Cobalamin and folate: recent developments.
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Anemia, Megaloblastic↗
Biomedical subjects
M Lumb
Publications and source records attributed to M Lumb.
Methylthioadenosine serves as a single carbon source to the folate co-enzyme pool in rat bone marrow cells.
[ribose-U-14C]Methylthioadenosine (MTA) was prepared by incubating methionine with [14C-U]ATP in the presence of methionine adenosyltransferase and the resulting S-adenosylmethionine was heated to release MTA. Labelled [14C]MTA, when incubated with rat bone marrow cells, yielded [14C]formate which was used in the synthesis of adenine and guanine. Unlike 14C from sodium, formate, serine and glycine, there was no decline in 14C utilization from MTA with bone marrow cells from rats in which cobalamin had been inactivated by exposure to nitrous oxide. It was concluded that methionine via MTA is a significant contributor of single-carbon units at the formate level of oxidation and that this pathway is maintained in cobalamin 'deficiency'.
Adenine↗
Linking and integrating computers for maternity care.
Functionally separate computer systems have been developed for many different areas relevant to maternity care, e.g. maternity data collection, pathology and imaging reports, staff rostering, personnel, accounting, audit, primary care etc. Using land lines, modems and network gateways, many such quite distinct computer programs or databases can be made accessible from a single terminal. If computer systems are to attain their full potential for the improvement of the maternity care, there will be a need not only for terminal emulation but also for more complex integration. Major obstacles must be overcome before such integration is widely achieved. Technical and conceptual progress towards overcoming these problems is discussed, with particular reference to the OSI (open systems interconnection) initiative, to the Read clinical classification and to the MUMMIES CBS (Common Basic Specification) Maternity Care Project. The issue of confidentiality is also briefly explored.
Confidentiality↗
Methylation of DNA in megaloblastic anaemia.
Methylation of cytosine residues in DNA samples, collected before and serially after cobalamin treatment from patients with cobalamin deficiency, was studied using restriction endonucleases Hpa II and Msp I and an epsilon globin gene probe. There was no evidence of hypomethylation in any of the samples. It was concluded that although hypomethylation of metabolites such as choline occurs, that of DNA is preserved in megaloblastic anaemia.
Anemia, Macrocytic↗
The substrate for folate polyglutamate biosynthesis in the vitamin B12-inactivated rat.
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Animals↗
Characterization of endogenous folate and incorporation of labelled folates into the brain of the South African fruit bat.
Folate in the brain of the South African fruit bat consists of 10-formyltetrahydropteroyglutamic acid and the tri-, tetra- and penta- forms of 5-methyltetrahydropteroylglutamic acid. Following parenteral injection, only 5-[3H]-methyltetrahydropteroylglutamic acid was taken up by the brain, but none of a dose of 14C-labelled tetrahydropteroylglutamic acid was detectable. Only trace smounts of the 5-methyltetrahydropteroylglutamic acid were converted into the formyl compounds and a small amount of methyltetrahydropteroyltriglutamic acid appeared after 96 h. There was no significant difference in vitamin B-12-deficient animals.
Animals↗
Selective inactivation of vitamin B12 in rats by nitrous oxide.
Exposure of rats to nitrous oxide rapidly inactivated the cytosol enzyme, methionine synthetase, but the mitochondrial enzyme, methylmalonyl CoA mutase, seemed to be unaffected, although both enzymes require vitamin B12.
5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
Role of vitamin B12 in folate coenzyme synthesis.
Normal red cells in man were found to contain predominantly folate pentaglutamates with smaller amounts of tetra- and hexapolyglutamates. There was no change in the type of polyglutamate present in red cells from patients with vitamin B12 deficiency and primary folate deficiency. In contrast to the fall in red cell polyglutamate concentration in vitamin B12 deficiency, there was a marked fall in short-chain folates in early folate deficiency (treated non-anaemic epileptics) and a fall in both short chain and long chain polyglutamates in patients with severe folate deficiency and megaloblastic anaemia. These differences in folate distribution within cells exclude a primary failure to transport methylfolate into cells as the lesion in vitamin B12 deficiency. The failure of folate polyglutamate synthesis in ivtamin B12 deficiency arises either from a failure to provide the proper substrate for polyglutamate synthesis or to a direct requirement for vitamin B12 for polyglutamate synthesis.
Anemia, Pernicious↗