Nerve
gases permanently inactivate AChE, so acetylcholine increases to toxic levels.
(Graphic illustrates general trends, not data.) |
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The original nerve gases, tabun, soman and sarin, were developed in Germany between
1936 and 1944. They were inspired by the preceding discovery of organophosphate
insecticides. (1) The two groups of chemicals share many similarities. (2)
Nerve gases
work primarily by inhibiting the normal cycling of the body's most basic neurotransmitter,
acetylcholine. As acetylcholine builds up in the nerves, muscles and brain, the
muscles become rigid and breathing becomes extremely difficult. Convulsions and
other neurological symptoms follow as the nervous system goes into a persistent
cycle of chaotic response.
Although the
public usually associates nerve gas with mass death, fatality rates in wartime
nerve gas attacks have generally been less than five per cent, largely due to
difficulties involved in delivering lethal levels of gas. The tragedy of nerve
gas is largely found in its survivors. (3)
Nerve gases
destroy the enzyme acetylcholinesterase (AChE), which normally breaks down acetylcholine
as needed. This severely depletes the body's reserves of AChE, and it takes a
long time to restore them to normal levels. Follow-up studies of the survivors
of the 1995 sarin attack in Tokyo found subnormal AChE even a year later in some
individuals. The slow recovery and recurring, persistent symptoms experienced
by Palestinian victims of the early 2001 gas attacks suggest a similar effect.
(4)(5)(6)(7)
The treatment
of acute nerve gas poisoning includes medications to alleviate symptoms and restore
AChE, such as atropine, pralidoxime, diazepam and tropicamide, with oxygen to
assist breathing. The patient should be monitored for heart, lung, and liver functioning,
given specific blood tests (eg. Ellman assay), and blood oxygen levels should
be monitored. (8)(9)
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