Reference

Metabolism of 13C galactose by lymphoblasts from patients with galactosemia determined by NMR spectroscopy

Metabolism of 13C galactose by lymphoblasts from patients with galactosemia determined by NMR spectroscopy. Wehrli, Suzanne L.; Reynolds, Robert; Chen, Jie; Yager, Claire; Segal, Stanton (Joseph Stokes Jr. Research Institute, NMR Core Facility, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA). Molecular Genetics and Metabolism, 77(4), 296-303 (English) 2002 Elsevier Science. CODEN: MGMEFF. ISSN: 1096-7192. DOCUMENT TYPE: Journal CA Section: 14 (Mammalian Pathological Biochemistry) To assess the pathways by which galactose is metabolized by galactose-1-phosphate uridyltransferase (GALT) deficient cells, lymphoblasts from 10 galactosemic patients with defined genotypes (six Q188R homozygotes, two S153L homozygotes, and two with homozygous deletions) were incubated with 1 mM 1- or 2-13C galactose for 2.5 and 5 h. The 13C-labeled metabolites were identified and quantified using NMR and the results were compared to that obtained with cells from eight normal individuals. Cells from galactosemic patients formed two to three times the galactose-1-phosphate (Gal-1P) in normal cells, no difference being obsd. between the various genotypes. Galactitol formation was not significantly different from normal cells. No labeled galactonate was detected. Cells with the Q188R and S135L mutations formed both labeled uridine diphosphogalactose (UDPgal) and uridine diphosphoglucose (UDPglu), but to a lesser extent than normals, whereas cells with the GALT deletion did not. The pattern of 13C enrichment of the ribose carbons of adenosine monophosphate upon incubation of the normal cells with 1-13C galactose paralleled that found for incubations with 1-13C glucose, which is consistent with galactose disposition through the Leloir pathway to glucose and its subsequent metab. to ribose. Cells with the GALT deletion formed no detectable labeled ribose, whereas cells from a patient homozygous for Q188R mutation formed labeled ribose in a pattern similar to normal albeit with lower enrichment. The results suggest that there is residual GALT activity and function of the Leloir pathway in the presence of the Q188R as well as S135L mutation.

Natural insecticides from Hippocratea excelsa and Hippocratea celastroides

Natural insecticides from Hippocratea excelsa and Hippocratea celastroides. Reyes-Chilpa, Ricardo; Jimenez-Estrada, Manuel; Cristobal-Telesforo, Elizabeth; Torres-Colin, Leticia; Villavicencio, Miguel Angel; Perez-Escandon, Blanca Estela; Mercado-Gonzalez, Roberto (Instituto de Quimica, Universidad Nacional Autonoma de Mexico. Circuito Exterior, Ciudad Universitaria, Coyoacan 04510, Mex.). Economic Botany, 57(1), 54-64 (English) 2003 New York Botanical Garden Press. CODEN: ECBOA5. ISSN: 0013-0001. DOCUMENT TYPE: Journal CA Section: 11 (Plant Biochemistry) Section cross-reference(s): 5, 17 Hippocratea excelsa and Hippocratea celastroides have therapeutic and insecticide applications in Mexican traditional medicine. The toxicity of H. excelsa root cortex has been previously demonstrated against the stored grain pest Sitophilus zeamais. To identify the active compds., several exts. (petroleum ether, CH2Cl2, acetone, methanol, and water) and compds. were obtained from the roots, and tested (1% wt./wt.) with a force-feeding assay against S. zeamais. All H. excelsa exts. showed high antifeedant activity, and elicited moderate mortality. The triterpenoid pristimerin and a mixt. of sesquiterpene evoninoate alkaloids, isolated from the hexane and methanol exts., resp., strongly reduced the insect feeding capacity. Other triterpenoids (friedelin, b-sitosterol, canophyllol) isolated from the hexane ext., and the alditol galactitol obtained from the water ext., were innocuous or had insignificant activity. The org. exts. from H. celastroides only showed moderate antifeedant activity, while the water ext. was innocuous. Galactitol was also obtained from this ext.