Biomaterial Database

[The role of N-quinones in the regulation of glucose-6-phosphate metabolism]. 1986

V A Lider, and S N Bogdanova

In experimental (white rats, rabbits) and clinical (erythrocytes, blood plasma) studies on 29 healthy subjects and patients it has been demonstrated that primary or secondary n-quinone deficiency is accompanied by increased tissue activity of glycolysis enzymes (aldolase, PGmutase) and aerobic pentose phosphate shunt (6 GPDH). Parallel rise in the amount of glycolysis metabolites (pyruvate and lactate) in the blood and the decline in blood plasma glucose level were observed. The changes in glucose-6-phosphate metabolism are, probably, secondary and reflect tissue structure alterations in the development of K and E avitaminosis.

UI	MeSH Term	Description	Entries
D008297	Male		Males
D010084	Oxidation-Reduction	A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).	Redox,Oxidation Reduction
D010427	Pentose Phosphate Pathway	An oxidative decarboxylation process that converts GLUCOSE-6-PHOSPHATE to D-ribose-5-phosphate via 6-phosphogluconate. The pentose product is used in the biosynthesis of NUCLEIC ACIDS. The generated energy is stored in the form of NADPH. This pathway is prominent in tissues which are active in the synthesis of FATTY ACIDS and STEROIDS.	Hexose Monophosphate Shunt,Pentose Phosphate Shunt,Pentose Shunt,Pentosephosphate Pathway,Pentose-Phosphate Pathway,Pentosephosphate Shunt,Hexose Monophosphate Shunts,Pathway, Pentose Phosphate,Pathway, Pentose-Phosphate,Pathway, Pentosephosphate,Pathways, Pentose Phosphate,Pathways, Pentose-Phosphate,Pathways, Pentosephosphate,Pentose Phosphate Pathways,Pentose Phosphate Shunts,Pentose Shunts,Pentose-Phosphate Pathways,Pentosephosphate Pathways,Pentosephosphate Shunts,Shunt, Hexose Monophosphate,Shunt, Pentose,Shunt, Pentose Phosphate,Shunt, Pentosephosphate,Shunts, Hexose Monophosphate,Shunts, Pentose,Shunts, Pentose Phosphate,Shunts, Pentosephosphate
D011809	Quinones	Hydrocarbon rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.
D011817	Rabbits	A burrowing plant-eating mammal with hind limbs that are longer than its fore limbs. It belongs to the family Leporidae of the order Lagomorpha, and in contrast to hares, possesses 22 instead of 24 pairs of chromosomes.	Belgian Hare,New Zealand Rabbit,New Zealand Rabbits,New Zealand White Rabbit,Rabbit,Rabbit, Domestic,Chinchilla Rabbits,NZW Rabbits,New Zealand White Rabbits,Oryctolagus cuniculus,Chinchilla Rabbit,Domestic Rabbit,Domestic Rabbits,Hare, Belgian,NZW Rabbit,Rabbit, Chinchilla,Rabbit, NZW,Rabbit, New Zealand,Rabbits, Chinchilla,Rabbits, Domestic,Rabbits, NZW,Rabbits, New Zealand,Zealand Rabbit, New,Zealand Rabbits, New,cuniculus, Oryctolagus
D005954	Glucosephosphate Dehydrogenase		Glucose-6-Phosphate Dehydrogenase,Dehydrogenase, Glucose-6-Phosphate,Dehydrogenase, Glucosephosphate,Glucose 6 Phosphate Dehydrogenase
D005958	Glucosephosphates
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D014811	Vitamin E Deficiency	A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)	Deficiency, Vitamin E,Deficiencies, Vitamin E,Vitamin E Deficiencies