How cooked meat may inflame the heart.

Among the chronic diseases that characterize aging is inflammation and deterioration of heart tissue. This cardiomyopathy  begins gradually as a symptomless death of muscle. If the damage becomes extensive, heart failure or degeneration of the arteries carrying blood from the heart can occur.

While viral and other diseases can trigger some cardiomyopathy, the primary cause of the condition remains unknown. However, a new study suggests that a share of this chronic disease may trace to consumption of heterocyclic amines (HCAs) - carcinogens that form in cooked meat (SN: 1/8/94, p.22).

Nutritionist Cindy D. Davis of the National Cancer Institute (NCI) in Bethesda, Md. and her coworkers decided to investigate this link after collaborators at NCI observed heart damage in monkeys with HCA-induced liver cancer. To determine whether the muscle degeneration was just a by-product of the cancer, the researchers administered high doses of two mutagenic HCAs - IQ and PhIP -- to cultured cells for 2 hours and to adult male rats for 2 weeks.

Both brief experiments triggered a loss of mitochondria in heart muscle cells. Mitochondria provide cells with energy and are essential to their survival. As a result, "we observed cell death - a lot in the cell-culture studies, much less in the animals," Davis says.

"We're not seeing cardiomyopathy per se," she points out, but adverse changes that "are suggestive of what might develop into cardiomyopathy" Moreover, Davis adds, these changes appear unrelated to liver cancer.

As in cancer studies, HCAs are not toxic to heart tissue unless transformed by liver enzymes. But once activated by those enzymes, HCAs circulate through the body and bind chemically -- as adducts --to DNA in the heart, Davis and her coauthors report in the February TOXICOLOGY AND APPLIED PHARMACOLOGY.

Davis says that, although important, the heart adducts don't appear to account fully for the damage seen. For instance, she notes, "While there are higher levels of DNA adducts in heart cells exposed to PhIP than in those exposed to IQ, IQ is more toxic to heart cells."

An alternative mechanism to explain the new findings might involve the generation of free radicals - biologically damaging molecular fragments - as a consequence of exposure to HCAs, speculates NCI's Elizabeth G. Snyderwine, a coauthor of the new paper.

Because any loss of cardiac mitochondria will foster myopathy, the study's mitochondrial finding "certainly warrants scientific follow-up," observes Neal D. Epstein of the National Heart, Lung, and Blood Institute's cardiology branch in Bethesda. However, he adds, owing to the "exorbitant doses" of HCAs used here, it's too early to extrapolate these findings to humans.