Abstract:

Excessive reactive oxygen species (ROS) can oxidativelydamageDNAto cause severe biological consequences. In thestudy, a natural flavonoid,myricitrin(myricetin-3-O-alpha-L-rhamnopyranoside), was found to have aprotectiveeffectagainsthydroxyl-inducedDNAdamage(IC50 159.86 +/- 54.24 mu g/mL). To investigate themechanism, it was determined by variousantioxidantassays. The results revealed thatmyricitrincould 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). Basedonthe mechanistic analysis, it can be concluded that: (i)myricitrincan effectively protectagainsthydroxyl-inducedDNAoxidativedamagevia ROS scavenging and deoxynucleotide radicals repairing approaches. Both approaches can be attributed to itsantioxidant. From a structure-activity relationship viewpoint, itsantioxidantability can be attributed to the ortho-dihydroxyl moiety, and ultimately to the stabilityofits 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) itsprotectiveeffectagainstDNAoxidativedamagemay be primarily responsible for the pharmacological effects, and offers promise as a new therapeutic reagent for diseases fromDNAoxidativedamage.