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(American Journal of Pathology. 2005;167:1371-1377.)
© 2005 American Society for Investigative Pathology

Absence of 12/15 Lipoxygenase Reduces Brain Oxidative Stress in Apolipoprotein E-Deficient Mice

Cinzia M. Chinnici*, Yuemang Yao*, Tao Ding*, Colin D. Funk{dagger} and Domenico Praticò*

From the Department of Pharmacology,* University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; and the Departments of Physiology and Biochemistry,{dagger} Queen’s University, Kingston, Ontario, Canada

The enzyme 12/15 lipoxygenase (12/15LO) has been implicated in the oxidative modification of lipoproteins and phospholipids in vivo. In addition, mice deficient in apolipoprotein E (ApoE–/–) are characterized by spontaneous hypercholesterolemia and a systemic increase in oxidative stress. Whereas the absence of 12/15LO reduces lipid peroxidation in the plasma and urine of ApoE–/– mice, the relative contribution of this enzyme to oxidative stress in the central nervous system remains unknown. Here, we provide the first in vivo evidence that 12/15LO modulates brain oxidative stress reactions using ApoE–/– mice crossbred with 12/15LO-deficient (12/15LO–/–) mice (12/15LO–/–/ApoE–/–). In chow-fed 12-month-old 12/15LO–/–/ApoE–/– mice, the amount of brain isoprostane iPF2{alpha}-VI, a marker of lipid peroxidation, and carbonyls, markers of protein oxidation, were significantly reduced when com-pared with 12/15LO-expressing controls (12/15LO+/+/ApoE–/–). These results were observed despite the fact that cholesterol, triglyceride, and lipoprotein levels were similar to those of ApoE–/– mice. These data indicate a functional role for 12/15LO in the modulation of oxidative reactions in the central nervous system, supporting the hypothesis that inhibition of this enzymatic pathway may be a novel therapeutic target in clinical settings involving increased brain oxidative stress.




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