Detail of "70649-54-6"

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Electrochemical investigation of the association of distamycin A with the manganese(III) complex of meso-tetrakis(N-methyl-4-pyridiniumyl)porphine and the interaction of this complex with DNA

Electrochemical investigation of the association of distamycin A with the manganese(III) complex of meso-tetrakis(N-methyl-4-pyridiniumyl)porphine and the interaction of this complex with DNA. Rodriguez, Marisol; Bard, Allen J. (Dep. Chem. Biochem., Univ. Texas, Austin, TX 78712, USA). Inorg. 70649-54-6 and 636-47-5 are cas registry numbers. These chemicals are also mentioned in this article. Chem., 31(7), 1129-35 (English) 1992. CODEN: INOCAJ. ISSN: 0020-1669. DOCUMENT TYPE: Journal CA Section: 6 (General Biochemistry) Section cross-reference(s): 72 Differential pulse voltammetry (DPV) was used to study the interaction of distamycin A (Dis) with the manganese(III) complex of meso-tetrakis(N-methyl-4-pyridiniumyl)porphine (MnIIIP) and that of this complex with calf thymus (CT) DNA. The addn. of distamycin to MnIIIP caused a diminution in the peak current and a pos. shift in the peak potential of the DPV wave for the redn. of MnIIIP. This effect on the peak current is a result of a decrease in the diffusion coeff. (D) of MnIIIP from Df = 1.2 ′ 10-6 cm2/s to Db = 7.2 (±0.2) ′ 10-8 cm2/s. An amperometric titrn. was used to show that two distamycins bind to one MnIIIP with an overall binding const. of K = 5 (±3) t 108 M-2, assuming a static equil. model, probably by axial coordination of the oxygen atom of the formyl end of Dis to Mn(III). The 23-mV pos. shift in the DPV peak potential of MnIIIP indicates that distamycin binds 2.5 times more strongly to MnIIP than to MnIIIP. The MnIIIP(Dis)2 complex interacts with sonicated CT DNA; DPV and amperometric titrn. were also used to investigate this interaction. .

The potential role of peroxynitrite in the vascular contractile and cellular energetic failure in endotoxic shock

The potential role of peroxynitrite in the vascular contractile and cellular energetic failure in endotoxic shock. Zingarelli, Basilia; Day, Brian J.; Crapo, James D.; Salzman, Andrew L.; Szabo, Csaba (Division of Critical Care, Children's Hospital Medical Center, Cincinnati, OH 45229, USA). British Journal of Pharmacology, 120(2), 259-267 (English) 1997 Stockton. CODEN: BJPCBM. ISSN: 0007-1188. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Here we have investigated the relative potency of Mn(III)tetrakis(4-benzoic acid) porphyrin (MnTBAP) and a range of related compds. in terms of inhibition of peroxynitrite-induced oxidn. and cytotoxicity. In addn., we tested the effects of MnTBAP on the vascular and the cellular energetic failure in rodent models of endotoxic shock. We obsd.In this article, certain chemicals are used. Some of their cas registry numbers are 14797-65-0 and 70649-54-6 a dose-related inhibition of the peroxynitrite-induced oxidn. of dihydrorhodamine 123 to rhodamine by MnTBAP, ZnTBAP and FeTBAP, but not by MnTMPyP [(5,10,15,20-tetrakis(N-methyl-4'-pyridyl)porphinato)-manganese (III)]. In addn., MnTBAP, ZnTBAP and FeTBAP, but not MnTMPyP prevented the suppression of mitochondrial respiration by authentic peroxynitrite in cultured J774 macrophages. In rat cultured aortic smooth muscle cells, MnTBAP protected against the suppression of mitochondrial respiration in response to authentic peroxynitrite, immunostimulation and nitric oxide (NO) donor compds. MnTBAP slightly reduced the amt. of nitrite/nitrate produced in response to immunostimulation in these cells. Administration of MnTBAP, 15 mg kg-1 i.v., before the administration of endotoxin (15 mg kg-1, i.v.) to rats ameliorated the development of vascular hyporeactivity and the development of endothelial dysfunction in the thoracic aorta ex vivo. MnTBAP also prevented the endotoxin-induced decrease in mitochondrial respiration, the development of DNA single strand breaks, and the depletion of intracellular NAD+ in peritoneal macrophages ex vivo. MnTBAP did not inhibit the expression by endotoxin of the inducible NO synthase in lung samples. MnTBAP did not alter survival rate in mice challenged with high dose endotoxin. Our findings, taken together with previous data demonstrating protective effects of NO synthase inhibitors against the endotoxin-induced contractile and energetic failure in the models of shock used in the current study, and with the known ability of peroxynitrite to cause cellular energy depletion, suggest a role for peroxynitrite in the pathogenesis of cellular energetic failure and contractile dysfunction in endotoxin shock. .