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PubMed2000

Reduction of oxidative stress and cytokine-induced neutrophil chemoattractant (CINC) expression by red wine polyphenols in zinc deficiency induced intestinal damage of rat.

Consumption of red wine has been associated with health promotion and disease prevention. We have previously found that the intestine of zinc-deficient (ZD) rats develop oxidative damage associated with inflammation. Here we have used this model to investigate whether red wine polyphenols could protect against intestinal injury and, if so, whether this protection was achieved through antioxidant and anti-inflammatory activity. The intestinal alterations induced by zinc deficiency such as morphological damage, increased TBA-RS level and CuZn-superoxide dismutase activity, and decreased glutathione peroxidase activity, did not develop with the administration to ZD rats of a suspension of dealcoholated red wine (RWS). The same treatment induced in control rats a decrease of TBA-RS level but also of glutathione peroxidase and catalase activity. Treatment with RWS to ZD rats prevented a marked mucosal macrophage and neutrophil infiltration. The expression of pro-inflammatory cytokines, such as tumor necrosis factor alpha and cytokine-induced neutrophil chemoattractant (CINC), was induced by zinc deficiency, whereas that of the anti-inflammatory interleukin-10 was suppressed. Treatment with RWS reduced CINC expression. These results report a novel activity of red wine polyphenols in downregulation of intestinal CINC expression, which likely protects cells against inflammatory processes.

Animals↗
PubMed2003

Electron transfer in flavocytochrome P450 BM3: kinetics of flavin reduction and oxidation, the role of cysteine 999, and relationships with mammalian cytochrome P450 reductase.

Cys-999 is one component of a triad (Cys-999, Ser-830, and Asp-1044) located in the FAD domain of flavocytochrome P450 BM3 that is almost entirely conserved throughout the diflavin reductase family of enzymes. The role of Cys-999 has been studied by steady-state kinetics, stopped-flow spectroscopy, and potentiometry. The C999A mutants of BM3 reductase (containing both FAD and FMN cofactors) and the isolated FAD domain are substantially compromised in their capacity to reduce artificial electron acceptors in steady-state turnover with either NADPH or NADH as electron donors. Stopped-flow studies indicate that this is due primarily to a substantially slower rate of hydride transfer from nicotinamide coenzyme to FAD cofactor in the C999A enzymes. The compromised rates of hydride transfer are not attributable to altered thermodynamic properties of the flavins. A reduced enzyme-NADP(+) charge-transfer species is populated following hydride transfer in the wild-type FAD domain, consistent with the slow release of NADP(+) from the 2-electron-reduced enzyme. This intermediate does not accumulate in the C999A FAD domain or wild-type and C999A BM3 reductases, suggesting more rapid release of NADP(+) from these enzyme forms. Rapid internal electron transfer from FAD to FMN in wild-type BM3 reductase releases NADP(+) from the nicotinamide-binding site, thus preventing the inhibition of enzyme activity through the accumulation of a stable FADH(2)-NADP(+) charge-transfer complex. Hydride transfer is reversible, and the observed rate of oxidation of the 2-electron-reduced C999A BM3 reductase and FAD domain is hyperbolically dependent on NADP(+) concentration. With the wild-type BM3 reductase and FAD domain, the rate of flavin oxidation displays an unusual dependence on NADP(+) concentration, consistent with a two-site binding model in which two coenzyme molecules bind to catalytic and regulatory regions (or sites) within a bipartite coenzyme binding site. A kinetic model is proposed in which binding of coenzyme to the regulatory site hinders sterically the release of NADPH from the catalytic site. The results are discussed in the light of kinetic and structural studies on mammalian cytochrome P450 reductase.

Amino Acid Sequence↗
PubMed2004

Reduction and oxidation of hydroperoxo rhodium(III) complexes by halides and hypobromous acid.

