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Science 21 October 1966:
Vol. 154. no. 3747, pp. 404 - 407
DOI: 10.1126/science.154.3747.404
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Articles

Dealkylation and Loss of Capacity for Reactivation of Cholinesterase Inhibited by Sarin

Larrel W. Harris 1, Joseph H. Fleisher 1, James Clark 1, and William J. Cliff 1

1 Biochemistry Branch, Medical Research Laboratory, U.S. Army Edgewood Arsenal, Maryland 21010

Inhibition of rat brain acetylcholinesterase by 32P-sarin in vivo results initially in 32P-isopropylmethylphosphonylated enzyme. The percentage of inhibited enzyme that could not be reactivated by pyridinium aldoxime methochloride (aged enzyme) approximated the amount of radioactivity identified as 32P-methylphosphonate. The 32P-isopropyl methylphosphonate not released fromthe inhibited enzyme by the oxime accounted for 51 ± 10 percent ( standard deviation) of the radioactivity fixed to brain tissue. It showed no correlation with aging and was probably bound to sites other than acetylcholinesterase.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Aging Pathways for Organophosphate-Inhibited Human Butyrylcholinesterase, Including Novel Pathways for Isomalathion, Resolved by Mass Spectrometry.
H. Li, L. M. Schopfer, F. Nachon, M.-T. Froment, P. Masson, and O. Lockridge (2007)
Toxicol. Sci. 100, 136-145
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Crystal Structure of Human Butyrylcholinesterase and of Its Complexes with Substrate and Products.
Y. Nicolet, O. Lockridge, P. Masson, J. C. Fontecilla-Camps, and F. Nachon (2003)
J. Biol. Chem. 278, 41141-41147
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Reactive Immunization.
P. Wirsching, J. A. Ashley, C.-H. L. Lo, K. D. Janda, and R. A. Lerner (1995)
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Science. ISSN 0036-8075 (print), 1095-9203 (online)