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Rackets and Radicals: Noise may cause gene damage in heart

Ben Harder

Exposure to loud, continuous sound can pepper free radicals throughout heart tissue and cause injury to cells' DNA that persists after the din subsides. This new finding from animal research adds to evidence that too much noise may be bad for the heart, but some scientists suggest that the changes may be no more than part of the body's general response to stress.

Research over the past 2 decades has suggested that in addition to causing hearing loss, excessive noise exposure contributes to high blood pressure (SN: 3/28/81, p. 198) and elevated death rates from diseases of the heart and arteries (SN: 5/7/83, p. 294). Researchers at the University of Pisa in Italy and elsewhere recently reported that noise exposure can damage cells' power-generating structures, or mitochondria.

According to Pisa geneticist Giada Frenzilli, loud sound sensed by the auditory system can trigger a surge in blood concentrations of the hormone norepinephrine, which stimulates heart cells to absorb too much calcium. That can weaken the membranes of the mitochondria and cause them to release free radicals.

To investigate whether free-radical activity induced by noise might damage DNA in cells' nuclei, Frenzilli and her colleagues blasted 10 male lab rats with white noise at 100 decibels, a volume heard in some dance clubs and loud industrial workplaces. Meanwhile, the scientists kept a similar group of rats in relative quiet.

Immediately after 12 hours of these regimens, the researchers removed heart cells from half the rats in each group. The remaining animals got another 24 hours of quiet before Frenzilli's team analyzed their cells.

Under microscopes, mitochondria from the noise-blasted rats had more broken membranes than did those from animals that had experienced quieter conditions. Mitochondria from rats given a day to recover from the din were no better off than those from the other animals exposed to loud noise.

The researchers then examined DNA in the cells' nuclei. Again, the sound-exposed animals displayed damage not suffered by the other rats and not lessened by a recovery day, the team reports in an upcoming Environmental Health Perspectives.

The persistence of the observed effects for at least a day is interesting, says Sandra L. McFadden of the State University of New York at Buffalo. Future research should determine how long the changes last, she says, since damaged DNA can often repair itself, even though cells meanwhile may be more susceptible to other threats. Studies could also test whether subsequent exposure to noise causes more damage or less, she says.

Other researchers note that shorter exposures or less earsplitting volumes might not have similar effects. They also note that the study doesn't address how sound stacks up against other sources of physiological stress.

Kevin K. Ohlemiller of the Central Institute for the Deaf in St. Louis suspects that a general stress response to the deafening noise, rather than any quality unique to sound-induced injury, fully accounts for the activity of the free radicals.

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References:

Lenzi, P., G. Frenzilli, et al. In press. DNA damage associated with ultrastructural alterations in rat myocardium following loud noise exposure. Environmental Health Perspectives.

Further Readings:

Raloff, J. 1983. Airport noise linked with heart disease. Science News 123(May 7):294.

______. 1982. Noise can be hazardous to our health. Science News 121(June 5):377.

______. 1981. Noise and high blood pressure. Science News 119(March 28):198.

Sources:

Giada Frenzilli
Dipartimento di Morfologia Umana e Biologia Applicata
Sez. Biologia e Genetica
University of Pisa
Via Roma
55-56126 Pisa
Italy

Sandra L. McFadden
Center for Hearing and Deafness
215 Parker Hall
University at Buffalo
Buffalo, NY 14214

Kevin K. Ohlemiller
Research Department
Central Institute for the Deaf
4560 Clayton Avenue
St. Louis, MO 63110


From Science News, Volume 163, No. 5, February 1, 2003, p. 68.