Aflatoxin G1-13C17is intended for use as an internal standard for the quantification of aflatoxin G1by GC- or LC-MS. Aflatoxin G1is a mycotoxin that has been found inA. terricola.1In vivo, aflatoxin G1is lethal to ducklings (LD50= 1.18 mg kg).2It induces hepatocellular carcinoma tumor formation and lethality in rats when administered at doses of 1.4 and 3 mg animal, respectively. Aflatoxin G1also inhibits liver and kidney succinate dehydrogenase and fumarase, as well as kidney cytochrome oxidase, NADH oxidase, α-glycerophosphate dehydrogenase, isocitrate dehydrogenase, and malate dehydrogenase in rats.3 1.Moubasher, A.H., el-Kady, I.A., and Shoriet, A.Toxigenic Aspergilli isolated from different sources in EgyptAnn. Nutr. Aliment.31(4-6)607-615(1977) 2.Wogan, G.N., Edwards, G.S., and Newberne, P.M.Structure-activity relationships in toxicity and carcinogenicity of aflatoxins and analogsCancer Res.31(12)1936-1942(1971) 3.Bai, N.J., Pai, M.R., and Venkitasubramanian, T.A.Mitochondrial function in aflatoxin toxicityIndian J. Biochem. Biophys.14(4)347-349(1977)
N-Desbutyl dronedarone is an active metabolite of the antiarrhythmic agent dronedarone .1,2,3It is formed from dronedarone by cytochrome P450s (CYPs) and monoamine oxidase (MAO) in human hepatocyte preparations.4N-Desbutyl dronedarone inhibits the binding of 3,3’,5-triiodo-L-thyronine to the thyroid hormone receptors TRα1and TRβ1(IC50s = 59 and 280 μM for the chicken and human receptors, respectively).1It inhibits CYP2J2-mediated formation of 14,15-EET from arachidonic acid and soluble epoxide hydrolase-mediated formation of 14,15-DHET from 14,15-EET (IC50s = 1.59 and 2.73 μM, respectively, in cell-free assays).2N-Desbutyl dronedarone decreases intracellular ATP levels in H9c2 rat cardiomyocytes (IC50= 1.07 μM) and inhibits mitochondrial complex I, also known as NADHdehydrogenase, and mitochondrial complex II, also known as succinate dehydrogenase, activities in isolated rat heart mitochondria (IC50s = 11.94 and 24.54 μM, respectively).3 1.Van Beeren, H.C., Jong, W.M.C., Kaptein, E., et al.Dronerarone acts as a selective inhibitor of 3,5,3’-triiodothyronine binding to thyroid hormone receptor-α1: in vitro and in vivo evidenceEndocrinology144(2)552-558(2003) 2.Karkhanis, A., Tram, N.D.T., and Chan, E.C.Y.Effects of dronedarone, amiodarone and their active metabolites on sequential metabolism of arachidonic acid to epoxyeicosatrienoic and dihydroxyeicosatrienoic acidsBiochem. Pharmacol.146188-198(2017) 3.Karkhanis, A., Leow, J.W.H., Hagen, T., et al.Dronedarone-induced cardiac mitochondrial dysfunction and its mitigation by epoxyeicosatrienoic acidsToxicol. Sci.163(1)79-91(2018) 4.Klieber, S., Arabeyre-Fabre, C., Moliner, P., et al.Identification of metabolic pathways and enzyme systems involved in the in vitro human hepatic metabolism of dronedarone, a potent new oral antiarrhythmic drugPharmacol. Res. Perspec.2(3)e00044(2014)
sn-Glycerol 3-phosphate lithium is synthesized via the cytosolic glycerol 3-phosphate dehydrogenase pathway. This process involves the conversion of dihydroxyacetone phosphate to sn-Glycerol 3-phosphate using NADH, which is generated during glycolysis.
(R)-(-)-1,2-Propanediol is the (R)-enantiomer of 1,2-Propanediol, which is derived from glucose through the expression of NADH-linked glycerol dehydrogenase genes in Escherichia coli.
CBR-6672, a type II NADHdehydrogenase inhibitor, demonstrates potent antimycobacterial activity against mycobacterium tuberculosis (Mtb) with a minimum inhibitory concentration (MIC) of 0.14 μM [1].