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Biomedical subjects

I Chanarin

Publications and source records attributed to I Chanarin.

At least 73 records · Page 4Linked to original sources
PubMed1982

Changes in the mean corpuscular red cell volume in women with beta-thalassaemia trait during pregnancy.

Thirty-eight women with beta-thalassaemia trait and thirty-five normal Asian women were studied retrospectively during normal pregnancies. The red cell size increased in both groups, with a mean increase of 2.3 fl (SD 2.3) in the women with beta-thalassaemia trait and a significantly higher increase of 4.3 fl (SD 2.1) in the normal Asian women. The rise in red cell size during pregnancy which is a physiological change, is thus impaired by defective globin-chain synthesis as well as by iron deficiency.

Erythrocyte Count↗
PubMed1982

Demonstration of vitamin B12 analogues in human sera not detected by microbiological assay.

Sera were absorbed with polyacrylamide beads to which purified human intrinsic factor was attached. This procedure removed the vitamin B12 analogues which are measured by microbiological assay with Lactobacillus leichmannii and Euglena gracilis and which are measured in an isotope dilution method using intrinsic factor. Such sera still contained B12 analogues that were assayed in an isotope dilution method using a non-intrinsic factor vitamin B12 binder. Such vitamin B12 analogues make up approximately half of the total vitamin B12 analogues in human serum.

Biological Assay↗
PubMed1982

A comparison of tetrahydrofolate and 5-formyltetrahydrofolate in correcting the impairment of thymidine synthesis in pernicious anaemia.

5-formyltetrahydrofolate and tetrahydrofolate were added to marrow cells from patients with untreated pernicious anaemia at 1, 5 and 50 nmol doses in the deoxyuridine suppression test. At all 3 dose levels formyltetrahydrofolate was significantly more effective in correcting the defect of thymidine synthesis in pernicious anaemia, than tetrahydrofolate. The data suggest that formylation of tetrahydrofolate is necessary for its normal utilization.

Anemia, Pernicious↗
PubMed1982

The effects of nitrous oxide on cobalamins, folates, and on related events.

The anaesthetic gas nitrous oxide (N2O), when inhaled for longer than 6 hr, produces megaloblastic anemia in man. Longer term inhalation, as in addicts, produces a syndrome similar to that due to B12 neuropathy, and long term exposure to low concentrations results in an increased abortion rate and neuropathy, particularly in dental personnel. N2O acts by oxidizing vitamin B12 from the active reduced cob[I]alamin form to the inactive cob[III]alamin form. In turn, this inactivates the enzyme methionine synthetase which requires both B12 and folate as cofactors. In the rat, hepatic methionine synthetase is completely inactivated after 3 hr exposure to a mixture of equal parts of N2O/O2. There is an impared uptake of folate analogues by the liver so that the plasma folate level rises and thereafter there is a considerable loss of folate into the urine. Hepatic folate concentration falls to 25% within 10 days of N2O exposure. There is a failure to synthesize folate polyglutamate (the active folate coenzyme) from all other than formyltetrahydrofolate. As oxidization of the methyl of methionine is an important source of formyl, the failure of methionine synthesis in turn appears to lead to the failure in supply of formate and, hence, a lack of the formylfolate substrate.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1982

Urinary folate loss following inactivation of vitamin B12 by nitrous oxide in rats.

Rats were injected with [2-14C]H4PteGlu daily for 3 d and thereafter one group left in air and a second group in an atmosphere of nitrous oxide/oxygen (1/1). Nitrous oxide inactivates cobalamin. The N2O-treated rats excreted large amounts of L. casei-active folate into the urine. The urinary folate co-chromatographed with authentic 3H-labelled 5-methyltetrahydrofolate. Both groups of animals excreted 14C-labelled breakdown products in the urine but there was no evidence of increased folate catabolism in the N2O-treated rats. It was concluded that the folate deficiency that develops in the N2O-treated rat is due to massive urinary loss of folate. This appears to be secondary to impaired cellular uptake of folate which leads to a raised plasma folate level.

Animals↗
PubMed1981

Changes in tissue folates accompanying nitrous oxide-induced inactivation of vitamin B12 in the rat.

The anesthetic gas, nitrous oxide, oxidizes cob(I)alamin and thus inactivates methionine synthetase which requires cobalamin as a coenzyme. The effect on folates in liver, kidney, marrow, plasma, and brain in rats breathing a 1/1 nitrous oxide/oxygen mixture is described. There is loss of folate from tissues, most marked in liver, that affects folate polyglutamates to a greater extent than folate monoglutamates. Both methyl- and nonmethyl-analogues are affected. There is a transient rise in the levels of 5-methyltetrahydropteroylpolyglutamate in all tissues 8 h after starting nitrous oxide, which falls thereafter. In marrow and brain there is also a transient rise in methyltetrahydropteroylmonoglutamate. Plasma folate increased markedly throughout the period of exposure to nitrous oxide. It is suggested that these changes are due to the action of nitrous oxide in depressing tissue uptake of folate from plasma, in promoting loss of folate into urine and in inhibiting folate polyglutamate synthesis.

