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- W78545189 abstract "Macrophage-mediated oxidation of low-density lipoprotein (LDL) is thought to play a key role during early atherogenesis, and cellular oxygenases were shown to mediate this process. As macrophage antioxidants may also contribute to the extent of cell-mediated oxidation of LDL, we analyzed the role of cellular reduced glutathione (GSH) and glutathione peroxidase (GPx) in LDL oxidation. The present study examined the effect of the macrophage GSH-GPx status on the ability of the cells to oxidize LDL. Upon incubation of J-774 A.1 macrophages for 20 h at 37°C with 50 μM of buthionine sulfoximine (BSO), an inhibitor of glutathione synthesis, cellular GSH content and GPx activity were reduced by 89 and 50%, respectively, and this effect was associated with a twofold elevation in macrophage-mediated oxidation of LDL. The BSO-treated cells contained high levels of peroxides, and released 32% more superoxide anions than nontreated cells in response to their stimulation with LDL in the presence of copper ions. To increase macrophage GSH content and GPx activity we have used L-2-oxothiazolidine-4-carboxylic acid (OTC), which delivers cysteine residues to the cells for GSH synthesis, and also selenium, which activates GPx and increases cellular glutathione synthesis. GSH content and GPx activity in J-774 A.1 macrophages were increased by 80 and 50%, respectively, following cells incubation with 2 mM OTC for 20 h at 37°C, and this was paralleled by a 47% inhibition in LDL oxidation by these cells. An inverse correlation was found between the extent of macrophage-mediated oxidation of LDL and cellular GSH content (r = .97), or GPx activity (r = .95). Upon incubation of J-774 A.1 macrophages with selenomethionine (10 ng/ml) for 1 week, cellular GSH content and GPx activity were increased by about twofold compared to control cells, and this effect was associated with a 30% reduction in cell-mediated oxidation of LDL. Dietary selenium supplementation (1 μg/d/mouse) to the atherosclerotic apolipoprotein E-deficient mice for a 6-month period, increased GSH content and GPx activity in the mice peritoneal macrophages by 36 and 30%, respectively, and this effect was associated with a 46% reduction in cell-mediated oxidation of LDL. Finally, the atherosclerotic lesion area in the aortas derived from these mice after selenium supplementation was found to be reduced by 30% compared to the lesion area found in nontreated mice. Our results demonstrate an inverse relationship between macrophage GSH content/GPx activity and cell-mediated oxidation of LDL. Intervention means to enhance the macrophage GSH-GPx status may thus contribute to attenuation of the atherosclerotic process." @default.
- W78545189 created "2016-06-24" @default.
- W78545189 creator A5052487247 @default.
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- W78545189 date "1998-01-01" @default.
- W78545189 modified "2023-09-30" @default.
- W78545189 title "Macrophage Glutathione Content and Glutathione Peroxidase Activity Are Inversely Related to Cell-Mediated Oxidation of LDL" @default.
- W78545189 cites W1506594192 @default.
- W78545189 cites W1516636175 @default.
- W78545189 cites W1523498318 @default.
- W78545189 cites W1535828429 @default.
- W78545189 cites W1562522900 @default.
- W78545189 cites W1590457525 @default.
- W78545189 cites W1597723737 @default.
- W78545189 cites W1625092822 @default.
- W78545189 cites W1775749144 @default.
- W78545189 cites W1810073570 @default.
- W78545189 cites W1824744945 @default.
- W78545189 cites W1841006369 @default.
- W78545189 cites W1964651215 @default.
- W78545189 cites W1965258539 @default.
- W78545189 cites W1970357567 @default.
- W78545189 cites W1972545405 @default.
- W78545189 cites W1976115068 @default.
- W78545189 cites W1978367775 @default.
- W78545189 cites W1979655335 @default.
- W78545189 cites W1981201921 @default.
- W78545189 cites W1987005612 @default.
- W78545189 cites W1988557610 @default.
- W78545189 cites W1996448872 @default.
- W78545189 cites W1999871971 @default.
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- W78545189 cites W2022456632 @default.
- W78545189 cites W2031596649 @default.
- W78545189 cites W2036001146 @default.
- W78545189 cites W2048890665 @default.
- W78545189 cites W2049646399 @default.
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- W78545189 cites W2104573407 @default.
- W78545189 cites W2109738937 @default.
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- W78545189 cites W2125570349 @default.
- W78545189 cites W2148207815 @default.
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- W78545189 cites W2184358165 @default.
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- W78545189 cites W2400802530 @default.
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- W78545189 doi "https://doi.org/10.1016/s0891-5849(97)00231-1" @default.
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