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Enzyme Research
Researchers at Massachusetts General Hospital publish new data on enzyme research
November 7th, 2009
Data detailed in '12/15-Lipoxygenase targets neuronal mitochondria under oxidative stress' have been presented. According to a study from the United States, "12/15-Lipoxygenase (12/15-LOX) is an important mediator of brain injury following experimental stroke in rodents. It contributes to neuronal death, but the underlying mechanism remains unclear." "We demonstrate here that in neuronal HT22 cells subjected to glutamate-induced oxidative stress, 12/15-LOX damages mitochondria, and this represents the committed step that condemns the cell to die. Importantly these events, including breakdown of the mitochondrial membrane potential, the production of reactive oxygen species, and cytochrome c release, can all be replicated by incubation of 12/15-LOX with mitochondria in vitro, without the need to add other cytosolic factors. Proteasome activity is required downstream of mitochondrial damage to complete the cell death cascade, but proteasome inhibition is only partially protective," wrote S. Pallast and colleagues, Massachusetts General Hospital. The researchers concluded: "These findings position 12/15-LOX as the central executioner in an oxidative stress-related neuronal death program." Pallast and colleagues published the results of their research in the Journal of Neurochemistry (12/15-Lipoxygenase targets neuronal mitochondria under oxidative stress. Journal of Neurochemistry, 2009;111(3):882-9). For additional information, contact S. Pallast, Massachusetts General Hospital, Neuroprotection Research Laboratory, Charlestown, Massachusetts USA.. The publisher of the Journal of Neurochemistry can be contacted at: Blackwell Publishing Inc., 350 Main St., Malden, MA 02148, USA. Keywords: United States, Charlestown, Cell Biology, Enzyme Research, Experimental Stroke, Lipoxygenase, Neurochemistry. This article was prepared by NewsRx editors from staff and other reports. Copyright 2009, NewsRx.com.
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