Help for stressed-out pigs - and smokers.

Help for stressed-out pigs--and smokers

One problem plaguing European hog producers far more than their American counterparts is a lethal susceptibility to stress--in their pigs, that is. Affected animals, thought to have a genetic weakness, succumb whenever they get excited -- in crowded feedlots, in transit to market, even in the throes of mating. The condition, which costs European farmers an estimated $560 million annually, can affect up to 90 percent of the pigs in West Germany and Belgium, according to zoologist Garry G. Duthie at the Rowett Research Institute in Aberdeen, Scotland. Duthie's work now indicates that these stress attacks -- characterized by a rapid heartbeat, hyperventilation, localized areas of bluishness on the skin and an ultimately fatal 1[deg.]C increase every five minutes in body temperature -- result from an unusual sensitivity to oxidative reactions.

His first clue was the seemingly promising treatment European pig farmers happened onto: dietary supplements of the premier antioxidant, vitamin E. Though the pigs he studied displayed classic symptoms of severe vitamin E deficiency, the condition developed even after they consumed normal dietary levels of the vitamin and incorporated normal levels in their tissues, Duthie found.

His new research suggests the problem is in the animals' cell membranes. In affected pigs, he reports, those membranes are more susceptible to "free radicals" -- reactive molecular fragments containing one or more unpaired electrons. These radicals can initiate damaging oxidative reactions.

Pigs receiving massive doses of vitamin E (235 international units per kilogram of food) incorporated it into blood plasma and muscle, Duthie found. However, only those with the stress-death susceptibility responded by leaking less pyruvate kinase and creatine kinase from their muscles into blood plasma. Blood levels of these enzymes--an indicator of cell-membrane leakiness -- are one gauge of tissue damage from oxidative reactions. Duthie also found lower levels of thre other key indicators of oxidative activity in vitamin-E-supplemented, stress-susceptible pigs -- plasma malonaldehyde, peroxidized red blood cells and pentane.

As a further measure of the animals' susceptibility to oxidative damage, Duthie incubated samples of red blood cells with hydrogen peroxide--a chemical that expoes the cells to oxygen radicals. The blood cells from stress-susceptible pigs showed 5.5 times more oxidation than those from stress-resistant pigs--or stress-tolerant animals fed massive vitamin E supplements.

In a related pilot study, Duthie applied the same test to gauge the oxidative potential of red blood cells from 40 men: 20 smokers -- who regularly subject their bodies to a large, oxidative burden -- and 20 age-matched nonsmokers. For two weeks before the test, each man took either 1,000 international units of vitamin E daily or a placebo pill. Blood cells from unsupplemented smokers oxidized three times more than those of nonsmokers or vitamin-E-supplemented smokers.

Duthie and his co-workers say such data hint that by reducing oxidative damage in smokers, prolonged vitamin E supplementation might "decrease the risk of developing diseases such as coronary heart disease and cancer."