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Education

Arsenic and Old Monarchs, Sugary Snacks Not for Cats, Odds and Ends

by Rachel Sheremeta Pepling
August 1, 2005 | A version of this story appeared in Volume 83, Issue 31

Arsenic and old monarchs

Rulers of the world are often remembered for their successes, defeats, or fits of insanity. King George III, ruler of England from 1760 to 1820, is remembered for all three. His reign is notable for the defeat of Napoleonic France, the loss of American colonies, and five episodes of long illness and mental derangement.

At one time, King George's moments of madness were attributed to psychiatric illness. In 1969, a review of the king's medical symptoms linked his bouts of mental instability to a hereditary metabolic disorder known as porphyria. King George suffered from porphyric symptoms such as lameness, abdominal pain, insomnia, temporary mental disturbances, and discolored urine. But the severity and late onset of the king's symptoms remained a mystery.

Now, researchers believe they've solved this mystery by pinning arsenic as the culprit. In the July 23 issue of the Lancet (2005, 366, 332), a study reveals that large concentrations of arsenic (17 ppm) were found in samples of the king's hair. Arsenic, which interferes with the synthesis of heme, can trigger porphyric episodes in genetically predisposed individuals, and likely exacerbated the severity and duration of his attacks.

But how did the king absorb the arsenic? Emetic tartar (potassium antimony tartrate) was often used to treat the king's symptoms. Arsenic and antimony often coexist in nature, and at the time, arsenic frequently contaminated antimony-based medicines, such as emetic tartar, by as much as 5%. King George was administered about 180 mg of antimony per day and received, potentially, up to 9 mg of arsenic daily. Not enough to kill him, but certainly enough for chronic poisoning.

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Credit: PHOTO BY VICTORIA GILMAN
Credit: PHOTO BY VICTORIA GILMAN

Sugary snacks not for cats

The July 25 debut issue of PLoS Genetics includes a study on cats' lack of preference for sweet compounds, including sugar and artificial sweeteners. Researchers from Monell Chemical Senses Center in Philadelphia found that cats don't produce one of the proteins that make up the sweet receptor on the tongues of other mammals. The gene responsible for producing the protein is a nonfunctional pseudogene in cats. Without the protein, the sweet receptor cannot function.

The researchers believe cats lost their sweet tooth during the evolution of a ca rnivorous diet of meat and fat. So while the sugary stuff is safe, the tuna is not.

Excluding the sweet-blindness, cats' sense of taste is still similar to all other mammals. Dogs, however, do have a functioning sweet receptor similar to humans, disposing them to a love for sugary carbohydrates. That Snickers stash may not be safe after all.

Odds and ends

A cautionary note came from Wendy Horn of Westfield, N.J., in response to the item on a skunk spray odor remover (C&EN, July 18, page 64). She used the solution with great success on her white Great Pyrenees. However, she suggests spot testing the solution on pets with dark coats because of the bleaching ability of the hydrogen peroxide. Wouldn't want to turn a black Lab blond by accident.

Also, a clarification from the July 18 issue: Researchers are modifying the feed mentioned in the item "Reeking Havoc" to result in lower levels of ammonia and hydrogen sulfide in swine manure. They are not lowering levels of the gases in the feed itself. Thanks to Dick Pfeiffer, a chemist in Ames, Iowa, for asking that we clear the air.

Patrick Flash, emeritus chemistry professor at Kent State University, Ashtabula, Ohio, is calling on the senses of humor of Newscripts readers. Flash is compiling a collection of old (1930s-70s) chemistry jokes, cartoons, and strange anecdotes for possible publication in the Journal of Chemical Education. Please send your items to pflash@kent.edu.


This week's column was written by Rachel Pepling . Please send comments and suggestions to newscripts@acs.org.

 

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