The oxidation of low-density lipoproteins (LDL) plays an important role in the development of atherosclerosis. Atherosclerosis is characterized by oxidative damage, which affects lipoproteins, the walls of blood vessels, and subcellular membranes. Several studies suggest that curcumin inhibits oxidation of LDL (87-90). Naidu and Thippeswamy examined the effect of cur-cumin on copper-ion-induced lipid peroxidation of human LDL by measuring the formation of thiobarbituric acid reactive substance (TBARS) and relative electrophoretic mobility of LDL on agarose gel. Curcumin inhibited the formation of TBARS effectively throughout the incubation period of 12 h and decreased the relative electrophoretic mobility of LDL (90). Curcumin at 10 ||M produced 40-85% inhibition of LDL oxidation. The inhibitory effect of curcumin was comparable to that of BHA but more potent than ascorbic acid. Further, curcumin significantly inhibited both the initiation and propagation phases of LDL oxidation.
Ramirez-Tortosa et al. evaluated the effect of curcumin on LDL oxidation susceptibility and plasma lipids in atherosclerotic rabbits (88). A total of 18 rabbits were fed for 7 weeks on a diet containing 95.7% standard chow, 3% lard, and 1.3% cholesterol, to induce atherosclerosis. The rabbits were divided into groups, two of which were also orally treated with turmeric extract at doses of 1.66 (group A) and 3.2 (group B) mg/kg body weight. A third group (group C) acted as a control. Plasma and LDL lipid composition, plasma a-tocopherol, plasma retinol, LDL TBARS, and LDL lipid hydroperoxides were assayed and aortic atherosclerotic lesions were evaluated. The low but not the high dosage of turmeric extracts decreased the susceptibility of rabbit LDL to lipid peroxidation. Both doses produced lower levels of total plasma cholesterol than the control group. Moreover, the lower dosage group had lower levels of cholesterol, phospholipids, and triglycerides than the 3.2-mg-dosage group.
Quiles et al. evaluated the antioxidant capacity of a C. longa extract on the lipid peroxidation of liver mitochondria and microsome membranes in atherosclerotic rabbits (87). Male rabbits fed a 3% (w/w) lard and 1.3% (w/w) cholesterol diet were randomly assigned to three groups. Two groups were treated with different dosages of a turmeric extract (A and B) and the third group (control) with a curcumin-free solution. Basal and in vitro 2,2'-azobis
(2-amidinopropane) dihydrochloride-induced hydroperoxide and TBARS production in liver mitochondria and microsomes was analyzed. Group A had the lowest concentration of mitochondrial hydroperoxides. In micro-somes, the basal hydroperoxide levels were similar in all groups but after the induction of oxidation, group C registered the highest value; TBARS production followed the same trend in mitochondria. These findings suggest that active compounds in curcuma extract may be protective against lipo-peroxidation of subcellular membranes in a dosage-dependent manner.
Asai and Miyazawa examined the effect of curcumin on lipid metabolism in rats fed a control, moderately high-fat diet (15 g soybean oil/100 g diet) and those given supplements of 0.2 g curcuminoids/100 g diet. Liver triacyl-glycerol and cholesterol concentrations were significantly lower in rats fed curcumin than in control rats (89). Plasma triacylglycerols in the very-low-density lipoproteins fraction were also lower in curcumin-fed rats than in control rats (p < .05). Hepatic acyl-CoA oxidase activity of the curcumin group was significantly higher than that of the controls. Furthermore, epididymal adipose tissue weight was significantly reduced with curcuminoid intake in a dose-dependent manner. These results indicated that dietary curcuminoids have lipid-lowering potency in vivo, probably due to alterations in fatty acid metabolism.
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