- A tiny protein called metallothionein (MT) may protect against alcohol's neurotoxic effects.
- The brain can make more of these proteins in response to alcohol consumption.
- One of an individual's different responses to alcohol may be related to his or her MT levels.
- Research indicates that MT can serve as an antioxidant throughout the body, including the brain.
Metallothionein (MT), a small protein found in most tissues throughout the body, may help "detoxify"
the brain from the effects of alcohol. A study published in the March issue of
Alcoholism:
Clinical & Experimental Research has found that the brain can synthesize more MT in response to
alcohol consumption, which may provide protection against its toxic effects.
"Alcohol's toxicity," explained Yutaka Suzuki, visiting scientist from the department of neurology at
the Nihon University School of Medicine and lead author of the study, "could be due to its production
of oxygen radicals. Metallothionein may protect against oxidative damage of the central nervous
system that is caused by overproduction of free radicals."
MT was initially identified in 1957 as a cadmium-binding protein. It has since been discovered to
also bind with and regulate a variety of essential trace minerals, such as zinc and copper. Research
suggests that both a deficiency as well as an excess of some minerals can cause heart disease,
diabetes, high blood pressure and cancer.
The MT protein interests toxicologists because it may protect against metal toxicity and possibly
against oxidative stress. It interests pharmacologists because it might have a role in cancer
chemotherapy. Nutritionists are interested because it appears to be a major storage protein for zinc,
which is of particular importance during fetal development. Biochemists and molecular biologists
might be interested in the regulation mechanisms of an extremely inducible protein. And now addiction
'"/>
Contact: Yutaka Suzuki, M.D., Ph.D.
QZU00375@nifty.ne.jp
81-3-3972-811 x2602
Alcoholism: Clinical & Experimental Research
13-Mar-2000
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