nidins). and comprises studies in which its oxidation has been chemically [20811], electrochemically [203,21113] and enzymatically induced [135,209,214]. Comparatively, an incredibly restricted number of research have addressed the implications that HDAC1 manufacturer quercetin oxidation has on its antioxidant properties. In actual fact, until really not too long ago, only the works by Ramos et al. [215] and by G sen et al. [211] had addressed this challenge. Employing the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay, Ramos et al. [215] reported that although some quercetin oxidation items retained the scavenging properties of quercetin, others had been slightly extra potent. Working with the DPPH, a hydrogen peroxide, and hydroxyl absolutely free radical scavenging assay, G sen et al. [211] reported that all quercetin oxidation goods have been less active than quercetin. From a structural point of view, the oxidative conversion of quercetin into its Q-BZF will not impact rings A and B from the flavonoid but drastically adjustments ring C, as its six-atom pyran ring is converted into a five-atom furan ring. Taking into consideration the three Bors’ criteria for optimal activity [191], the cost-free radical scavenging capacity of Q-BZF is expected to be substantially significantly less than that of quercetin by the sole fact that its structure lacks the C2 three double bond needed for radical stabilization. According to the latter, it appears affordable toAntioxidants 2022, 11,13 ofassume that an ultimate consequence in the oxidation of quercetin could be the relative loss of its original free radical scavenging potency. According to the earlier research of Atala et al. [53], in which the oxidation of various flavonoids resulted within the formation of mixtures of Aurora B Formulation metabolites that largely retained the ROS-scavenging properties of the unoxidized flavonoids, the assumption that oxidation leads to the loss of such activity needed to be revised. Within the case of quercetin, the mixtures of metabolites that resulted from its exposure to either alkaline situations or to mushroom tyrosinase didn’t differ in terms of their ROS-scavenging capacity, retaining each mixtures close to one hundred from the original activity. Even though the exact chemical composition from the aforementioned oxidation mixtures was not established [53], early research by Zhou and Sadik [135] and much more not too long ago by He m kovet al. [205] demonstrated that when it r comes to quercetin, no matter the methods employed to induce its oxidation (i.e., totally free radical, enzymatic- or electrochemically mediated), an basically similar set of metabolites is formed. Prompted by the unexpected retention from the cost-free radical scavenging activity in the mixture of metabolites that arise from quercetin autoxidation (Qox), Fuentes et al. [57] investigated the potential of Qox to shield 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 having a 20-fold higher potency than that of quercetin (productive at 10 ). The composition of Qox, as analyzed by HPLC-DAD-ESIMS/MS, incorporated eleven significant metabolites [57]. Every single 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 able to account for the protection afforded by Qox. The latt
