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Clue to cigarettes' role in emphysema.

Though the link between cigarette smoking and emphysema seems firmly established, researchers are still puzzling over the precise chemical role of tobacco smoke in the destruction of lung tissue. Chemists at Louisiana State University in Baton Rouge have teased out a new clue: a biologically aggressive role for a chemical produced by interactions between relatively nontoxic chemicals in smoke and in the lung.

The body is peppered with proteases, valuable enzymes that foster the breakdown of proteins. Within the lung, however, these enzymes must be held in check to avoid the risk that they will begin a wholesale chopping up of structural tissue -- a process that can lead to emphysema. Nature has seeded the lung with antiproteases to inhibit these enzymes. Suppression of the antiproteases is the most widely accepted explanation for how smoking leads to emphysema. The remaining question has been how smoke shuts down antiproteases.

Juan J. Moreno and William A. Pryor now describe evidence indicating that peroxynitrite (O = NOO-) is one of the agents responsible. Many biochemists had suspected that the antiproteases' nemesis was a potent, biologically damaging free radical, such as hydroxyl (HO.) -- and that peroxynitrite production constituted one step along the path to creation of the radical. But in the May/June CHEMICAL RESEARCH IN TOXICOLOGY, Moreno and Pryor show that peroxynitrite can by itself inactive the most abundant lung antiprotease, alpha-1PI.

Peroxynitrite forms during reactions between two free radicals: nitric oxide (NO) in smoke and the superoxide (O2-) produced in the lung. "Though neither of the parent compounds are powerful oxidants," Pryor notes, "together they form a potent oxidant." Indeed, their offspring appears to inactivate the lung-protecting alpha-1PI by donating an oxygen atom to methionine, one of its amino-acid building blocks.
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Title Annotation:reaction of lungs to tobacco smoke
Publication:Science News
Article Type:Brief Article
Date:Jun 13, 1992
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