Oxygen atom transfer from trans-L(H(2)O)RhOOH(2+) [L = [14]aneN(4) (L(1)), meso-Me(6)[14]aneN(4) (L(2)), and (NH(3))(4)] to iodide takes place according to the rate law -d[L(H(2)O)RhOOH(2+)]/dt = k(I)[L(H(2)O)RhOOH(2+)][I(-)][H(+)]. At 0.10 M ionic strength and 25 degrees C, the rate constant k(I)/M(-)(2) s(-)(1) has values of 8.8 x 10(3) [L = (NH(3))(4)], 536 (L(1)), and 530 (L(2)). The final products are LRh(H(2)O)(2)(3+) and I(2)/I(3)(-). The (NH(3))(4)(H(2)O)RhOOH(2+)/Br(-) reaction also exhibits mixed third-order kinetics with k(Br) approximately 1.8 M(-)(2) s(-)(1) at high concentrations of acid (close to 1 M) and bromide (close to 0.1 M) and an ionic strength of 1.0 M. Under these conditions, Br(2)/Br(3)(-) is produced in stoichiometric amounts. As the concentrations of acid and bromide decrease, the reaction begins to generate O(2) at the expense of Br(2), until the limit at which [H(+)] 2(NH(3))(4)(H(2)O)RhOH(2+) + O(2); i.e., the reaction has turned into the bromide-catalyzed disproportionation of coordinated hydroperoxide. In the proposed mechanism, the hydrolysis of the initially formed Br(2) produces HOBr, the active oxidant for the second equivalent of (NH(3))(4)(H(2)O)RhOOH(2+). The rate constant k(HOBr) for the HOBr/(NH(3))(4)(H(2)O)RhOOH(2+) reaction is 2.9 x 10(8) M(-)(1) s(-)(1).

Journal Article↗
PubMed2006

Binaphthalene molecules with tetrathiafulvalene units: CD spectrum modulation and new chiral molecular switches by reversible oxidation and reduction of tetrathiafulvalene units.

By combining the features of binaphthalene and tetrathiafulvalene (TTF), compounds 1-4 were designed for studies of chiral molecular switches. Absorption and CD spectral studies clearly indicate that the CD spectra resulting from axial chiral binaphthalene units can be modulated through the redox reactions of TTF units, which means new chiral molecular switches can be established on the basis of binaphthalene molecules with TTF units. The reference compound 5, which has one TTF unit rather than two as in the case of compounds 1, 3, and 4, failed to show such property, hinting that the presence of two or more TTF units is required for the realization of CD spectrum modulation. In addition, the manner of the CD spectrum modulation has been found to be dependent on the way TTF units are linked to the binaphthalene skeleton, in terms of the linker length, the positions for substitution, and the number of TTF units.

Journal Article↗
PubMed2007

Oxidative and reductive carbodiazenylation of nonactivated olefins.

Procedures for the carbodiazenylation of nonactivated olefins with a wide range of aryldiazonium salts have been developed. The azo compounds obtained can serve as valuable precursors for beta-arylamines (carboamination products), beta-amino acids, ketones, and various heterocyclic structures.

Journal Article↗
PubMed2002

Improvement of aortic wall distensibility and reduction of oxidative stress by pioglitazone in pre-diabetic stage of Otsuka Long-Evans Tokushima fatty rats.

We tested the hypothesis that pioglitazone (insulin sensitizer) reduces oxidative stress and improves aortic wall distensibility in the pre-diabetic stage of Otsuka Long-Evans Tokushima Fatty rats, type 2 diabetes mellitus (DM) model. 20 DM and 9 nonDM male rats were divided into 3 groups: treated-DM, untreated-DM, and untreated-nonDM. Pioglitazone (0.01%) was mixed in chow in the treated group from 15 to 20 weeks of age. At baseline and 20 weeks, plasma malondialdehyde (MDA) was measured. At 20 weeks, intravascular ultrasound images and aortic pressure were simultaneously recorded. Stiffness parameter beta was calculated from the cyclic variations of aortic diameter and pressure. From an excised thoracic aorta, aortic wall collagen was measured, and the morphology was histopathologically evaluated by hematoxylin-eosin staining. At 20 weeks, MDA (nmol/ml) in treated-DM (2.3 +/- 0.3) was lower than in untreated-DM (3.2 +/- 0.6, p < 0.0001). beta in treated-DM (0.53 +/- 0.21) was smaller than that in untreated-DM (0.88 +/- 0.26, p = 0.0067). Aortic wall collagen (mg/100 mg dry weight) did not decrease in treated-DM (22.3 +/- 3.2 vs untreated-DM : 19.6 +/- 4.7). Lumen/medial area ratio (L/M) increased in treated-DM (2.79 +/- 0.40 vs untreated-DM : 2.22 +/- 0.20, p = 0.0041, untreated-nonDM : 2.25 +/- 0.55, p = 0.0075). MDA was significantly correlated with beta (r = 0.65, p = 0.0005) or L/M (r = -0.60, p = 0.0008). Pioglitazone may reduce oxidative stress and contribute to improvement of aortic wall stiffness without decrease in collagen content at an early prediabetic stage of type 2 DM.

