Molecule of the Month : Cleo watched the bitter berry work and opted for the asp

John Emsley looks at atropine, the poisonous product of the deadly nightshade

Tom Wilkie
Tuesday 21 February 1995 00:02

It costs less than £5 to buy a gram of atropine - enough to poison the wife and lay a trail of spiked bottles of tonic water on the shelves of a local supermarket. So thought an Edinburgh biochemistry lecturer, Dr Paul Agutter. His plan to kill his wife, Alexandria, almost succeeded last August, but this month he was found guilty of attempted murder and jailed for 12 years.

By an amazing coincidence, one of the first bottles of his poisoned tonic ended up in the home of Dr Geoffrey Sharwood-Smith, a consultant anaesthetist who was familiar with the symptoms of atropine. His wife and son became ill after drinking it, and he informed the hospital where they had been taken that he thought they had been poisoned by atropine.

In the next few days five other local people were admitted suffering from atropine symptoms, including Mrs Agutter. Analysis of her gin and tonic proved it had more atropine than the supermarket tonics, revealing her husband's intentions: to dispose of her and marry his mistress.

Atropine is metabolised by the body, leaving only traces by the time death occurs. And it is a non-irritant toxin, so there are no inflamed internal organs for a pathologist to find.

In the US, atropine has caused deaths among teenagers who have tried to get high by drinking tea made from the leaves of an ornamental bush called angel's trumpet. This plant produces a lot of atropine, and can induce hallucinations in small doses, although too much can cause paralysis and memory loss. Sometimes it kills.

A better-known natural source of atropine is deadly nightshade (Atropa belladonna), one berry of which can kill a child - although it rarely does because its bitter taste immediately acts as a warning and a repellent. Atropine can be detected at concentrations as low as one part in 10,000.

Professor John Mann of Reading University, author of Murder, Magic and Medicine (Oxford University Press) says Cleopatra investigated belladonna when seeking the best poison for committing suicide. A slave given it died a quick but painful death. Asp venom was equally rapid, but tranquil.

In Renaissance times, belladonna became fashionable as an eye cosmetic. Women squeezed the juice of a berry into their eyes and the atropine would cause the pupil to dilate, giving them a doe-eyed look. Actresses continued to use it in this century and, until quite recently, ophthalmic surgeons used it to examine inside the eye.

Atropine is a white, odourless crystalline powder that melts at 114C, and was first isolated in 1833 by two German chemists, Geiger and Hess, from the black, shiny, cherry-sized berries of the deadly nightshade. It is still extracted from this tall bush, which is native to woodland around the Mediterranean, and cultivated in France. Deadly nightshade is rare in Britain, but not unknown.

Atropine is not very soluble in water, and doctors who administer it medically choose atropine sulphate, which is very soluble. The amounts given are tiny and typical doses are less than a milligram - an ounce is enough for 50,000 doses. Larger amounts lead to blurred vision, excitement and delirium, but to kill someone requires about a gramme.

In the body, atropine blocks acetylcholine, a molecule used to carry messages across nerve junctions. The first effect is to dry up bodily fluids - saliva, tears, mucous, sweat and urine - and this is why it is given before operations. At various times atropine has been prescribed for hay fever, colds, bedwetting and diarrhoea.

Yet while deadly, it is also an antidote for other poisons, such as the carbamate and organophosphate insecticides used in agriculture. It is also an antidote for the deadliest of chemicals, the nerve gases. This curious duality of toxin and treatment stems from the effect that atropine has on its target organs, the nerve endings. Soldiers in the 1992 Gulf war carried atropine and pralidoxime to inject themselves in the event of a nerve gas attack.

These chemicals kill by interfering with the enzyme that removes acetylcholine messengers after they have done their job. Without the enzyme's mediating action, nerve endings are stimulated unchecked, the victim goes into convulsions and spasms, and death follows within minutes. Atropine and pralidoxime restore normal nerve function: atropine immediately calms the nerve endings, while the pralidoxime releases the enzyme blocked by the nerve gas so it can begin to do its job again.

Not every living thing is adversely affected by atropine. David Hopper and Peter Trudgill of the University of Wales, Aberystwyth, are researching soil bacteria that feed off the poison, breaking the molecule down to extract its carbon and nitrogen. Their work, funded by the Government's Biotechnology Directorate, aims to find new pharmaceuticals and enzymes that might be used in automatic sensors to detect atropine-like chemicals, such as cocaine.

The writer is science writer in residence at Imperial College, London, and author of `The Consumer's Good Chemical Guide', WH Freeman, £18.99.

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