title: Metabolic pathways in Anopheles stephensi mitochondria.
abstract: No studies have been performed on the mitochondria of malaria vector mosquitoes. This information would be valuable in understanding mosquito aging and detoxification of insecticides, two parameters that have a significant impact on malaria parasite transmission in endemic regions. In the present study, we report the analyses of respiration and oxidative phosphorylation in mitochondria of cultured cells [ASE (Anopheles stephensi Mos. 43) cell line] from A. stephensi, a major vector of malaria in India, South-East Asia and parts of the Middle East. ASE cell mitochondria share many features in common with mammalian muscle mitochondria, despite the fact that these cells are of larval origin. However, two major differences with mammalian mitochondria were apparent. One, the glycerol-phosphate shuttle plays as major a role in NADH oxidation in ASE cell mitochondria as it does in insect muscle mitochondria. In contrast, mammalian white muscle mitochondria depend primarily on lactate dehydrogenase, whereas red muscle mitochondria depend on the malate-oxaloacetate shuttle. Two, ASE mitochondria were able to oxidize proline at a rate comparable with that of alpha-glycerophosphate. However, the proline pathway appeared to differ from the currently accepted pathway, in that oxoglutarate could be catabolized completely by the tricarboxylic acid cycle or via transamination, depending on the ATP need.
authors.affiliation: Department of Molecular Biosciences, School of Veterinary Medicine, University of California Davis, 1 Shields Avenue, Davis, CA 95616, USA. cgiulivi@ucdavis.edu
authors.forename: Cecilia
authors.initials: C
authors.lastname: Giulivi
authors.forename: Catherine
authors.initials: C
authors.lastname: Ross-Inta
authors.forename: Ashley A
authors.initials: AA
authors.lastname: Horton
authors.forename: Shirley
authors.initials: S
authors.lastname: Luckhart
mesh_terms: D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D000852:Anopheles / Q000166:cytology / Q000378:metabolism*; D000968:Antimycin A / Q000494:pharmacology; D050260:Carbohydrate Metabolism; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / Q000494:pharmacology; D002460:Cell Line; D019069:Cell Respiration / Q000187:drug effects; D002853:Chromatography, Liquid; D002952:Citric Acid Cycle; D018698:Glutamic Acid / Q000378:metabolism; D007303:Insect Vectors / Q000378:metabolism*; D008288:Malaria / Q000635:transmission; D008293:Malates / Q000378:metabolism; D053858:Metabolic Networks and Pathways; D008928:Mitochondria / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption; D019289:Pyruvic Acid / Q000378:metabolism; D053719:Tandem Mass Spectrometry
chemical_list: D000596:Amino Acids; D008293:Malates; D009840:Oligomycins; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; D018698:Glutamic Acid; D000968:Antimycin A; C030298:malic acid; D019289:Pyruvic Acid