Irisin is an exercise-regulated myokine inducing browning of white adipose tissue and has gained interest as a potential new strategy to combat obesity and its associated disorders, such as type 2 diabetes mellitus (T2DM). The aim of this study is to evaluate the circulating serum irisin levels in obesity and T2DM and also to elucidate possible relationships between serum irisin levels with anthropometric and metabolic parameters of obesity and T2DM. One hundred fifty newly diagnosed T2DM patients as well as 150 nondiabetic control subjects were enrolled in this study. Nondiabetic controls were then stratified according to their body mass index (BMI) into three subgroups; lean, overweight, and obese. Serum irisin levels were evaluated by enzyme-linked immunosorbent assay. Serum irisin levels were significantly decreased in T2DM patients compared with nondiabetic controls. Obese nondiabetic controls had significantly higher serum irisin levels compared with lean nondiabetic controls. In both nondiabetic controls and T2DM patients, serum irisin was significantly positively correlated with BMI (r 5 0.985, P < 0.001 and r 5 0.218, P 5 0.007, respectively), fat mass (r 5 0.959, P < 0.001 and r 5 0.202, P 5 0.013, respectively), fat-free mass (r 5 0.606, P < 0.001 and r 5 0.194, P 5 0.017, respectively), fat-free mass index (r 5 0.820, P < 0.001 and r 5 0.179, P 5 0.028, respectively), waist-to-hip ratio (r 5 0.880, P < 0.001 and r 5 0.194, P 5 0.017, respectively), fasting insulin (r 5 0.989, P < 0.001 and r 5 0.207, P 5 0.011, respectively), and HOMA-IR (r 5 0.989, P < 0.001 and r 5 0.185, P 5 0.023, respectively), whereas; significantly negatively correlated with insulin sensitivity (r 5 20.992, P < 0.001 and r 5 20.187, P 5 0.022, respectively). In this study, we demonstrated that circulating serum irisin levels were increased in obese nondiabetic subjects, while decreased in T2DM patients. Moreover, serum irisin levels were correlated with anthropometric and metabolic markers of obesity and T2DM. V C 2016 IUBMB Life, 68(7): [544][545][546][547][548][549][550][551][552][553][554][555][556] 2016

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The kinetics of permanganate oxidation of P-phenylalanine in aqueous perchlorate media at a constant ionic strength of 3.0 mol dm-3 has been studied spectrophotometrically. A first-order reaction in [MnO,] and a fractional order with respect to P-phenylalanine were observed. The results obtained at various hydrogen-ion concentrations indicate that the protonated species of both the amino acid and permanganate play a role in the kinetics. Kinetic evidence for the formation of an intermediate complex between the amino acid and the oxidant is presented. The activation parameters were calculated and found to be ASs = -1 60.1 4 8.23 J K-l mol-l, AHs = 34.04 f 1.02 k J mol-l, and AG' = 81.77 f 3.47 k J mol-l, respectively. A mechanism consistent with the kinetic results is discussed.Permanganate ion in acidic media has been used extensively as a potent oxidant for studying the oxidation kinetics of many organic substrates including amino acids.'-7 In some cases the mechanistic approach has been based on intermediate complex formation and in others the results have been interpreted by a free-radical mechanism, in the absence of kinetic or spectrophotometric evidence. The mechanisms suggested by various authors are not uniform, indicating that a wide variety of mechanisms is possible depending on the nature of the reactive species of permanganate as well as of the amino acids.

Aroclors 1242 and 1254 were anaerobically dechlorinated by microorganisms eluted from polychlorinated biphenyl (PCB)-contaminated River Raisin (RR) and Silver Lake (SL) sediments. Dechlorination occurred primarily from the meta positions. H4IIE rat hepatoma cell bioassays for ethoxyresorufin-O-deethylase (EROD) induction potency, a measure of aryl hydrocarbon receptor-mediated toxic potential, revealed that the potencies of the Aroclors were considerably reduced after dechlorination. The decreases in EROD induction potencies were dependent on the extent of dechlorination of the non-ortho-substituted and monoortho-substituted PCBs. Calculated 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalents (TEqs calc ) for the PCB mixtures were 5.7, 0.08, and 0.05 pM TEq calc /mole of PCBs for non-, RR-, and SL-dechlorinated Aroclor 1242, and 7.8, 1.6, and 1.0 pM TEq calc / mole of PCBs for non-, RR-, and SL-dechlorinated Aroclor 1254, respectively. Correspondence between TEqs assay determined using the H4IIE bioassay and TEqs calc indicated that no unexpected synergistic interactions occurred among components of the dechlorinated mixtures. These results indicate that the dioxinlike toxicities of PCB mixtures are substantially reduced by microbial reductive dechlorination, and that a constant ratio of TEq to total PCBs cannot be assumed in risk assessments.

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Abstract-Aroclors 1242 and 1254 were anaerobically dechlorinated by microorganisms eluted from polychlorinated biphenyl (PCB)-contaminated River Raisin (RR) and Silver Lake (SL) sediments. Dechlorination occurred primarily from the meta positions. H4IIE rat hepatoma cell bioassays for ethoxyresorufin-O-deethylase (EROD) induction potency, a measure of aryl hydrocarbon receptor-mediated toxic potential, revealed that the potencies of the Aroclors were considerably reduced after dechlorination. The decreases in EROD induction potencies were dependent on the extent of dechlorination of the non-ortho-substituted and monoortho-substituted PCBs. Calculated 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalents (TEqs calc ) for the PCB mixtures were 5.7, 0.08, and 0.05 pM TEq calc /mole of PCBs for non-, RR-, and SL-dechlorinated Aroclor 1242, and 7.8, 1.6, and 1.0 pM TEq calc / mole of PCBs for non-, RR-, and SL-dechlorinated Aroclor 1254, respectively. Correspondence between TEqs assay determined using the H4IIE bioassay and TEqs calc indicated that no unexpected synergistic interactions occurred among components of the dechlorinated mixtures. These results indicate that the dioxinlike toxicities of PCB mixtures are substantially reduced by microbial reductive dechlorination, and that a constant ratio of TEq to total PCBs cannot be assumed in risk assessments.

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