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ShareJune 18, 1997 — Shock can kill. A heart attack, stroke, infection or injury can cause
the profound disturbance of normal cellular functioning that doctors
call shock - a biochemical and metabolic catastrophe that can lead to
cell death and even death of the entire organism.
University of Maryland School of Medicine researchers have found a
potentially powerful new weapon for medicine's war on shock.
Ironically, it's an oncogene implicated in a kind of cancer called
B-cell lymphoma, from which it gets its name - bcl-2. The products of
the bcl-2 gene help prevent cell death, which is a boon to a cancer
cell, although ultimately harmful to its human host.
Now bcl-2 may prove helpful in preventing cell death caused by shock.
Dr. Benjamin F. Trump, professor and chairman of pathology at the
medical school in Baltimore, and colleagues will present results of a
study of bcl-2's protective effects, at the 20th Annual Conference on
Shock, on June18 in Indian Wells, California.
"The precise mechanism by which bcl-2 inhibits cell death remains to
be defined," said Trump, "but we believe that its protective action
arises from its anti-oxidant properties, its interference with the
cellular signaling process, and its modification of calcium ion
transport within the cell."
Oxidants, which can damage cells, are released in enormous quantities
by infection, inflammation and ischemia - a blockage of blood flow -
making them a far greater threat than one might think, the pathologist
pointed out.
For more than a decade, Trump's research has focused on the role
played by ionized or electrically charged calcium, which can increase
rapidly within cells after they are damaged, activating biochemical
and metabolic changes that can lead to cell death.
Dr. Masato Ichimiya, a surgeon and research fellow in Trump's lab, and
Dr. Paul Amstad, associate professor of pathology at the University of
Maryland School of Medicine, engineered normal cells from rats'
kidneys to express extra bcl-2. Those cells proved more resistant
than normal controls to death from treatment with hydrogen peroxide.
The toxicity of hydrogen peroxide was further reduced by pretreating
cells with a chemical that binds calcium ions.
After treatment with another chemical that releases calcium ions, the
amount of positively charged intracellular calcium increased in both
bcl-2 cells and controls, but calcium levels in cells containing bcl-2
dropped again much more rapidly.
Trump said his lab's findings suggest that bcl-2 protects against two
kinds of cell death, apoptosis and oncosis. In apoptosis, most
frequently seen in normal or "programmed" cell death, a cell shrinks,
breaks into fragments and is absorbed by other housecleaning cells
known as phagocytes. Oncosis, in which a cell swells and bursts, is
more typical of cell death from shock following traumatic injury,
infection or ischemia.
"Cells overexpressing bcl-2 may prevent oxidant-induced cell death in
part by increasing the cells' ability to effectively buffer the
effects of increased calcium ions," Trump and Ichimiya concluded. "This could be significant in developing effective methods of
preventing and treating shock, which is a major cause of death.
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