidant ability can be attributed to the ortho-dihydroxyl moiety, and ultimately to the stability of its oxidized form ortho-benzoquinone; (ii) its ROS scavenging is mediated via metal-chelating, and direct radical-scavenging which is through donating hydrogen (H center dot) and electron (e); and (iii) its protective effect against DNA oxidative damage may be primarily responsible for the pharmacological effects, and offers promise as a new therapeutic reagent for diseases from DNA oxidative damage.


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