The Experts below are selected from a list of 33 Experts worldwide ranked by ideXlab platform

Donald D Koblin - One of the best experts on this subject based on the ideXlab platform.

  • aging chronic administration of ethanol and acute exposure to nitrous oxide effects on vitamin b12 and folate status in rats
    Mechanisms of Ageing and Development, 1992
    Co-Authors: Barbara W Everman, Donald D Koblin
    Abstract:

    Abstract Elderly patients with alcoholism often require surgery and receive nitrous oxide (N 2 O) as a component of their anesthetic. Since aging, ethanol, and N 2 O may all perturb folate and/or vitamin B 12 metabolism, we examined the combined influence of these parameters on vitamin B 12 /folate status in a rodent model. Aged male Fischer 344 rats (24 months old) were given a liquid ethanol diet (35% of calories as ethanol) and control rats were pair-fed a liquid diet with carbohydrate substituting for the caloric content of ethanol. After receiving liquid diets for 7 weeks, rats were exposed to 60% N 2 O/40% O 2 for 6 h. Urinary excretion of formic Acid, Formiminoglutamic Acid (FIGLU), and methylmalonic Acid (MMA) were used as indirect markers of folate/vitamin B 12 status. In both the aged ethanol-fed and control groups, excretion of formic Acid and FIGLU markedly increased the first day after N 2 O exposure and returned towards background values by the second day. No changes occurred in MMA excretion. Exposure to N 2 O decreased methionine synthase activities in liver, kidney and brain, and recovery of methionine synthase activities occurred over a period of 4 days in both the aged ethanol-fed and control groups. Ethanol treatment for 7 weeks combined with acute exposure to N 2 O did not deplete the aged rats of folate or vitamin B 12 in blood, liver, kidney or brain. Thus, in this animal model, aging, chronic ethanol administration, and acute N 2 O exposure did not act synergistically to produce prolonged and severe disturbances in folate and vitamin B 12 metabolism.

A A Spence - One of the best experts on this subject based on the ideXlab platform.

  • nitrous oxide and Formiminoglutamic Acid excretion in surgical patients and anaesthetists
    BJA: British Journal of Anaesthesia, 1991
    Co-Authors: P J Armstrong, P W H Rae, W M Gray, A A Spence
    Abstract:

    We have investigated the possible toxicity of nitrous oxide on vitamin B 12 and its sequelae upon folic Acid metabolism using the urine form-iminoglutamic Acid excretion test, an index of the functional state of folate metabolism. Ten control subjects not exposed to nitrous oxide and five patients receiving limb surgery under local anaesthesia excreted normal amounts of form-iminoglutamic Acid in urine for 6 days. Fifty patients received nitrous oxide anaesthesia for similar surgery and, of these, 22 had a dose-dependent increase in excretion on the first 2 days after operation. There were large individual variations. Exposure to 70% nitrous oxide appeared to cause abnormal metabolism of folate when exposure was greater than 90 min. Ten anaesthetists demonstrated normal excretion of Formiminoglutamic Acid; their exposure to nitrous oxide was typical of that in other studies of theatre environmental pollution.

I Chanarin - One of the best experts on this subject based on the ideXlab platform.

  • increased urinary excretion of Formiminoglutamic Acid in nitrous oxide treated rats and its reduction by methionine
    FEBS Journal, 2005
    Co-Authors: Rosemary Deacon, Janet Perry, M J Lumb, I Chanarin
    Abstract:

    Inhalation of nitrous oxide oxidises cob(I)alamin and inactivates methionine synthetase of which cobalamin is a co-enzyme. The biochemical changes in the rat following exposure to nitrous oxide resemble in some detail the changes present in patients with untreated pernicious anemia due to deficiency of cobalamin. There is a marked increase in the excretion of Formiminoglutamic Acid in the urine following exposure to nitrous oxide. A significant decrease is produced, while on N2O, by giving methionine. The explanation for these findings is discussed in the light of recent data on the effects of cobalamin inactivation.

P J Armstrong - One of the best experts on this subject based on the ideXlab platform.

  • nitrous oxide and Formiminoglutamic Acid excretion in surgical patients and anaesthetists
    BJA: British Journal of Anaesthesia, 1991
    Co-Authors: P J Armstrong, P W H Rae, W M Gray, A A Spence
    Abstract:

    We have investigated the possible toxicity of nitrous oxide on vitamin B 12 and its sequelae upon folic Acid metabolism using the urine form-iminoglutamic Acid excretion test, an index of the functional state of folate metabolism. Ten control subjects not exposed to nitrous oxide and five patients receiving limb surgery under local anaesthesia excreted normal amounts of form-iminoglutamic Acid in urine for 6 days. Fifty patients received nitrous oxide anaesthesia for similar surgery and, of these, 22 had a dose-dependent increase in excretion on the first 2 days after operation. There were large individual variations. Exposure to 70% nitrous oxide appeared to cause abnormal metabolism of folate when exposure was greater than 90 min. Ten anaesthetists demonstrated normal excretion of Formiminoglutamic Acid; their exposure to nitrous oxide was typical of that in other studies of theatre environmental pollution.

Rosemary Deacon - One of the best experts on this subject based on the ideXlab platform.

  • increased urinary excretion of Formiminoglutamic Acid in nitrous oxide treated rats and its reduction by methionine
    FEBS Journal, 2005
    Co-Authors: Rosemary Deacon, Janet Perry, M J Lumb, I Chanarin
    Abstract:

    Inhalation of nitrous oxide oxidises cob(I)alamin and inactivates methionine synthetase of which cobalamin is a co-enzyme. The biochemical changes in the rat following exposure to nitrous oxide resemble in some detail the changes present in patients with untreated pernicious anemia due to deficiency of cobalamin. There is a marked increase in the excretion of Formiminoglutamic Acid in the urine following exposure to nitrous oxide. A significant decrease is produced, while on N2O, by giving methionine. The explanation for these findings is discussed in the light of recent data on the effects of cobalamin inactivation.