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CHEMICALS USED TO PROTECT SOLDIERS IN 1991 GULF WAR CAN DAMAGE TESTES,
ANIMAL STUDIES SHOW
By Mohamed B. Abou-Donia, Ph.D.
Duke University Medical Center
January 8, 2003

http://www.eurekalert.org/pub_releases/2003-01/dumc-cut010803.php

DURHAM, N.C. -- A combination of chemicals given to protect Gulf War
soldiers against deadly diseases and nerve gas may have inadvertently
damaged their testes and sperm production, according to animal experiments
at Duke University Medical Center.

The new study could explain why some veterans have experienced infertility,
sexual dysfunction, and other genitourinary symptoms, said Mohamed Abou
Donia, Ph.D., a Duke pharmacologist.

Three chemicals were given to soldiers to protect them against insect-borne
diseases and nerve-gas poisoning: the insect repellent DEET, the insecticide
permethrin, and the anti-nerve gas agent pyridostigmine bromide.

In a study designed to mimic those same conditions, Abou Donia and his
colleagues gave rats equivalent doses to what the soldiers received. When
given together, the chemicals caused extensive cell degeneration and cell
death with various structures of the testes, he found. The damage was even
more severe among rats that were exposed to moderately stressful situations
in addition to the chemicals.

Results of the study, funded by the Department of Defense, are published in
the Jan. 10, 2003 issue of The Journal of Toxicology and Environmental
Health.

"It appears that moderate stress, combined with the three chemicals, caused
the most severe deterioration in testicular structure and sperm production,
and these conditions were likely experienced by some Gulf War soldiers in
the combat environment," said Abou Donia, principal investigator of the
study.

"Interestingly, the chemically-treated rats don't look or behave any
differently than normal rats, just as the soldiers don't show any outward
signs of disease," said Abou Donia. "But under a microscope, you can see
clear and well-defined damage to a variety of testicular structures."

Abou Donia's team found the most pervasive cell damage within basal germ
cells and spermatocytes, which give rise to mature sperm. The three
chemicals combined with stress caused these cells to detach from one
another, slough off, and develop holes known as "vacuoles." Such changes are
well-known stages in the progression toward programmed cell death, known as
apoptosis. The more cells that die, the greater the suppression of
"spermatogenesis" or sperm production, said Abou Donia.

In fact, pathologic exams showed that most of the developing stages of sperm
were interrupted, and some of the stages were absent altogether among rats
treated with all three chemicals and stressful conditions.

Similar cell degeneration occurred in the seminiferous tubules, where
developing sperm are produced, and Sertoli cells that support and nurture
the developing germ cells.

"On every objective measure, the testes showed severe degeneration in the
presence of multiple chemicals, suggesting that the chemicals have a
synergistic or additive effect," said Abou Donia.

BRAIN DEFICITS COINCIDE WITH REPRODUCTIVE DAMAGE

The testicular damage corresponds to equally devastating brain changes in
the same rats exposed to the chemicals plus stress, said Abou Donia.
Findings from those experiments were published in the August 2002, issue of
Neurobiology of Disease.

In that study, Abou Donia's team showed that chemicals and stress increased
the permeability of the blood-brain barrier, allowing substances that would
normally be blocked to enter the brain. Moreover, the researchers found
large numbers of dead neurons, or nerve cells, in regions of the brain that
control muscle strength and movement (cortex); balance and coordination
(cerebellum); and memory, cognition and mood (hippocampus). Yet the animals
appeared normal to the naked eye.

Similarly, Gulf War veterans have complained of deficits in these very
functions for more than a decade, while clinical exams show no obvious signs
of disease.

"The brain deficits we found in rats reside in specific areas of the brain
that we can't measure in living humans," said Abou Donia. "This is why the
deficits are so difficult to assess clinically and why animal studies are so
critical to understanding the cellular damage."

Complicating the diagnostic process even further is the sheer volume of
brain cells that must die before clinical deficits become obvious, he said.
The human brain contains billions of nerve cells and supporting cells, so
the loss of brain cells does not produce immediate and overt symptoms.
Often, it takes repeated exposures to chemicals before the brain is depleted
of enough neurons to trigger deficits, he said.

However, once the damage occurs, little can be done to repair it. Extensive
nerve cell death causes "holes" in the brain and thus permanent deficits,
because neurons cannot regenerate like other cells in the body.

"Many of the effects we see with chemical exposure are similar to those of
aging, which is also associated with fewer neurons," said Abou Donia. He
said his ongoing research should help prevent such debilitating conditions
in the future.

"The military used these chemicals with the best of intentions, to protect
soldiers from indigenous diseases in the Gulf War region," he said. "Without
protection, there may have been thousands of deaths. But it appears that the
precautions prevented one set of problems while creating another. Now, our
task is to discern the mechanisms of illness in order to provide the
soldiers with maximum protection and the least risk of chemically induced
injury."

Duke colleagues Hagir B. Suliman, Ph.D., Wasiuddin A. Khan, Ph.D., and Ali
A. Abdel-Rahman were co-authors of the paper.

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