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Biomedical subjects

A L Tappel

Publications and source records attributed to A L Tappel.

At least 109 records · Page 6Linked to original sources
PubMed1982

Glutathione peroxidase activities of animal tissues.

1. Selenium-dependent, selenium-independent and total glutathione peroxidase activities were measured in liver, kidney, heart, lung, intestine and stomach of a variety of animals, mostly mammals. 2. Total glutathione peroxidase activity of liver was highest in the order: hamster greater than gerbil approximately equal to rabbit greater than mouse greater than rat. Total glutathione peroxidase activity was adequate in the livers of other mammals and in the kidney, heart, lung, intestine and stomach of all mammals. 3. The total glutathione peroxidase activities in the following tissues correlated significantly: liver and kidney; heart and lung; and intestine and stomach. Selenium-dependent glutathione peroxidase activities in rat tissues correlated with reported activities of copper-superoxide dismutase in the same tissues. 4. Considering the phylogenetic distribution of total glutathione peroxidase activities, the rodent limb of the phylogenetic tree has the highest activities.

Amphibians↗
PubMed1982

Carbon tetrachloride-mediated expiration of pentane and chloroform by the intact rat: the effects of pretreatment with diethyl maleate, SKF-525A and phenobarbital.

Measurements were made of pentane, a produce of lipid peroxidation, and chloroform (CHCl3), a product of the reproductive metabolism of carbon tetrachloride (CCl4), expired by rats administered CCl4 plus either phenobarbital (PB), 2-diethylaminoethyl-2,2-diphenyl valerate hydrochloride (SKF-525A), or diethyl maleate (DEM). In rats fed a standard laboratory diet, treatment with PB prior to injection of CCl4 increased expiration of both CHCl3 and pentane. SKF-525A pretreatment decreased the metabolism of CCl4 and CCl4-induced lipid peroxidation. DEM, a depleter of intracellular glutathione, increased lipid peroxidation. In rats fed 10% corn oil diets that contained either 0 or 40 IU of dl-alpha-tocopherol acetate, oxidant stresses caused by glutathione depletion and CCl4-intoxication were found to be additive.

Animals↗
PubMed1982

Lipid peroxidation during chronic inflammation induced in rats by Freund's adjuvant: effect of vitamin E as measured by expired pentane.

Expired pentane, a product of omega 6-unsaturated fatty acid hydroperoxide decomposition, and foot volume were measured following injection of Freund's adjuvant into the hind feet of vitamin E-deficient rats injected 1 wk previously with either 0 or 100 mg of dl-alpha-tocopherol acetate/100 g body weight. Vitamin E inhibited pentane production after 21 and 28 days. This is the first demonstration in vivo of increased lipid peroxidation and its inhibition by vitamin E during adjuvant-induced chronic inflammation. By 28 days, foot volume was significantly less in vitamin E-injected rats (162%) than in vitamin E-deficient rats (207%).

Animals↗
PubMed1981

The role of peroxidation during chronic and acute exposure to ethanol as determined by pentane expiration in the rat.

Weanling rats were fed one of 3 diets containing 0, 11 or 200 international units (IU) dl-alpha-tocopherol acetate/kg diet for 4 weeks. Following this period, the drinking water was replaced with an 18% solution of ethanol (v/v). An isocaloric D-glucose solution was substituted for the drinking water of a control group of rats fed the vitamin-E-deficient diet for 4 weeks. The 4 treatment groups were maintained on the diet and drinking regimen for 20 weeks. Basal levels of expired pentane were determined at weeks 0, 1, 3, 5, 7 and 9. Chronic ethanol consumption did not influence basal pentane production during the 9-week treatment. Basal levels of expired pentane were affected by dietary vitamin E. Rats supplemented with vitamin E had basal pentane levels less than one-half of the level of rats fed a vitamin-E-deficient diet (p less than 0.001). After 14 weeks of treatment, the 2 groups of rats fed a vitamin-E-deficient diet were administrated p.o. an acute dose of 6 g of ethanol/kg body wt. Pentane expired above basal levels during the following 4-hr period correlated with the amount of hepatic triglycerides determined at the conclusion of the experiment. The etiology of ethanol toxicity is a complex and multifactorial system made up of many biological variables that influence lipid peroxidation. The appropriate choices of experimental designs and methods are important in examining the role of lipid peroxidation.

