On February 13, 2017, North Korean Kim Jong-nam, half-brother of North Korean le

Question

On February 13, 2017, North Korean Kim Jong-nam, half-brother of North Korean                        leader Kim Jong-un suddenly died in Malaysia. According to the authorities he                        was murdered by poisoning with VX, a chemical agent that was found on his face.

            According to the New York Times, “The VX molecule interferes with the way                     glands and muscles function by blocking an enzyme that allows them to relax.                   That causes muscles to clench uncontrollably and, eventually, prevents a victim                   from being able to breathe. The lethal dose for VX ranges from about 10                                   milligrams via skin contact to 25 to 30 milligrams if inhaled. Early symptoms can                include pinprick pupils, runny nose, wheezing and muscle twitching. Death can                   occur anywhere from within a few minutes to hours, depending on the dose and                 the method of contact.”

            a) Which neurotransmitter system is affected by VX. If you use google to find the              answer, make sure to explain how the ‘evidence’ in the paragraph above                                    would have led you to the same conclusion, even if you weren’t stumped.              Make sure to include the words muscles, glans, pinprick pupils, and                                   muscle twitching in your answer.

            b) What would you suggest as an antidote to VX? Why would it work? What                                would the side effects of the antidote be, particularly if you mistakenly                          took it without being exposed to VX?

Explanation / Answer

VX or Venomous agent X is a synthetic chemical compound that is highly toxic. It was developed by the military for use in chemical warfare.

VX and Sarin gas (another toxic nerve agent) have a similar mode of action i.e. they are acetylcholinesterase inhibitor. They work by inhibiting the enzyme acetylcholiesterase.

Under normal conditions, on stimulation of a motor neuron, a neurotransmitter acetylcholine is released into the space between a neuron and an adjacent muscle cell. Acetylcholine, when taken up by the muscle cell stimulates muscle contraction. To avoid a continous state of muscle contration, acetylcholine is broken down by the enzyme acetylcholinesterase .

BUt when a person is exposed to VX gas, the enzyme is not functional and hence results in a build up of acetylcholine in the space between the neuron and muscle cell. This results in a continous contraction of the muscle cell leading to twitching of muscles and fatigue. Prolonged exposure results in paralysis and death by asphyxiation. One of the early signs of exposure is pinprick pupils.

One way of treating VX poisoning is by administering the antidote atrophine.

Atrophine binds to acetylcholine receptors and blockes them from binding to the neurotransmitter. Hence, the build up of acetylcholine due to VX exposure does not result in constant muscle contraction.

Side effect of atrophine include ventricular fibrillation (irregular and uncoordinated contraction of cardiac muscles of the ventricles), dizziness, nausea, blurred vision, dialated pupils and photophobia.

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