The potassium salt of the new mixed-polyoxotungstate anion [ Eu3( H, O), (SbW, O, ) (W50,&]l8-(1) has been prepared from WO, , Sb, O, , Eu(N0,),*6H20, and KOH in water and isolated in crystalline form as K, , H, [ Eu, ( H, O), (SbW, O, ) (W,O,,),]*25.5 H, O. It crystallizes in the monoclinic space group C2/m, with a = 30.250(7), b = 18.568(5& c = 22.101 (6) A, p = 109.19(8)", and, core is co-ordinated by a B-type a-SbWgO, unit and three W,018 units with tetrahedral conformation. Each Eu3+ in the core exhibits eight-co-ordination by oxygen atoms belonging to H20, SbWgO, , and W,018 units. The intramolecular energy transfer from the 0-W charge-transfer levels for the polyoxotungstate crystalline lattices to the emitting 50, level of Eu3+ takes place efficiently at least over 6.9 A which is the largest distance between W and Eu atoms in the anion. A comparison of the lifetime and quantum yield of the emission among (1 ), [Eu(W,0,,), Ig-, and [Eu(SiW,,O,),]l3-indicates that the hopping of a Cr electron between WO, octahedra is the predominant deactivation channel of the O-+W charge-transfer levels, which reduces drastically the communication with the excited levels of Eu3+.

The crystal structures of oxidized and photoreduced decatungstates are compared. Three specimens of decatungstate complexes were prepared in mixed solvents of H2O–CH3CN and were characterized by X-ray diffraction. Unit cell parameters are as follows: (C6H16N)4[W10O32]·2CH3CN; DECA Mr=2841.4, monoclinic, P21⁄n, a=14.617(2), b=17.783(3), c=11.755(2) Å, β=100.27(2)°, V=3006.5(9) Å3, Z=2; (C6H16N)4[H1.5W10O32]·8H2O; RED1 Mr=2905.4, monoclinic, P21⁄n, a=15.902(3), b=12.233(2), c=15.673(4) Å, β=93.76(2)°, V=3042(1), Å3  Z=2; Na4[H1.8W10O32]·14H2O; RED2 Mr=2696.7, monoclinic, C2⁄m, a=16.123(5), b=12.636(3), c=12.168(4) Å, β=117.40(2)°, V=2202(1) Å3, Z=2; There is no obvious change in the anion frame among the three decatungstate complexes. Photoreduced decatungstates may coordinate protons which neutralize excess charge injected into anions. It is concluded that the structure of W10O32 is not largely altered up to two-electron reduction.

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In recent work, it was shown that V-containing polyoxometalates such as (n-Bu4N)7SiW9V3O40 or (n-Bu4N)9P2W15V3O62, as well as eight other V-containing precatalysts tested, evolve to a high activity, long catalytic lifetime (> or = 30,000-100,000 total turnovers) 3,5-di-tert-butylcatechol dioxygenase, in which Pierpont's complex [VO(DBSQ)(DTBC)]2 (where DBSQ is 3,5-di-tert-butylsemiquinone and DTBC is the 3,5-di-tert-butylcatecholate dianion) was identified as a common catalyst or catalyst resting state (Yin, C.-X.; Finke, R. G. Vanadium-Based, Extended Catalytic Lifetime Catechol Dioxygenases: Evidence For a Common Catalyst. J. Am. Chem. Soc. 2005, 127 (25), 9003-9013). Herein, those findings are followed up by studies aimed at answering the following questions about this record catalytic lifetime 3,5-di-tert-butylcatechol dioxygenase catalyst: (i) What is the key to how V leaches from, for example, seemingly robust V-containing polyoxometalate precatalysts? (ii) What is the key to the sigmoidal, apparently autocatalytic kinetics observed? (iii) What can be learned about the underlying reactions that form [VO(DBSQ)(DTBC)]2? (iv) Finally, do the answers to (i-iii) lead to any broader insights or concepts? Key findings from the present work include the fact that the reaction involves a novel, autoxidation-product-induced dioxygenase, that is, one in which the undesired autoxidation of the 3,5-di-tert-butylcatechol substrate to the corresponding benzoquinone and H2O2 turns on the desired dioxygenase catalysis via a V-leaching process which eventually yields Pierpont's complex, [VO(DBSQ)(DTBC)]2. Plausible reactions en route to [VO(DBSQ)(DTBC)]2 consistent with the kinetic data, the role of H2O2, and the relevant literature are provided. The results provide a prototype example of the little observed but likely more general concept of an autoxidation-product-initiated reaction. The results also provide considerable simplification of, and insight into, the previously disparate literature of V-based 3,5-di-tert-butylcatechol dioxygenase catalysis.

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Autophagy was enhanced in white adipose tissues of mice fed a high-fat diet. The suppression of autophagy in white adipose tissue ameliorated liver steatosis, inflammation, and fibrosis. Adipocyte autophagy contributes to the liver pathogenesis of nonalcoholic fatty liver disease. BACKGROUND & AIMS:Although nonalcoholic fatty liver disease (NAFLD) is closely associated with obesity, the role of adipose tissue in NAFLD is not well-understood. Because autophagy has been reported to be involved in the degradation of lipid droplets, we investigated the role of adipose tissue autophagy in the liver pathogenesis of NAFLD.METHODS: C57BL/6J mice and adipocyte-specific Atg7knockout mice (Adipoq-Atg7 KO mice) were fed a high-fat diet (HFD).RESULTS: HFD feeding for up to 4 months increased both inguinal and epididymal white adipose tissue (iWAT and eWAT, respectively; the former represents subcutaneous fat, and the latter represents visceral fat) in mice. After HFD feeding, autophagy flux in both types of white adipose tissue was increased, and the levels of Rubicon, a negative autophagy regulator, were decreased, suggesting autophagy promotion.Adipoq-Atg7 KO mice exhibited suppressed autophagy in both iWAT and eWAT. Adipocyte-specific Atg7 KO enhanced HFDinduced iWAT hypertrophy. On the other hand, eWAT levels in Adipoq-Atg7 KO mice were increased after 1 month of HFD feeding but decreased after 4 months of HFD feeding compared with those in wild-type controls. Cleaved caspase 3 and JNK pathway protein expression in eWAT was increased without cytokine elevation in Adipoq-Atg7 KO mice fed an HFD compared with wild-type mice fed an HFD. Adipocyte-specific Atg7 KO decreased serum free fatty acid levels and ameliorated HFD-induced steatosis, liver inflammation, and fibrosis.CONCLUSIONS: Autophagy was enhanced in the white adipose tissues of mice fed an HFD. Autophagy inhibition in white adipose tissues ameliorated the liver pathology of NAFLD via adipose-liver crosstalk.

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