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Glucose triggers brain cell death in rats after hypoglycemic coma

The rats could remain hypoglycemic without evidence of significant oxidative stress for at least 60 minutes," says Swanson, who is also professor and vice-chair of neurology at the University of California, San Francisco. "It was only when we gave them glucose to reverse the hypoglycemia that the oxidative stress occurred. This was a real surprise."

The researchers then discovered that oxidative stress and neuron death were prevented when the rats were given an inhibitor of NADPH oxidase, indicating a key role for this enzyme.

"It is well-established that mitochondria can be a source of oxidative stress," says Swanson. "But in this setting, oxidative stress comes from an entirely different source." He adds that the normal role of NADPH oxidase in the brain is "completely unknown."

The authors also found that the degree of oxidative stress was directly dependent upon the amount of glucose given. "We think that this stems from a known link between glucose and NADPH oxidase," Swanson says. "Glucose is a precursor for NADPH, which in turn is used by NADPH oxidase in generating oxidative stress."

Swanson explains that the results have implications for both basic and clinical science. For basic science, he says, "this calls for a reconsideration of our concepts about the causes of oxidative stress in other settings especially in ischemic stroke, where the blood supply to the brain is diminished and theres a big burst of oxidative stress when the blood returns. That burst has always been blamed on oxygen, but it may be that glucose is the culprit. And it may depend on how much glucose is put in."

In terms of clinical science, Swanson observes that "as clinicians, our first reaction when we see a patient in hypoglycemic coma is to give lots of glucose, fast. But our rodent model makes it clear that overshooting glucose levels is very bad for rat brains. The way we treat patients for hypoglycemia may have to be reevaluat
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Contact: Steve Tokar
steve.tokar@ncire.org
415-221-4810 x5202
University of California - San Francisco
4-Apr-2007


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