Our results unveiled that Cd2+ treatment led to the marked upregulation of several antioxidant enzymes (e.g., metallothionein-1G, superoxide dismutase, pyridoxal kinase, etc.), enzymes associated with glutathione biosynthesis and homeostasis (e.g., glutathione S-transferases, glutathione

synthetase, glutathione peroxidase, etc.), and proteins involved in cellular energy metabolism (e.g., glycolysis, JIB 04 pentose phosphate pathway, and the citric acid cycle). Additionally, we found that Cd2+ treatment resulted in the elevated expression of two isoforms of dimethylarginine dimethylaminohydrolase (DDAH I and II), enzymes known to play a key role in regulating nitric oxide biosynthesis. Consistent with these findings, we observed elevated formation of nitric oxide in human skin (GM00637) and lung (IMR-90) fibroblast cells following Cd2+ exposure. The upregulation of DDAH I and II suggests a role of nitric oxide synthesis in Cd2+-induced toxicity in human cells.”
“A series of tetranuclear oxo/hydroxo clusters comprised of three Fe centers and a redox-inactive metal (M) of various charge is reported. Crystallographic studies show an unprecedented Fe3M(mu(4)-O)(mu(2)-OH) core that remains intact upon changing M or the oxidation state of iron.

Electrochemical studies reveal that the reduction potentials (E-1/2) span a window of 500 mV and depend upon the Lewis acidity of M. Using the pK(a) of the M-aqua complex as a measure JQEZ5 price of Lewis acidity, these compounds display a linear dependence between E-1/2 and acidity, with a slope of similar to 70 mV per pK(a) unit. The current study of [Fe3MO(OH)] and previous ones of [Mn3MOn] (n = 2,4) moieties support the generality of the above relationship between the reduction potentials of heterometallic oxido clusters and Dinaciclib supplier the Lewis acidity of incorporated cations, as applied to clusters

of different redox-active metals.”
“We have previously isolated a cDNA clone coding for Xenopus AP-2rep (activator protein-2 repressor), a member of the Kruppel-like factor family, and reported its expression pattern in developing Xenopus embryos. In the present study, the physiological function of AP-2rep in the morphogenetic movements of the dorsal mesoderm and ectoderm was investigated. Embryos injected with either AP-2rep or VP16repC (a dominant-negative mutant) into the dorsal marginal zone at the 4-cell stage exhibited abnormal morphology in dorsal structures. Both AP-2rep and VP16repC also inhibited the elongation of animal cap explants treated with activin without affecting the expression of differentiation markers. Whole-mount in situ hybridization analysis revealed that expression of brachyury and Wnt11 was greatly suppressed by injection of VP16repC or AP-2rep morpholino, but expression was restored by the simultaneous injection of wild-type AP-2rep RNA.