Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive oxygen species (ROS) play important roles in the pathogenesis of vascular disease states. In particular, superoxide anion participates in endothelial dysfunction mainly owing to its rapid interaction with NO, but also as it causes direct biological effects and serves as a progenitor for many other ROS. Detection of ROS in intact tissues and cells is much more difficult than in chemical systems. We describe advantages and potential pitfalls of chemiluminescent methods of vascular ROS detection. Lucigenin and luminol-enhanced chemiluminescent methods are described in the detection of vascular superoxide and peroxynitrite production and NAD(P)H oxidase activity. We also describe the use of new chemiluminescent probes, including cypridina luciferin analogs (coelenterazine; CLA and MCLA) and pholasin. The validity of some of these chemiluminescent methods (in particular lucigenin-enhanced chemiluminescence) recently has been questioned. It has been suggested that lucigenin itself, especially at high concentrations (>50 micromol/L), may produce superoxide via redox cycling. Using intact human vascular rings and vascular homogenates, we show that lucigenin, particularly at lower concentrations (5 micromol/L), provides an accurate assessment of the rate of superoxide production as assessed by close correlations with the SOD inhibitable ferricytochrome c reduction assay. Chemiluminescent techniques provide a useful approach for vascular ROS measurements, but should be always interpreted in the context of measurements obtained using other complementary techniques.
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PMID:Measurement of vascular reactive oxygen species production by chemiluminescence. 1602 77

A mixture of trans-10, cis-12 (t10,c12) and cis-9, trans-11 (c9,t11) conjugated linoleic acid (CLA mixture) reduced atherosclerosis in animals, thus the effect of these isomers on endothelial dysfunctions leading to inflammation and atherosclerosis is of interest. We gave 75 healthy postmenopausal women a daily supplement of 5.5 g of oil rich in either CLA mixture, an oil rich in the naturally occurring c9,t11 CLA (CLA milk), respectively, or olive oil for 16 wk in a double-blind, randomized, parallel intervention study. We sampled blood and urine before and after the intervention. The ratios of total cholesterol:HDL cholesterol and concentrations of C-reactive protein, fibrinogen, and plasminogen activator inhibitor-1 were significantly higher in women supplemented with the CLA mixture than in those supplemented with CLA milk. Plasma triacylglycerol was significantly higher and HDL cholesterol was lower in women supplemented with the CLA mixture than with olive oil. Both CLA supplements increased lipid peroxidation, a marker of in vivo oxidative stress measured as urinary free 8-iso-prostaglandin F(2alpha). However, the CLA mixture increased lipid peroxidation more than the CLA milk did. The plasma cytokines interleukin-6 and tumor necrosis factor-alpha were not affected by the treatments, nor were any of the other variables measured. In conclusion, oil containing trans-10,cis-12 CLA has several adverse effects on classical and novel markers of coronary vascular disease, whereas the c9,t11 CLA isomer is more neutral, except for a small but significant increase in lipid peroxidation compared with olive oil.
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PMID:An oil mixture with trans-10, cis-12 conjugated linoleic acid increases markers of inflammation and in vivo lipid peroxidation compared with cis-9, trans-11 conjugated linoleic acid in postmenopausal women. 1864 Nov 89