The document discusses the role of free radicals in the development of atherosclerosis. It provides details on: - What free radicals are and their sources in the body - How free radicals can damage LDL cholesterol and lead to atherosclerosis - The process of atherosclerosis where macrophages take up oxidized LDL and become foam cells that accumulate in artery walls - The role of antioxidants like superoxide dismutase in neutralizing free radicals and preventing oxidative damage

1. Role of free radical in the development of atherosclerosis Jan S. Purba Depart. Neurologi. FK UI/RSCM Jakarta

2. Oxidation causes body damage Don’t let rust attack you

5. Normal metabolism in Physiological Condition Mitochondria Endogen Antioxidant BALANCE Free Radical

13. Adhesion of monocytes onto endothelial cells and their foamy change

16. Severe atherosclerosis of the aorta

17. Microphotography of arterial wall with calcified (violet colour) atherosclerotic plaque (haematoxillin & eosin stain)

18. Light micrograph of a fibrofatty plaque in the coronary artery. FC = fibrous cap; MP = myeloproliferative; C = cap are calcified F= healed fissure; A = adventitia is the outermost area of the artery [From Gravanis MB. Histopathology of atherosclerosis. In: Atlas of Atherosclerosis: Risk Factors and Treatment , edited by Wilson PWF. Philadelphia, PA: Current Medicine, 2002.]

27. Enzymatic pathway for detoxification of reactive oxygen species

28. Under normal conditions, ROS are cleared from the cell by the action of superoxide dismutase (SOD), catalase, or glutathione (GSH) peroxidase. The main damage to cells results from the ROS-induced alteration of macromolecules such as polyunsaturated fatty acids in membrane lipids, essential proteins, and DNA.

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34. Under normal conditions, ROS are cleared from the cell by the action of superoxide dismutase (SOD), catalase, or glutathione (GSH) peroxidase. The main damage to cells results from the ROS-induced alteration of macromolecules such as polyunsaturated fatty acids in membrane lipids, essential proteins, and DNA.

36. SOD Intestine M cells Intestinal SOD/Gliadin (GliSODin ® ) transport and pharmacology: SOD/Gliadin Phase 2: Initial Immune Contact & Activation Phase 3: Gearing-up whole body immune response Phase 1: Digestive absorption }

41. Terima Kasih