[RuIII(EDTA)(H2O)]- mediated oxidation of cellular thiols by HSO5-

The [RuIII(EDTA)(H2O)]- (EDTA4-= ethylenediaminetetraacetate) complex is shown to mediate the oxidation of thiols, RSH (RSH = cysteine, glutathione, N-acetylcysteine, and penicillamine), with peroxomonosulfate ion (HSO5-). The kinetics of the catalytic oxidation process were studied using toppedflow and rapid scan spectrophotometry as a function of [RuIII(EDTA)(H2O)-], [HSO5-], and [RSH] at a constant pH (6.2). Spectral analyses and kinetic data are suggestive of a catalytic pathway in which the RSH reacts with the [RuIII(EDTA)] catalyst complex to form [RuIII(EDTA)(SR)]2- intermediate species. In a subsequent step the HSO5- ion reacts directly with the coordinated S-atom of [RuIII(EDTA)(SR)]2- yielding the disulfido species, RSSR, as a major oxidation product (as identified using HPLC and ESI-MS analyses) under the employed conditions. Based on the experimental data, a working mechanism is proposed for the [RuIII(EDTA)] catalyzed oxidation of thiols

Oxidation of captopril by hydrogen peroxide and peroxomonosulfate ion catalyzed by a ruthenium(III) complex: kinetic and mechanistic studies

The complex [RuIII(edta)(H2O)]− (edta4− = ethylenediaminetetraacetate) catalyzes the oxidation of captopril (CapSH) using primary oxidants, hydrogen peroxide (H2O2) and peroxomonosulfate (HSO5−). The kinetics of the oxidation reaction were studied as a function of both oxidant (H2O2, HSO5−) and substrate (CapSH) concentrations using stopped-flow and rapid scan stopped-flow techniques. Spectral and kinetic data are suggestive of a pathway involving rapid formation of the intermediate complex [RuIII(edta)(CapS)]2− followed by direct attack of the oxidant (H2O2 or HSO5−) at the S atom of the coordinated CapS−. ESI–MS and HPLC analysis of the reaction products showed that captopril disulfide (CapSSCap) is the major oxidation product. A probable mechanism in agreement with the spectral and kinetic data is presented

[RuIII(EDTA)(H2O)]− catalyzed oxidation of biologically important thiols by H2O2

[RuIII(EDTA)(H2O)]− (EDTA4− = ethylenediaminetetraacetate) catalyzes oxidation of biological thiols, RSH (RSH  =  cysteine, glutathione, N-acetylcysteine, penicillamine) using H2O2 as precursor oxidant. The kinetics of the oxidation process were studied spectrophotometrically as a function of [RuIII(EDTA)(H2O)]−, [H2O2], [RSH], and pH (4–8). Spectral analyses and kinetic data are suggestive of a catalytic pathway in which the RSH reacts with [RuIII(EDTA)] catalyst complex to form [RuIII((EDTA)(SR)]2− intermediate species. In the subsequent reaction step the oxidant, H2O2, reacts directly with the coordinated S of the [RuIII((EDTA)(SR)]2− intermediate leading to formation of the disulfido (RSSR) oxidation product (identified by HPLC and ESI-MS studies) of thiols (RSH). Based on the experimental results, a working mechanism involving oxo-transfer from H2O2 to the coordinated thiols is proposed for the catalytic oxidation

NaCl pretreatment alleviates salt stress by enhancement of antioxidant defense system and osmolyte accumulation in mungbean (<i style="">Vigna radiata</i> L. Wilczek)

