Cobalamin deficiency and subacute combined degeneration after nitrous oxide anesthesia: A case report Sung C. Ahn, DO, Allen W. Brown, MD Archives of Physical Medicine and Rehabilitation Volume 86, Issue 1, Pages 150-153 (January 2005) DOI: 10.1016/j.apmr.2004.01.019 Copyright © 2005 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions
Fig 1 Active cobalamin with cobalt in its reduced form (Co+). N2O inactivates cobalamin by irreversibly oxidizing cobalt to the Co++ and Co+++ forms. Archives of Physical Medicine and Rehabilitation 2005 86, 150-153DOI: (10.1016/j.apmr.2004.01.019) Copyright © 2005 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions
Fig 2 Cobalamin (B12) is converted to methylcobalamin (MB12) in the cytoplasm where it binds to methionine synthetase (MS). N2O inactivates methylcobalamin plus methionine synthetase, preventing the catalytic conversion of N5-methyltetrahydrofolate (MTHF) and homocysteine to 5-methylenetetrahydrofolate (THF) and methionine. The other cobalamin-dependent coenzyme, deoxyadenosylcobalamin (DB12), catalyzes reactions important for carbohydrate and lipid synthesis. Abbreviation: CoA, coenzyme A. (Used by permission, adapted from Flippo TS, Holder WD. Arch Surg 1993;128:1391–95, figure p. 1394. 1993 AMA). Archives of Physical Medicine and Rehabilitation 2005 86, 150-153DOI: (10.1016/j.apmr.2004.01.019) Copyright © 2005 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions