Amounts Of Cholesterol Oxides Research Articles

Antibodies against electronegative LDL inhibit atherosclerosis in LDLr-/- mice

In order to determine the effect of antibodies against electronegative low-density lipoprotein LDL(-) on atherogenesis, five groups of LDL low receptor-deficient (LDLr-/-) mice (6 per group) were immunized with the following antibodies (100 microg each): mouse anti-LDL(-) monoclonal IgG2b, rabbit anti-LDL(-) polyclonal IgG or its Fab fragments and mouse irrelevant monoclonal IgG and non-immunized controls. Antibodies were administered intravenously one week before starting the hypercholesterolemic diet (1.25% cholesterol) and then every week for 21 days. The passive immunization with anti-LDL(-) monoclonal IgG2b, polyclonal antibody and its derived Fab significantly reduced the cross-sectional area of atherosclerotic lesions at the aortic root of LDLr-/- mice (28.8 +/- 9.7, 67.3 +/- 17.02, 56.9 +/- 8.02 microm(2) (mean +/- SD), respectively) compared to control (124.9 +/- 13.2 microm(2)). Vascular cell adhesion molecule-1 protein expression, quantified by the KS300 image-analyzing software, on endothelium and the number of macrophages in the intima was also decreased in aortas of mice treated with anti-LDL(-) monoclonal antibody (3.5 +/- 0.70 per field x 10) compared to controls (21.5 +/- 3.5 per field x 10). Furthermore, immunization with the monoclonal antibody decreased the concentration of LDL(-) in blood plasma (immunized: 1.0 +/- 1.4; control: 20.5 +/- 3.5 RLU), the amount of cholesterol oxides in plasma (immunized: 4.7 +/- 2.7; control: 15.0 +/- 2.0 pg COx/mg cholesterol) and liver (immunized: 2.3 +/- 1.5; control: 30.0 +/- 26.0 pg COx/mg cholesterol), and the hepatic content of lipid hydroperoxides (immunized: 0.30 +/- 0.020; control: 0.38 +/- 0.15 ng/mg protein). In conclusion, antibodies against electronegative LDL administered intravenously may play a protective role in atherosclerosis.

Formation of Cholesterol Oxides in Irradiated Raw and Cooked Chicken Meat During Storage

The objective of this study was to determine the effect of electron-beam irradiation on the oxidation of cholesterol in raw and cooked chicken meats with different packaging and storage times. Patties were prepared with skinless chicken breasts and legs. Half of the patties were used for raw meat study and the other half for cooked meat work. For cooked samples, patties were cooked in an electric oven to an internal temperature of 70 C. Raw and cooked meat patties were either aerobically or vacuum-packaged before irradiation. Irradiated patties were stored at 4 C up to 2 wk, and the amounts of cholesterol oxides in the patties were analyzed at 0, 7, and 14 d of storage. In raw chicken meat with vacuum packaging, 7β-hydroxycholesterol and β-epoxide were the only two cholesterol oxides present in significant amounts. In raw chicken meat with aerobic packaging, 7α-hydroxycholesterol and 7-keiocholesterol, which were not detected in vacuum-packaged raw chicken meat, were found. 7β-Hydroxycholesterol in raw chicken meat was increased by irradiation and storage time, regardless of packaging. The kinds of cholesterol oxides found in cooked meat were basically the same as those found in raw chicken, but the levels in cooked meats at all storage time were higher than those of the raw meats. With vacuum packaging, irradiation had no consistent effect on the amount of β-epoxide, 7α-hydroxycholesterol, or 7-ketocholesterol, but storage significantly influenced the amount of 7-ketocholesterol, 7β-hydroxycholesterol, and total cholesterol oxides in cooked chicken meat. With aerobic packaging, irradiation significantly increased the formation of 7α-hydroxycholesterol, 7β-hydroxycholesterol, and 7-ketocholesterol in cooked meat stored for 0 and 7 d. After 14 d of storage, however, irradiation had minor effects on the formation of cholesterol oxides in aerobically packaged cooked chicken.

Oxidation of cholesterol in butter during storage - effects of light and temperature

The objective of this study was to determine whether the exposure of three types of butter to different light and temperature conditions during a storage period of 6 weeks would result in a significant increase in cholesterol oxidation products (COPS) and, in addition, to assess whether a relationship exists between the amount of cholesterol oxides, the light source, the storage temperature and the type of butter. As standard indicator substances, 25-hydroxycholesterol, 7-ketocholesterol, 7β-hydroxycholesterol and 7α-hydroxycholesterol were used, and their prevalence was assessed using an HPLC method. With the exception of UV-light at room temperature, negligible increases in the formation of cholesterol oxides were detected in the first 3 weeks of storage. However, it was remarkable that in all three types of butter at refrigerator temperatures, a special light for food contributed more to the development of COPS than did a daylight lamp.

DIETARY OILS AND TOCOPHEROL SUPPLEMENTATION ON CHOLESTEROL OXIDE FORMATION IN FREEZE‐DRIED CHICKEN MEAT DURING STORAGE

ABSTRACTThe influence of dietary oils [fish (FO), flax (LO), palm (PO) and sunflower (SO) oil] and tocohperol supplementation on the oxidation of cholesterol and lipids of chicken meat was investigated. Lipid oxidation in chicken meat powders was determined by thiobarbituric acid reactive substances (TBARS) and cholesterol oxidation products were estimated by capillary gas chromatography (GC) after trimethylsilylation. Peak identities from GC were confirmed by mass spectrometry. Freeze‐dried chicken meat powder, stored in contact with air at room temperature for four months showed the presence of 7α‐ and 7β‐hydroxycholesterol, 7‐ketocholesterol, α and β‐epoxide, and cholestane‐triol. Total cholesterol oxides contents significantly (P < 0.05) increased with storage. The amount of cholesterol oxides in the meat powder was the highest in FO and SO group, and lowest in PO group. Lipid and cholesterol oxidation were accelerated by the presence of long‐chain PUFA. Lipid and cholesterol stability of chicken meat were improved by the dietary supplementation of tocopherol.