Antioxidant Delays Type 1 Diabetes
A synthetic antioxidant delays and often prevents the onset of autoimmune
or type 1 juvenile diabetes in mice, researchers reported in the journal
Diabetes.
"We've all
heard a lot about how oxidative stress can damage cells and how we should
take vitamins that work as antioxidants," co-author Jon Paganelli, formerly
of the University of Colorado Health Sciences Center in Denver and now
assistant professor of pediatrics at the University of Pittsburgh, told
United Press International.
The particular
antioxidant we used in this study works very well at scavenging free radicals.
The study showed the role that the generation of these particular free
radicals has in causing some of the damage to cells important in making
insulin. It is not the cause for all of the damage, but it plays a significant
part," Paganelli said.
In autoimmune
diabetes, the immune system misidentifies beta cells and attacks them.
Inflammatory cells release free radicals that damage and kill the beta
cells, eventually causing the body to make less insulin, leading to diabetes.
Approximately 1 million people in the United States have type 1 diabetes
and some 30,000 new cases are diagnosed each year.
The antioxidant
used in the study protected beta cells from the free radicals mistakenly
created and released destructively by the immune system. The antioxidant
also blocked the ability of the immune system to recognize beta cells,
the target of the autoimmune attack in diabetes.
"These data
show that antioxidants protect against diabetes on two fronts. They not
only mop up destructive oxygen radicals, but also alter the immune response,"
said co-author Dr. James Crapo, professor of medicine at National Jewish
Medical and Research Center in Denver. "That suggests the intriguing possibility
that we might one day treat a variety of autoimmune diseases by altering
the oxidant/antioxidant balance of immune system."
"This study
goes one step further than previous research in saying that free radicals
are involved in killing beta cells. That's important," Dr. Scott Campbell,
vice president of research programs at the American Diabetes Association
in Alexandria, Va., told UPI. "And this research suggests the potential
development of an alternative therapy to keep that from happening and preventing
type 1 diabetes from developing."
The synthetic
antioxidant, developed by Crapo and colleagues several years ago, is licensed
by Incara Pharmaceuticals Corp. of Triangle Park, N.C. The compound, named
AEOL 10113, imitates the action of the naturally occurring antioxidant
superoxide dismutas, but is more potent and lasts longer in the body.
The researchers
injected 10 mice with AEOL 10113 on the day before transplanting into them
diabetes-causing T cells. After the transplants, they gave the mice the
antioxidant four times, the last time on day 9. The five mice that did
not get the antioxident all developed diabetes by day 13.
The mice treated
with AEOL 10113 showed no signs of diabetes until day 21. Half were still
diabetes-free at four weeks.
"We were surprised
and pleased that the mice remained healthy for almost two weeks after the
antioxidant treatments ended," Piganelli said. "That suggested to us that
the antioxidant had altered the cells of the immune system."
Further experiments
showed the antioxidant prevented the mouse immune system from recognizing
certain antigens, molecules that trigger an immune response. This suggests
the antioxidant might be useful in combination with other antigens to treat
other autoimmune diseases.
Additional
animal experiments are planned to prove the safety and potency of the antioxidant
in animals before human trials are planned.
"Obviously
we have a long way to go," Crapo said. "But we believe that these findings
have opened a very promising new line of research."
The National
Institutes of Health and the National Heart Lung and Blood Institute funded
the research. Incara Pharmaceuticals provided the antioxidant.
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