Kinetic study of flavonoid reactions with stable radicals

The antiradical activities of some flavonols (kaempferol, quercetin, robinetin, quercetagetin, and myricetin), flavones (apigenin, baicalein, and luteolin), flavanones (naringenin and dihydroquercetin), and flavanols [(+)-catechin and (-)-epicatechin] were determined by measuring the reaction kinetics with 2,2-diphenyl-1-picrylhydrazyl (DPPH) and alpha,gamma-bisdiphenylene-beta-phenylallyl (BDPA) radicals. The reactions, which follow the mixed second-order rate law, were investigated under pseudo-first-order conditions by use of a large excess of flavonoids, and their stoichiometry was determined by spectrophotometric titration. The results confirm stoichiometric factors of 1, 2, and 3 for flavonoids with one, two, and three hydroxyl groups in the B-ring, respectively, excluding kaempferol, which, despite a single OH group in the B-ring, has a factor of 2, which is explained by the 3-OH group supporting the reaction with free radicals. Structure-activity considerations indicate for the present series of flavonoids the importance of multiple OH substitutions and conjugation. The logarithms of reaction rate constants with the OH, DPPH, and BDPA radicals correlate well with the reduction potential of the flavonoids.     

Gas-phase ligation of Fe+ and Cu+ ions with some flavonoids

It was assumed that gas-phase ligation of metal monocations by flavonoids might provide some insight on the intrinsic antioxidant activity of the latter. Thus, the ligation of Fe+ and Cu+ ions by apigenin (1), luteolin (2), kaempferol (3), quercetin (4), myricetin (5), and naringenin (6) was investigated in the gas phase in a Fourier transform mass spectrometer (FTMS). Both of the metal ions, which were produced by laser desorption ionization (LDI), bind consecutively to two neutral flavonoid molecules either with or without the simultaneous loss of some part (H, CO, H2O) of the latter. The flavonoids are present in the instrument at steady concentrations. The formation of flavonoid positive ions by charge exchange is also a common observation but is accompanied, in some cases, by a loss of H, CO, or H2O fragments. The reaction paths and observed fragmentations are presented. The results are supported by DFT B3LYP calculations that indicate a preference for metal ion attack at C-ring and not at the B-ring site considered to be mainly responsible for flavonoid antioxidant activity.     

Induction of inflammatory host immune responses by organisms belonging to the genera Chlamydia/Chlamydophila

Chlamydia/Chlamydophila are a family of intracellular gram-negative bacteria that infect their hosts primarily via mucosal epithelia. Chronic disease associated with bacterial persistence, inflammation and tissue damage are common sequelae of infection with these organisms. Human epithelial cell lines respond to infection by releasing pro-inflammatory cytokines and chemokines such as interleukin (IL)-6 and IL-8, and upregulating the expression of mRNA encoding Iκ-Bα, the endogenous inhibitor of NF-κB. However, Iκ-Bα is not upregulated in response to bacterial lipopolysaccharide (LPS). The failure of epithelial cells to respond to LPS is associated with the absence of surface expression of CD14. Identification of the components of Chlamydia/Chlamydophila that can induce pro-inflammatory mediators coupled with the mechanisms by which epithelial cells detect infection and respond accordingly will advance the development of preventative strategies.     

Induction of inflammatory host immune responses by organisms belonging to the genera Chlamydia/Chlamydophila

Chlamydia/Chlamydophila are a family of intracellular gram-negative bacteria that infect their hosts primarily via mucosal epithelia. Chronic disease associated with bacterial persistence, inflammation and tissue damage are common sequelae of infection with these organisms. Human epithelial cell lines respond to infection by releasing pro-inflammatory cytokines and chemokines such as interleukin (IL)-6 and IL-8, and upregulating the expression of mRNA encoding Iκ-B, the endogenous inhibitor of NF-κB. However, Iκ-B is not upregulated in response to bacterial lipopolysaccharide (LPS). The failure of epithelial cells to respond to LPS is associated with the absence of surface expression of CD14. Identification of the components of Chlamydia/Chlamydophila that can induce pro-inflammatory mediators coupled with the mechanisms by which epithelial cells detect infection and respond accordingly will advance the development of preventative strategies.