 Protection against nerve agents
An enzyme found naturally in the blood could protect soldiers against nerve agents, writes Cath O’Driscoll in Chemistry & Industry |
 An enzyme found naturally in the blood could help to protect soldiers from brain damage caused by exposure to nerve agents. In recent rat studies, scientists have found that the enzyme, known as GOT, was ‘very successful’ in protecting the animals against damaging neurological problems caused by exposure to the chemical paraoxon, commented Gadi Lipiner, ceo of the Israeli company Braintact which carried out the work. A derivative of the organophosphorus insecticide parathion, paraoxon is a useful model compound for nerve agents, such as sarin, soman and VX.
While the exact details of the study are still top secret, based on these results the firm is to begin a three-year study, funded by the US military, to look at GOT’s ability to protect against sarin damage in rats, pigs and then primates.
The enzyme’s effectiveness relies on its ability to bind to, and chemically inactivate, a chemical called glutamate, also found naturally in the blood and brain, Lipiner explains. In normal healthy individuals, glutamate’s role is to carry nerve impulses across the gaps between cells. But when brain cells are damaged or dying, either as a result of disease or injury – or by exposure to nerve agents – they release much more glutamate than normal, over-exciting and killing nearby nerve cells.
‘The influence of glutamate on the CNS is very strong,’ Lipiner said. While other effects are also responsible for the impaired cognitive abilities and coordination seen with nerve agents, glutamate is one of the main causes.
The work with nerve agents follows on from previous research to look at other types of brain injury, caused by head trauma, stroke or disease. Earlier this year, Vivian Teichberg at the Weizmann Institute of Science, together with researchers at the Beer Sheva University in Israel, showed that activation of GOT in blood was useful in mopping up toxic glutamate spills, and preventing much of the damage that occurs after such brain injury in rats.
‘If we can judge from the work on rats, it appears that most of the damage [that occurs after brain injury] is due to excess glutamate since we can entirely prevent the brain cell death after traumatic injury,’ Teichberg said.
Braintact now owns an exclusive licence to use this method, which is also the basis of the work with nerve agents. It is hoped that clinical trials in people, ‘for either stroke or traumatic brain injury’, could start some time next year.
But while the idea seems to ‘make a lot of sense, there may be problems too,’ cautioned Robert Fern, a researcher in cell physiology and pharmacology at the UK’s University of Leicester. ‘Glutamate is the major excitatory neurotransmitter of the brain needed for brain functioning, so they’ll need to be careful about side effects when they try to reduce levels.’
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