Tea Chemical May
Prevent Brain Damage
By Will Boggs, MD, Reuters Health
NEW YORK (Reuters Health)
- Chemicals found in green tea and other plants may prevent the
brain damage that occurs after strokes and other brain injuries,
say researchers from the University of California, San Francisco
``In stroke, as well as other conditions, cells sometimes take
an active role in causing their own death,'' Dr. Raymond Swanson
from UCSF and the Veterans Affairs Medical Center told Reuters
Health. ``In this case, it is overactivation of a normal DNA repair
system, the PARP/PARG system, that paradoxically causes cells
to die. By blocking this system we can rescue cells that would
otherwise go on to die.''
The PARP/PARG system is activated by the release of cell-damaging
oxygen radicals, a phenomenon called oxidative stress, and when
cells become overexcited by various toxins, the researchers note.
Swanson and associates tested the effects in the laboratory
of two plant-derived chemicals on brain cells under stress--gallotannin
and nobotanin B. Gallotannin is found in green tea and other plants.
Nobotanin B, a similar chemical, comes from the Brazilian glory
bush. Both chemicals block PARG activity.
Blockers of PARP activity have already been used to prevent
brain cell death, the authors explain, but as PARG blockers, gallotannin
and nobotanin B were 10 to 1,000 times more potent in preventing
brain cell death caused by oxygen radicals. And gallotannin was
100 times more effective than antioxidants, chemicals that can
soak up the toxic oxygen molecules.
Both gallotannin and nobotanin B also blocked brain cell death
from chemicals that normally overexcite the cells, the report
At the life-saving doses, neither chemical had cell-damaging
side effects, according to the report in the Proceedings of the
National Academy of Sciences, though gallotannin did cause some
ill effects just above its most effective dose.
``The findings confirm that cell death (in our case neural cell
death) after oxidative stress is not simply a passive process,
but rather involves active participation by the cells themselves,''
Swanson explained. ``In other words, oxidative stress triggers
responses in cells which can be deleterious to the cells, and
blocking this response can improve cell survival.''
``These compounds may have promise as (cell-protecting) agents,''
the authors conclude.
SOURCE: Proceedings of the National Academy of Sciences 2001;98:12227-
Reference Source 89