Alcoholic Intoxication↗
PubMed1981

Carbon tetrachloride-induced lipid peroxidation: simultaneous in vivo measurements of pentane and chloroform exhaled by the rat.

Simultaneous measurements of pentane, an index of lipid peroxidation, and chloroform (CHCl3), an index of carbon tetrachloride (CCl4) metabolism, were made on samples of breath from rats injected with 30 microliter CCL4/100 g body wt. In the first 3 h after administration of CCl4, rats fasted overnight metabolized less CCl4 and exhaled less pentane than did fed rats. Multiple injections of CCl4 decreased both the metabolism of CCl4 to CHCl3 and the level of in vivo lipid peroxidation following administration of a subsequent dose of CCl4. Dietary vitamin E provided limited protection from CCl4-induced lipid peroxidation and had no effect on the rate of CCl4 metabolism to CHCl3.

Animals↗
PubMed1981

In vivo lipid peroxidation: measurement via exhaled pentane and protection by vitamin E.

Lipid peroxidation occurs in animal tissue when antioxidant protective systems are lacking. Among the protective systems in animals are the biological antioxidant vitamin E and selenium-glutathione peroxidase, a decomposer of peroxides. Lipid peroxidation also occurs when a variety of chemical oxidants are introduced into a animal. The most recently developed technique for measurement of lipid peroxidation in vivo is the analysis of expired air for volatile hydrocarbon products of lipid hydroperoxide decomposition. Pentane is derived from the major fatty acids of the animal body, those of the omega 6-un-saturated fatty acid family, while ethane is derived from omega 3-unsaturated fatty acids. The technique of measuring volatile hydrocarbons has been used by a number of investigators to show increased lipid peroxidation in animals fed diets deficient in antioxidant nutrients and in animals exposed to ozone or injected with iron, halogenated hydrocarbons, or peroxides. Evidence that volatile hydrocarbons are produced during lipid peroxidation, the similarities of results obtained by different investigators who have measured lipid peroxidation by volatile hydrocarbon production, and the relative effects of nutritional and chemical treatments on production of volatile hydrocarbons by laboratory animals or humans are reviewed.

Fatty Acids, Unsaturated↗
PubMed1980

Respiratory pentane: a measure of in vivo lipid peroxidation applied to rats fed diets varying in polyunsaturated fats, vitamin E, and selenium and exposed to nitrogen dioxide.

Pentane is one decomposition product of omega 6-unsaturated lipid hydroperoxides. The measurement of respiratory pentane is one of the most sensitive in vivo tests of lipid peroxidation. This measurement was applied to test the ability of a low level, short-term exposure of rats of nitrogen dioxide to induce lipid peroxidation. When exposed to 4.48 ppm nitrogen dioxide for 60 min, no increase in pentane production was detected. For 10 weeks prior to exposure, the rats were fed Torula yeast-based diets with 10% stripped lard or 10% stripped corn oil. The ratios of basal pentane production by rats fed the following antioxidants were for corn oil- and lard-fed rats, respectively: 40 I.U. vitamin E/kg and 0 selenium: 0 vitamin E and 0.1 ppm selenium: 0 vitamin E and 0 selenium, 1:2.2:5.8 and 1:1.9:3.5. Pentane production was significantly (P<0.05) greater by corn oil-fed rats than by lard-fed rats only when both vitamin E and selenium were absent from the diet.

Animals↗
PubMed1980

Vitamin E and selenium protection from in vivo lipid peroxidation.

