nidins). and comprises studies in which its DNMT3 Formulation oxidation has been chemically [20811], electrochemically [203,21113] and enzymatically induced [135,209,214]. Comparatively, a very limited quantity of research have addressed the implications that quercetin oxidation has on its antioxidant properties. Actually, till incredibly recently, only the operates by Ramos et al. [215] and by G sen et al. [211] had addressed this situation. Utilizing the two,2-diphenyl-1-picrylhydrazyl (DPPH) assay, Ramos et al. [215] reported that while some quercetin oxidation solutions retained the scavenging properties of quercetin, other folks had been slightly extra potent. Utilizing the DPPH, a hydrogen peroxide, and hydroxyl free radical scavenging assay, G sen et al. [211] reported that all quercetin oxidation items had been significantly less active than quercetin. From a structural point of view, the oxidative conversion of quercetin into its Q-BZF does not have an effect on rings A and B on the flavonoid but drastically modifications ring C, as its six-atom pyran ring is converted into a five-atom furan ring. Taking into consideration the 3 Bors’ criteria for optimal activity [191], the free radical scavenging capacity of Q-BZF is expected to become considerably significantly less than that of quercetin by the sole fact that its structure lacks the C2 3 double bond required for radical stabilization. Depending on the latter, it seems affordable toAntioxidants 2022, 11,13 ofassume that an ultimate consequence with the oxidation of quercetin will be the relative loss of its original absolutely free radical scavenging potency. According to the earlier studies of Atala et al. [53], in which the oxidation of numerous flavonoids resulted within the formation of mixtures of metabolites that largely retained the ROS-scavenging properties on the unoxidized flavonoids, the assumption that oxidation CCKBR Accession results in the loss of such activity needed to be revised. Inside the case of quercetin, the mixtures of metabolites that resulted from its exposure to either alkaline conditions or to mushroom tyrosinase did not differ when it comes to their ROS-scavenging capacity, retaining both mixtures close to 100 of your original activity. Although the precise chemical composition with the aforementioned oxidation mixtures was not established [53], early studies by Zhou and Sadik [135] and more not too long ago by He m kovet al. [205] demonstrated that when it r comes to quercetin, regardless of the strategies employed to induce its oxidation (i.e., absolutely free radical, enzymatic- or electrochemically mediated), an basically comparable set of metabolites is formed. Prompted by the unexpected retention on the free radical scavenging activity of the mixture of metabolites that arise from quercetin autoxidation (Qox), Fuentes et al. [57] investigated the possible of Qox to defend Hs68 (from a human skin fibroblast) and Caco2 (from a human colonic adenocarcinoma) cells against the oxidative harm induced by hydrogen peroxide or by the ROS-generating non-steroidal anti-inflammatory drug (NSAID) indomethacin [21618]. When exposed to either of those agents, the quercetinfree Qox mixture afforded total protection using a 20-fold greater potency than that of quercetin (helpful at 10 ). The composition of Qox, as analyzed by HPLC-DAD-ESIMS/MS, incorporated eleven significant metabolites [57]. Each and every of these metabolites was isolated and assessed for its antioxidant capacity in indomethacin-exposed Caco-2 cells. Interestingly, out of all metabolites, only a single, identified as Q-BZF, was in a position to account for the protection afforded by Qox. The latt