Age Factors↗
PubMed2001

Reduction of oxidative stress and AT1 receptor expression by the selective oestrogen receptor modulator idoxifene.

1. The beneficial vasoprotective effects of oestrogens are hampered by their side effects on secondary sexual organs. Selective oestrogen receptor modulators (SERM) such as idoxifene may exert beneficial vascular effects without influencing cancerogenesis in breast or uterus. 2. In order to investigate vascular effects of selective oestrogen receptor modulators, we examined the impact of idoxifene on production of reactive oxygen species as well as AT1 receptor expression in vascular smooth muscle cells (VSMC). 3. Idoxifene caused a concentration- and time-dependent down-regulation of AT1 receptor mRNA expression, as assessed by Northern analysis. The maximal effect was reached with 10 micromol l(-1) idoxifene after a 4 h incubation period (33+/-7% of control levels). Western blots showed a similar down-regulation of AT1 receptor protein to 36+/-11% of control levels. 4. Confocal laserscanning microscopy using the redox sensitive marker 2',7'-dichlorofluorescein (DCF) and measurement of NAD(P)H oxidase activity in cell homogenates revealed that idoxifene effectively blunted the angiotensin II-induced production of reactive oxygen species. 5. In order to investigate the signal transduction involved in SERM-induced modulation of AT1 receptor expression, VSMC were preincubation with PD98059, genistein, wortmannin, or N(omega)-Nitro-L-arginine. The results suggested that idoxifene caused AT1 receptor down-regulation through nitric oxide-dependent pathways. 6. In conclusion, idoxifene reduces angiotensin II-evoked oxidative stress in VSMC. This could in part be explained by idoxifene-induced down-regulation of AT1 receptor expression. These results demonstrate that the selective oestrogen receptor modulator idoxifene may exert beneficial vascular effects which could be useful for therapeutic regimen in postmenopausal women at risk for cardiovascular diseases.

Angiotensin Receptor Antagonists↗
PubMed2003

Reduction of oxidative stress augments natriuretic effect of furosemide in moderate heart failure.

BACKGROUND: The significance of antioxidant therapy in heart failure has not been fully examined. This study evaluated whether vitamin C has beneficial effects on renal function or augments the renal effects of furosemide in patients with heart failure. METHODS: There were 2 protocols. In protocol 1, plasma level of thiobarbituric acid-reactive substances (TBARS) and renal function were assessed before and after intravenous infusion of vitamin C or placebo in 8 patients with moderate congestive heart failure (CHF) treated with enalapril. In protocol 2, a randomized crossover study was performed in patients with moderate CHF treated with either an ACE inhibitor (enalapril) (n = 10) or an angiotensin II receptor antagonist (losartan) (n = 9) and in asymptomatic patients with impaired left ventricular function treated with enalapril (n = 8). TBARS and renal function were assessed before and after intravenous infusion of furosemide alone, coinfusion of furosemide with placebo and vitamin C, or coinfusion of furosemide with vitamin C and a kallikrein inhibitor (nafamostat mesilate). RESULTS: In protocol 1, although vitamin C reduced TBARS, it did not affect renal function. In protocol 2, TBARS was higher in patients with moderate CHF than in asymptomatic patients. Vitamin C augmented natriuretic effect of furosemide (from 179 +/- 98 to 192 +/- 104 micromol/min, P <.01) only in patients with moderate CHF treated with enalapril but not in the other 2 groups. Nafamostat mesilate prevented this augmentation. CONCLUSIONS: In patients with CHF treated with enalapril, counteraction of the increased oxidative stress by vitamin C may contribute to the augmented natriuretic effect of furosemide through the renal kinin-nitric oxide pathway.

Angiotensin-Converting Enzyme Inhibitors↗