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Lipid peroxidation product measurement

Oxidative damage to membrane polyunsaturated fatty acids leads to the formation of numerous lipid peroxidation products, some of which can be measured as index of oxidative stress, including hydrocarbons, aldehydes, alcohols, ketones, and short carboxylic acids. [Pg.275]

Lipid peroxidation activity. Solubilized green tea, administered orally to rats for 5 weeks, reduced lipid peroxidation products. The treatment produced increased activity of glutathione (GSFf) peroxidase and GSH reductase, increased content of reduced GSH, a marked decrease in lipid hydroperoxides and malondialdehyde in the liver, an increase in the concentration of vitamin A by about 40%. A minor change in the measured parameters was observed in the blood... [Pg.18]

Antioxidant activity was also tested in a liver microsome system. In this study, mice were treated by oral intubation (2 times/wk) with 0.2 ml olive oil alone or containing CLA (0.1 ml), linoleic acid (0.1 ml), or dl-a-tocopherol (lOmg). Four weeks after the first treatment, liver microsomes were prepared and subsequently subjected to oxidative stress using a non-enzymatic iron-dependent lipid peroxidation system. Microsomal lipid peroxidation was measured as thiobarbituric acid-reactive substance (TBARS) production using malondialdehyde as the standard. It was found that pretreatment of mice with CLA or dl-a-tocopherol significantly decreased TBARS formation in mouse liver microsomes (p < 0.05) (Sword, J. T. and M. W. Pariza, University of Wisconsin, unpublished data). [Pg.269]

Figure 2. Lipid peroxidation as measured by TBA reacting products (absorbance at 532 nm) in liver mitochondria for... Figure 2. Lipid peroxidation as measured by TBA reacting products (absorbance at 532 nm) in liver mitochondria for...
We have used the thiobarbituric acid reaction to measure the steady state level of lipid peroxidation products accumulating in vivo in vital organs and subcellular particles (Zalkin and Tappel, 1960 Zalkin et al., 1960). Some of these results in terms of equivalent peroxide and free radicals are shown in Table II, where they are compared in amount with known toxicity of lipid peroxides and the lethality of ionizing radiations. Advantages and limitations of the thiobarbitiuic acid have been discussed previously. Comparison of the amounts of lipid peroxides found in vitamin E-deficient animals with the known lethality of ionizing radiation and... [Pg.498]

Likewise, results on lipid peroxidation products are not consistent, both in animal and in human studies. In addition to the variation with diet and exercise, different methods of measuring these products have been used. As an increase in lipid peroxidation products does not necessarily imply a state of disease, it is crucial to compare such results to inflammatory markers. No studies measuring such markers have indicated that CLA causes inflammation. [Pg.192]

There is some support for a role for free radicals in the pathogenesis of ischaemic colitis from animal studies. Murthy and Qi (1992) used a spin trap to demonstrate increased production of free radicals up to 60 min after reperfusion, whereas Douglas etal. (1989) demonstrated increases in malondialdehyde and conjugated dienes (presumptive measures of lipid peroxidation) in a rat model of ischaemic colitis. There is no data relating to human ischaemic colitis. [Pg.152]

Guyan et al. 1990) have used several markers of lipid peroxidation (9-cis-, 11-tmns-isomer of linoleic acid, conjugated dienes and ultraviolet fluorescent products) to demonstrate significant increases in the duodenal aspirate after secretin stimulation in patients with acute and clinic pancreatitis. They interpreted this as indicating induction of hepatic and pancreatic drug-metabolizing enzymes in the face of a shortfidl of antioxidant defences, more marked in chronic pancreatitis. Subsequent studies in patients with chronic pancreatitis have confirmed decreased serum concentrations of selenium, -carotene and vitamin E compared with healthy controls (Uden et al., 1992). Basso aol. (1990) have measured increases in lipid peroxides in the sera of patients with chronic... [Pg.152]

Ohnishi (Sakamoto etal., 1991) has described an oligomeric derivative of prostaglandin Bi (PGB2) and ascorbic acid. In a rat bilateral carotid occlusion-reperfiision injury complicated by haemorrhagic hypotension, this compound reduced a-phenyl-r-butyl nitrone (PBN) spin-trapped radicals and thiobarbituric acid-reactive products (TBARs) (a measure of lipid peroxidation) in isolated... [Pg.267]


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