Animals↗
PubMed1981

Recovery of tissue folates after inactivation of cobalamin by nitrous oxide. The significance of dietary folate.

The anesthetic gas, nitrous oxide (N2O), oxidizes the cobalt moiety in the vitamin B12 molecule and in this way inactivates methionine synthetase which requires reduced cobalamin. In rats this is followed by a disappearance of folates from the tissues, this loss being most marked in the liver. Returning the animals to a normal atmosphere leads to restoration of most of the pre-N2O folate levels within 5 days. The plasma folate, which rises on exposure to N2O, falls within several hours. The restoration of tissue folates does not take place if the rats are placed on a low folate diet after withdrawal from an N2O environment. Thus the fall in tissue folate levels is due to loss from the body either by excretion or increased catabolism and not to redistribution of folate. Return of normal folate levels requires a dietary source of folate.

Animals↗
PubMed1981

Erythroid colony growth in vitro from human peripheral blood null cells: evidence for regulation by T-lymphocytes and monocytes.

Colony assays in methylcellulose of primitive erythroid precursors (BFU-E) were carried out from the null cell fraction of normal human peripheral blood lymphoid cells. There was little proliferation or maturation of BFU-E as assessed by both the number and the size of colonies formed, when null cells alone were cultured. Culture of null cells with up to 8 X 10(5) autologous T-lymphocytes per ml led to considerable stimulation of colony growth and maturation. Culture of null cells with peripheral blood monocytes also resulted in the indication of BFU-E growth, although the response was inferior to the seen with T-cells. Co-culture of null cells together with both T-cells and monocytes resulted in a uniformly greater response than with either alone, and this was shown to be due to a positive interaction between these two cell types.

Cell Division↗
PubMed1981

Megaloblastic change is a feature of colonies derived from an early erythroid progenitor (BFU-E) stimulated by monocytes in culture.

The morphology of stained preparations of cells from human bone marrow and peripheral blood erythroid colonies cultured in methylcellulose, were examined by light microscopy. Although the morphology of 7 d erythroid colonies (CFU-E) was largely normoblastic, bone marrow and peripheral blood erythroid burst (BFU-E) showed a variable degree of megaloblastic and culture system and the deoxyuridine suppression test demonstrated active thymidine synthesis. Megaloblastic morphology was correlated with the growth induced by the addition of monocytes to erythroid progenitors. It was concluded that megaloblastosis was a feature of the erythroblasts derived from an early BFU-E which required monocytes for their development.

Bone Marrow Cells↗
PubMed1981

The effect of nitrous oxide-induced inactivation of cobalamin on plasma amino acid levels in the rat.

Rats were maintained in an atmosphere of equal volumes of oxygen/nitrous oxide (1/1) for up to 7 d and plasma levels of methionine, glycine, serine, histidine, homocysteine and S-methylcysteine were measured. There was a fall in plasma methionine and a rise in plasma serine levels. There were no significant changes in glycine and histidine levels. Homocysteine and S-methylcysteine were not detected in rat plasmas. The fall in plasma methionine was due to loss of cobalamin-dependent methionine synthetase activity. The rise in plasma serine may be due to decline in its metabolism via methenyltetrahydrofolate cyclohydrolase which is concerned in oxidizing the methenyl-carbon ( =CH-), initially derived as a methylene-carbon (-CH2-)from serine, to formate (-CHO).

Amino Acids↗
PubMed1981

Changes in plasma folate levels in rats inhaling nitrous oxide.

Inhalation of nitrous oxide, which inactivates vitamin B12, is followed by a rise in the plasma folate level. The concentration of plasma folate remains elevated throughout the period of exposure to nitrous oxide. Returning the rats to the air is followed by a fall to pre-exposure plasma folate levels within 24 h.

Animals↗
PubMed1981

Megaloblastic anaemia after pelvic radiotherapy for carcinoma of the cervix.

A 71-year-old woman was treated with radiotherapy for carcinoma of the cervix. Nine year later she was found at laparotomy to have a thickened narrow ileum. At the time she had an iron-deficiency anaemia and when this was treated the blood picture changed to that of a severe megaloblastic anaemia. This was due to cobalamin deficiency resulting from malabsorption of cobalamin by the damaged ileum.

Aged↗
PubMed1981

Comparison of serum vitamin B12 estimation by saturation analysis with intrinsic factor and with R-protein as binding agents.

It has been reported that serum vitamin B12 levels assayed by saturation analysis methods may give misleadingly high results, so much so that the diagnosis of vitamin B12 deficiency may be obscured. This defect was ascribed largely to assays using a vitamin B12 binder other than pure intrinsic factor. To test out this hypothesis two assays were set up, one using saliva (non-intrinsic factor R-binder) and the other using human gastric (intrinsic factor) as B12-binding agents. Both assays were able to differentiate sera from patients with pernicious anaemia from those from control subjects. Published results accumulated over the past 10 years indicate that properly designed and performed saturation analysis vitamin B12 assays are as reliable as microbiological assay methods for detecting low serum B12 levels. The failure of some methods to do does not appear to be due to the nature of the B12-binding agent.

Anemia, Pernicious↗