thiobarbituric-acid and Edema

The changes in the composition of bile can lead to the process of it's crystallization in the gallbladder. In bile model it was shown that inflammation with the generation of reactive oxygen metabolites may induce and influence the cholesterol monohydrate crystal formation within supersaturated bile. The aim of this study was to investigate the ability to detect traces of reactive oxygen metabolites, thiobarbituric acid reactive compounds and dien, in order to compare cholesterol and bilirubin contents in bile and serum during different conditions of inflammation in the gallbladder's wall. In every bile sample a reference to free radical reaction was found. There was an increase in MDA during higher degree of inflammation in the gallbladder, but no alteration in the dien content was observed. In case of common bile duct stones the bilirubin in the serum and in the gallbladder was parallelly high, but in other cases there were no significant correlation. In an occluded gallbladder with hydrops the content of protein was significantly higher in 85% of the cholesterol stones. As a conclusion, free radical reactions in the wall of gallbladder as well as in bile can induce gallstone formation. Further studies are needed to clarify the time which is sufficient to change the composition of bile and the degree of inflammation which lead to the onset of stone formation.

Topics: Bile; Bilirubin; Cholecystitis; Cholelithiasis; Cholesterol; Crystallization; Edema; Female; Free Radicals; Gallbladder; Gallbladder Diseases; Gallstones; Humans; Male; Malondialdehyde; Proteins; Reactive Oxygen Species; Thiobarbiturates

It has been suggested that canthaxanthin (CX), beta-carotene, and other carotenoids may inhibit carcinogenesis via antioxidant activity. CX has been shown to inhibit lipid peroxidation in liposomes; this experiment was designed to assess the antioxidant activity of CX in biological membranes. Chicks were fed semipurified diets supplemented with placebo beadlets or CX beadlets (5 g beadlets/kg diet; 0.5 g CX/kg diet) for five weeks. Diets were deficient in vitamin E and selenium to maximize the power of detecting an antioxidant effect of CX and to induce exudative diathesis, which is a vitamin E and selenium deficiency disease of chicks. Dietary CX had no effect on the onset, incidence, or severity of exudative diathesis. Liver homogenates from CX-fed chicks exhibited significantly (p = 0.02) decreased formation of thiobarbituric acid-reactive substances over time in ferrous ion-induced peroxidations. Because dietary CX increased hepatic alpha-tocopherol content, subsequent peroxidations were conducted in membrane fractions prepared from placebo and CX livers matched for alpha-tocopherol content. In this system, CX was marginally but inconsistently protective against peroxidation at both 15 torr O2 (p = 0.12) and 150 torr O2 (p = 0.07). Nanomolar changes in hepatic alpha-tocopherol, unlike CX, substantially altered rates of peroxidation. These results suggest that under these conditions, dietary CX increased resistance to lipid peroxidation primarily by enhancing membrane alpha-tocopherol levels and secondarily by providing weak direct antioxidant activity.

Topics: Animals; Antioxidants; Canthaxanthin; Carotenoids; Chickens; Diet; Edema; Female; Lipid Peroxidation; Liver; Male; Membrane Lipids; Poultry Diseases; Selenium; Thiobarbiturates; Vitamin E; Vitamin E Deficiency