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The Yin and Yang of Oxidation in the Development of the Fatty Streak

Arteriosclerosis Thrombosis and Vascular Biology · 1996 · Vol. 16(7) · pp. 831–842

Mohamad Navab✉(University of California, Los Angeles)Judith A. Berliner(University of California, Los Angeles)Andrew D. Watson(University of California, Los Angeles)Susan Hama(University of California, Los Angeles)Mary Territo(University of California, Los Angeles)Aldons J. Lusis(University of California, Los Angeles)Diana M. Shih(University of California, Los Angeles)Brian J. Van Lenten(University of California, Los Angeles)Joy S. Frank(University of California, Los Angeles)Linda L. Demer(University of California, Los Angeles)Peter A. Edwards(University of California, Los Angeles)Alan M. Fogelman(University of California, Los Angeles)

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Abstract

Recent data support the hypothesis that the fatty streak develops in response to specific phospholipids contained in LDL that become trapped in the artery wall and become oxidized as a result of exposure to the oxidative waste of the artery wall cells. The antioxidants present within both LDL and the microenvironments in which LDL is trapped function to prevent the formation of these biologically active, oxidized lipids. Enzymes associated with LDL and HDL (eg, platelet activating factor acetylhydrolase) or with HDL alone (eg, paraoxonase) destroy these biologically active lipids. The regulation and expression of these enzymes are determined genetically and are also significantly modified by environmental influences, including the acute-phase response or an atherogenic diet. The balance of these multiple factors leads to an induction or suppression of the inflammatory response in the artery wall and determines the clinical course.

Paraoxonase enzyme and polymorphisms Antioxidant Activity and Oxidative Stress Cynara cardunculus studiesFatty streakParaoxonaseEnzymePON1BiochemistryChemistryInternal medicineEndocrinologyBiologyCholesterol