Some of the vitamins and many of the metals that are being considered at this symposium interact in lipid peroxidation. Some of these interactions have been studied in vivo. Measurement of in vivo lipid peroxidation in the rat is accomplished by gas chromatographic analysis of pentane, a minor peroxidation product that is exhaled in the breath. In the rat, lipid peroxidation is proportional to dietary polyunsaturated lipids when the animal is deficient in antioxygenic agents. The chain-breaking antioxidant vitamin E is the main protector against in vivo lipid peroxidation. Dietary selenium, through its involvement in the biosynthesis of glutathione peroxidase, functions in a secondary antioxygenic role as a hydroperoxide reducer. In rats fed a vitamin E-deficient diet, injection of some hydroperoxides, iron, or vitamin C leads to initiation of in vivo lipid peroxidation, apparently by decomposing hydroperoxides to free radicals. Carbon tetrachloride, a toxic halogenated hydrocarbon, is metabolized by liver microsomes and initiates in vivo lipid peroxidation in the liver. These examples show that practical information on interactions involving in vivo lipid peroxidation can be obtained by studies that use the pentane method.

Animals↗
PubMed1979

Steady state and pre-steady state kinetic properties of rat liver selenium-glutathione peroxidase.

The kinetic properties of partially purified rat liver selenium-glutathione peroxidase were studied under various conditions. Steady state kinetic measurements show sigmoidal saturation curves, parabolic double reciprocal plots, and Hill coefficients greater than unity. Although these kinetic results appear to show cooperative interactions between subunits, they more reflect the presence of several oxidation-reduction forms of the catalytic site. A substrate-induced transition between enzyme forms was evidence by the occurrence of a lag in the attainment of the final steady state velocity under certain preincubation conditions. This hysteretic behavior was evident only when the enzyme was incubated in the absence of reduced glutathione, the donor substrate. Thus, reduced glutathione induces the transition to the fully active form of the enzyme, a slow process requiring about 0.5 min after addition of glutathione, depending on conditions. The length, tau, of the lag period is dependent on the concentrations of enzyme and glutathione, but to a first approximation, this lag period is independent of the concentration of the hydroperoxide acceptor substrate. The lag period is also relatively independent of the nature of the hydroperoxide species. A model for the transition process that is compatible with these observations and with the possible oxidation-reduction properties of the selenium moiety of the enzyme is suggested.

Animals↗
PubMed1979

Donor substrate specificity and thiol reduction of glutathione disulfide peroxidase.

By isolation of a mixed disulfide product of glutathione and cysteine, glutathione peroxidase was shown to be highly specific for only one donor substrate. Using the coupled assay of NADPH and yeast glutatione reductase, which is highly specific for flutathione disulfide, it was shown that the apparent inhibition of glutathione peroxidase by mercaptoethanol can be described kinetically and that it is competitive with glutathione. Also, when limiting amounts of hydroperoxide were present in the reaction mixture with mercaptoethanol or cysteine, the total amount of glutathione disulfide produced decreased as compared with that in a reaction mixture without mercaptoethanol or cysteine. This finding is consistent with enzymatic formation of mixed disulfides. Data presented suggest that the selenium in glutathione peroxidase was oxidized to a seleninic acid in the absence of glutathione. These results can be explained by a mechanism for glutathione peroxidase wherein the selenium atom is the only atom in the enzyme that undergoes oxidation reduction.

Animals↗
PubMed1979

Volatile hydrocarbon and carbonyl products of lipid peroxidation: a comparison of pentane, ethane, hexanal, and acetone as in vivo indices.

A study was undertaken to determine whether respiratory hexanal and acetone as well as pentane and ethane could be measured as potential indices of lipid peroxidation in vivo. The tests of induction of lipid peroxidation in rats included injection of iron-dextran and the vitamin E deficiency status. Injection of 460 mg of iron/100 g body wt over a 28-day period increased pentane and ethane production 4- and 6-fold, respectively. Hexanal production was increased 7-fold after injection of 60 mg of iron/100 g body wt, and then it fell back to the preinjection level in spite of continued injection of iron-dextran. Acetone production was lower in iron-injected rats than in controls, and it was ca. 10-fold higher in fasted vitamin E-deficient rats than in vitamin E-supplemented rats, being ca 48 and 5 nmol/100 g/min, respectively. It was observed that halomethane injection did not increase hexanal production, while acetone and pentane production were increased. Pentane and hexanal, but not acetone, were found to arise from decomposition of linoleic acid hydroperoxide in vitro. It was concluded that hydrocarbon gases are better indices of lipid peroxidation than hexanal, which is enzymatically metabolized, and acetone, the production of which is dominated by factors such as altered carbohydrate metabolism.

Acetone↗