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Evidence for carbon tetrachloride-induced lipid peroxidation in vivo by 23Na relaxation times t1
No full textWe report here the results of a study performed on the livers of rats intoxicated with CCl4 in order to investigate the dependence of 23Na n.m.r. parameters on specific cell alterations. In this connection, CCl4 represents a useful probe, since the hepatocellular damaging effects induced by this aliphatic halocarbon have been extensively investigated.
The t1relaxationtimes of intracellular sodium ion under physiological conditions in the presence of the paramagnetic shift reagent dysprosium tripolyphosphate were investigated. The significant increase of t1 in the livers of rats intoxicated with CCl4 with respect to the t1relaxationtimes of normal rats was studied.
Evidence is given that neither liver cell necrosis nor fat accumulation nor proliferative processes affected the observed t1 lengthening. However, when t1relaxationtimes were measured in the livers of vitamin E-treated rats subsequently intoxicated with CCl4 a significant shortening of t1 with respect to the times measured in intoxicated rats was observed. We report the results of the present study, taking into consideration that peroxidation of microsomal lipids is the key factor in the CCl4-induced liver injury process and that vitamin E exerts an antioxidant action against CCl4-induced microsomal lipidperoxidation
On the question of membrane-lipid peroxidation in the liver of rats fed a choline-devoid diet
No full textDecrease in linoleic acid metabolites as a potential mechanism in cancer risk reduction by conjugated linoleic acid
No full textPrevious research suggested that conjugated linoleic acid (CLA) feeding during the period of pubescent mammary gland development in the rat resulted in diminished mammary epithelial branching which might account for the reduction in mammary cancer risk. Terminal end buds (TEB) are the primary sites for the chemical induction of mammary carcinomas in rodents. One of the objectives of the present study was to investigate the modulation of TEE density by increasing levels of dietary CLA and to determine how this might affect the risk of methylnitrosourea-induced mammary carcinogenesis. The data show a graded and parallel reduction in TEE density and mammary tumor yield produced by 0.5 and 1% CLA. No further decrease in either parameter was observed when CLA in the diet was raised to 1.5 or 2%. Thus, optimal CLA nutrition during pubescence could conceivably control the population of cancer-sensitive target sites in the mammary gland. Since both CLA and linoleic acid are likely to share the same enzyme system for chain desaturation and elongation, it is possible that increased CLA intake may interfere with the further metabolism of linoleic acid. Fatty acid analysis of total lipid showed that CEA and CLA metabolites continued to accumulate in mammary tissue in a dose-dependent manner over the range 0.5-2% CLA. There was no perturbation in tissue linoleic acid, however, linoleic acid metabolites (including 18:3, 20:3 and 20:4) were consistently depressed by up to 1% CLA, Of particular interest was the significant drop in 20:3 (arachidonic acid), which is the substrate for the cyclooxygenase and lipoxygenase pathways of eicosanoid biosynthesis, Thus the CLA dose-response effect on arachidonic acid suppression corresponded closely with the CLA dose-response effect on cancer protection in the mammary gland. This information is critical in providing new insights regarding the biochemical action of CLA
Recognition and quantitation of cis-vaccenic and eicosenoic fatty acids in olive oils by 13C nuclear magnetic resonance spectroscopy
No full textNon-random peroxidation of different classes of membrane phospholipids in live cells detected by metabolically integrated cis-parinaric acid
No full textQuantitative assays of lipid peroxidation in intact, living cells are essential for evaluating oxidative damage from various sources and for testing the efficacy of antioxidant interventions. We report a novel method based on the use of cis-parinaric acid (PnA) as a reporter molecule for membrane lipid peroxidation in intact mammalian cells. Using four different cell lines (human leukemia HL-60, K562 and K/VP.5 cells, and Chinese hamster ovary (CHO) fibroblasts), we developed a technique to metabolically integrate PnA into all major classes of membrane phospholipids, i.e., phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol and cardiolipin, that can be quantified by HPLC with fluorescence detection. Integrated PnA constituted less than 1% of lipid fatty acid residues, suggesting that membrane structure and characteristics were not significantly altered. Low concentrations (20-40 mu M) of tert-butyl hydroperoxide (t-BuOOH) caused selective oxidation of PnA residues in phosphatidylserine and phosphatidylethanolamine of K562 cells and K/VP.5 cells while cell viability was unaffected. At higher t-BuOOH concentrations (exceeding 100 mu M), however, a progressive, random oxidation of all major phospholipid classes occurred and was accompanied by significant cell death. In HL-60 cells, phosphatidylethanolamine, phosphatidylserine and cardiolipin were sensitive to low concentrations of t-BuOOH, while phosphatidylcholine and phosphatidylinositol were not affected. Phosphatidylinositol was the only phospholipid that responded to the low concentrations of t-BuOOH in CHO cells, At high t-BuOOH concentrations, again, all phospholipid classes underwent extensive oxidation, All phospholipids were nearly equally affected by peroxidation induced by a initiator of peroxyl radicals, 2,2'-azobis-(2,4-dimethylvaleronitrile) (AMVN), in K562 cells. In gamma-irradiated (4-128 Gy) CHO cells, phosphatidylserine was the most affected phospholipid class (34% peroxidation) followed by phosphatidylinositol (24% peroxidation) while the other three phospholipid classes were apparently unaffected, Since loss of PnA fluorescence is a direct result of irreparable oxidative loss of its conjugated double bond system, the method described allows for selective and sensitive monitoring of oxidative stress in live cells without interference from cell repair mechanisms
Characterization of conjugated diene fatty acids in milk, dairy products and lamb tissues
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