This study reexamined the mechanisms
for oxidative organic degradation
by the binary mixture of periodate and H2O2 (PI/H2O2) that was recently identified as a new advanced
oxidation process. Our findings conflicted with the previous claims
that (i) hydroxyl radical (•OH) and singlet oxygen
(1O2) contributed as the primary oxidants, and
(ii) •OH production resulted from H2O2 reduction by superoxide radical anion (O2
•–). PI/H2O2 exhibited
substantial oxidizing capacity at pH < 5, decomposing organics
predominantly by •OH. The likelihood of a switch
in the major oxidant under varying pH conditions was revealed. IO4
– as the major PI form under acidic conditions
underwent one-electron reduction by H2O2 to
yield radical intermediates, whereas H2I2O10
4– preferentially occurring at pH >
7 caused 1O2 generation through two-electron
oxidation of
H2O2. PI reduction by O2
•– was suggested to be a key reaction in •OH production,
on the basis of the electron paramagnetic resonance detection of methyl
radicals in the dimethyl sulfoxide solutions containing PI and KO2, and the absence of deuterated and 18O-labeled
hydroxylated intermediates during PI activation using D2O and H2
18O2. Finally, simple oxyanion
mixing subsequent to electrochemical PI and H2O2 production achieved organic oxidation, enabling a potential strategy
to minimize the use of chemicals.
Studies suggest that time-restricted feeding (TRF) may prevent obesity and its commodities. At present, little is known about how TRF impacts immune cells, and whether such an effect is linked to altered metabolic parameters under condition of a high-fat diet (HFD)-induced obesity. To address these issues, we conducted a study in which we determined whether TRF has therapeutic efficacy against weight gain, adiposity, as well as associated immune cell disturbance found in obese mice. Six-week-old male C57BL/6 mice were fed a low-fat diet (LFD) or HFD ad libitum for six weeks, after which time a subgroup of HFD mice was switched to the 10 h TRF paradigm (HFD-TRF) for additional eight weeks. We found that TRF intervention reduced HFD-induced weight gain. Even with comparable fat mass and mean adipocyte area, the HFD-TRF group had lower mRNA levels of proinflammatory cytokine Tnfα and chemokine Ccl8, along with reduced numbers of adipose tissue macrophages (ATM), CD11c+ ATM, and CD8+ T cell compared to the HFD group, while maintaining CD8+ to CD4+ ratio at levels similar to those in the LFD group. Furthermore, TRF intervention was effective in improving glucose tolerance and reducing HOMA-IR. Taken together, our findings suggest that TRF restores the obesity-induced alteration in immune cell composition, and this effect may in part contribute to health benefits (including insulin sensitivity) of practicing TRF.
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