593-600Enhancement of salt (NaCl) tolerance by pretreatment with sublethal dose (50 mM) of NaCl was investigated in V. radiata seedlings. NaCl stress caused drastic effects on roots compared to shoots. Accompanying reductions in length, number of root hairs and branches, roots became stout, brittle and brown in color. Salt stress caused gradual reduction in chlorophyll, carotenoid pigment contents and chlorophyll fluorescence intensity also. Superoxide dismutase and catechol peroxidase activities increased under stress in both roots and leaves. But catalase activity showed an increase in roots and decrease in leaves. In these seedlings, the oxidative stress has been observed under salinity stress and the level of proline, H2O2 and malondialdehyde content were increased. But pretreatment with sublethal dose of NaCl was able to overcome the adverse effects of stress imposed by NaCl to variable extents by increasing growth and photosynthetic pigments of the seedlings, modifying the activities of antioxidant enzymes, reducing malondialdehyde and H2O2 content and increasing accumulation of osmolytes like proline. Thus, mungbean plants can acclimate to lethal level of salinity by pretreatment with sublethal level of NaCl, improving their health and production under saline condition

[Ru^III(EDTA)(H₂O)]⁻ catalyzed oxidation of biologically important thiols by H₂O₂

<p>[Ru^III(EDTA)(H₂O)]⁻ (EDTA⁴⁻ = ethylenediaminetetraacetate) catalyzes the oxidation of biological thiols, RSH (RSH = cysteine, glutathione, N-acetylcysteine, penicillamine) using H₂O₂ as precursor oxidant. The kinetics of the oxidation process were studied spectrophotometrically as a function of [Ru^III(EDTA)(H₂O)]⁻, [H₂O₂], [RSH], and pH (4–8). Spectral analyses and kinetic data are suggestive of a catalytic pathway in which the RSH reacts with [Ru^III(EDTA)] catalyst complex to form [Ru^III((EDTA)(SR)]²⁻ intermediate species. In the subsequent reaction step the oxidant, H₂O₂, reacts directly with the coordinated S of the [Ru^III((EDTA)(SR)]²⁻ intermediate leading to formation of the disulfido (RSSR) oxidation product (identified by HPLC and ESI-MS studies) of thiols (RSH). Based on the experimental results, a working mechanism involving oxo-transfer from H₂O₂ to the coordinated thiols is proposed for the catalytic oxidation.</p

Ameliorative effect of apple cider vinegar and p-coumaric acid combination in Ex ovo antimicrobial and in vivo wound healing models

Background: Apple cider vinegar (ACV) is most commonly used in sweet and sour Chinese cuisine. This study aimed to overcome the side effects of raw ACV, by increasing the concentration of p-Coumaric acid (p-CA), a polyphenolic component of ACV. The combination (diluted ACV with p-CA) has also been compared with individual raw ACV and p-CA to confirm if the overall dosage of the ACV can be reduced to avoid side effects and if the combination therapy had any better effect than the individual component itself. Objective: To evaluate and compare antioxidant, antimicrobial, and wound healing effects of ACV and p-CA combination with individual components ACV and p-CA. Methods: The antimicrobial properties of the samples were assessed by determining the Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) using the broth microdilution method, and zone of inhibition (ZOI) and an ex ovo study was also done to evaluate the antimicrobial effect of the samples in live embryo. For the evaluation of the test samples excision wound was created in Swiss male albino mice weighing 25–30 g of either sex to estimate parameters like wound contraction rate, WBC and platelet count, SOD and GSH levels. Histopathological analysis of the skin was also done. Result: In DPPH and ABTS antioxidant assays, the combined sample (ACV + p-CA) had lower IC50. The combination therapy also showed the best antimicrobial potential against P. aeruginosa and B. subtilis. In this context, ex-ovo antimicrobial study results showed that diluted ACV + p-CA treated live embryo samples had the least bacterial growth after 48 h, in comparison with non-treatment group as well as individually ACV and p-CA treated samples. In vivo study depicted that the highest dose of the combination test sample had the best wound contraction rate and antioxidant marker enzymes elevation compared to diseased control proving the potency to restore the wound healing progression. Conclusion: ACV and p-CA combination can be used with daily intake as this combination can prevent microbial contamination and oxidative stress additionally can repair wounds more safely than raw ACV