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Biomedical subjects

M Lumb

Publications and source records attributed to M Lumb.

46 records · Page 3Linked to original sources
PubMed1980

The effect of nitrous oxide inactivation of vitamin B12 on rat hepatic folate. Implications for the methylfolate-trap hypothesis.

Rats exposed to N20 show a decrease in liver folate to about 25% of the initial value after 10 days. There is a transient increase in the amount of 5-methylterrahydropteroylpolyglutamate in the first 24 h, but thereafter the content decreases. The level of 5-methyltetrahydropterolymonoglutamate declines without any transitory increase. The transient accumulation of 5-methyltetrahydropteroylpolyglutamate is due to failure of methionine synthetase. Thereafter the decrease in the amount of methylfolate makes it improbable that trapping of methylfolate is the explanation for failure of folate metabolism in vitamin B12 deficiency.

Animals↗
PubMed1980

Marrow cells from patients with untreated pernicious anaemia cannot use tetrahydrofolate normally.

Folate analogues were added to human bone marrow cells to determine their effect on deoxyuridine utilization in the deoxyuridine suppression test. Formyltetrahydrofolates fully corrected the impairment of dU utilization in pernicious anaemia marrows but tetrahydrofolate was relatively ineffective. All these analogues were effective in megaloblastic marrows from folate deficient patients. Formyltetrahydrofolates also enhanced dU utilization by normal human marrows whereas methyltetrahydrofolate reduced its use. In terms of the methylfolate trap hypothesis, the expectation that cobalamin-deficient marrows would be able to use tetrahydrofolate normally was not realized.

Anemia, Megaloblastic↗
PubMed1980

Inactivation of methionine synthase by nitrous oxide.

Exposure of rats to a 50% N2O/oxygen mixture led to a rapid loss of methionine synthase activity in both liver and brain. This enzyme has vitamin B12 as a cofactor. There was impaired conversion of deoxyuridine to deoxythymidine by bone marrow cells and this defect followed loss of methionine synthase activity. There was no homocystinuria. Withdrawal of N2O was followed by a relatively slow recovery of methionine synthase activity over four days. The inactivation of vitamin B12 by N2O promises to be a valuable tool in the study of vitamin B12 metabolism.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1979

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↗
PubMed1978

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↗
PubMed1976

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↗