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MEMBRANE LIPID PEROXIDATION: PROPAG...

LEUNG, HON-WING.

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MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS./
作者:	LEUNG, HON-WING.
面頁冊數:	141 p.
附註:	Source: Dissertation Abstracts International, Volume: 42-04, Section: B, page: 1417.
Contained By:	Dissertation Abstracts International42-04B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8122381

MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS.
LEUNG, HON-WING.

MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS. - 141 p.

Source: Dissertation Abstracts International, Volume: 42-04, Section: B, page: 1417.

Thesis (Ph.D.)--University of Rochester, 1981.

Peroxidation of the membrane polyunsaturated lipids is believed to be the mechanism of toxicity for many xenobiotics. Vitamin E protects against lipid peroxidation by scavenging free radicals. It has been proposed that ascorbate may reduce (alpha)-tocopherol radicals produced in the inhibition of lipid peroxidation, such that the relatively large reducing potential of cellular ascorbate could be efficiently delivered to lipid radicals via the lipid-soluble (alpha)-tocopherol. In order to evaluate the importance of this interaction between ascorbate and (alpha)-tocopherol in protecting against membrane lipid peroxidation, peroxidation studies in microsomes and liposomes were performed. The time course of microsomal lipid peroxidation induced by FeSO(,4) in the presence of ascorbate exhibited a delay in the onset of peroxidation consistent with an antioxidant function of ascorbate, possibly mediated through endogenous Vitamin E. At pH 5, where ferrous iron was stabilized, both Vitamin C and Vitamin E showed a dose-dependent inhibition of peroxidation in liposomes, but Vitamin E was about 40 times as effective as Vitamin C as an antioxidant. When both Vitamin E and Vitamin C were present together in the same liposome system, peroxidation was inhibited more effectively than the sum of either vitamin alone. These data suggest that interaction between the two antioxidants yields an enhanced delivery of antioxidant protection.Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS.
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245 1 0 $a MEMBRANE LIPID PEROXIDATION: PROPAGATION AND INHIBITION BY ANTIOXIDANTS.
300 $a 141 p.
500 $a Source: Dissertation Abstracts International, Volume: 42-04, Section: B, page: 1417.
502 $a Thesis (Ph.D.)--University of Rochester, 1981.
520 $a Peroxidation of the membrane polyunsaturated lipids is believed to be the mechanism of toxicity for many xenobiotics. Vitamin E protects against lipid peroxidation by scavenging free radicals. It has been proposed that ascorbate may reduce (alpha)-tocopherol radicals produced in the inhibition of lipid peroxidation, such that the relatively large reducing potential of cellular ascorbate could be efficiently delivered to lipid radicals via the lipid-soluble (alpha)-tocopherol. In order to evaluate the importance of this interaction between ascorbate and (alpha)-tocopherol in protecting against membrane lipid peroxidation, peroxidation studies in microsomes and liposomes were performed. The time course of microsomal lipid peroxidation induced by FeSO(,4) in the presence of ascorbate exhibited a delay in the onset of peroxidation consistent with an antioxidant function of ascorbate, possibly mediated through endogenous Vitamin E. At pH 5, where ferrous iron was stabilized, both Vitamin C and Vitamin E showed a dose-dependent inhibition of peroxidation in liposomes, but Vitamin E was about 40 times as effective as Vitamin C as an antioxidant. When both Vitamin E and Vitamin C were present together in the same liposome system, peroxidation was inhibited more effectively than the sum of either vitamin alone. These data suggest that interaction between the two antioxidants yields an enhanced delivery of antioxidant protection.
520 $a It has further been proposed that ascorbate and glutathione are in redox balance. Experiments were, therefore, conducted to examine the significance of their interaction. In vitro equilibrium studies indicated that glutathione could reduce dehydroascorbate to a slight extent, but ascorbate could not reduce oxidized glutathione disulfide. NO(,2) oxidized ascorbate 11 times faster than glutathione. Similarly, the guinea pig lung levels of glutathione and ascorbate was lowered by NO(,2) exposure. Diethyl maleate treatment decreased the lung glutathione concentration but the ascorbate concentration was unaffected. Simultaneous exposure of the glutathione-deficient animals to NO(,2) resulted in a further depression of lung glutathione concentration, but the ascorbate concentration was decreased to an extent identical to that of the NO(,2)-exposed animal. The data, therefore, suggest that the reduction of oxidized ascorbate is not mediated by glutathione. The two reductants probably operate independently during oxidant stress.
520 $a One of the major products of lipid peroxidation is the highly toxic lipid hydroperoxide, which may be detoxified enzymatically with the glutathione peroxidases. It is also believed that lipid hydroperoxides can be decomposed by metal ions and hemoproteins to secondary free-radical products that can initiate lipid peroxidation. Such branching reactions, which may increase the rate of lipid free-radical formation, has been referred to as propagation. In order to fully understand the basic mechanism of the propagation of lipid peroxidation, the non-enzymatic decomposition of linoleate hydroperoxide was studied. Free ferrous iron decomposed linoleate hydroperoxide and chelation with EDTA completely prevented decomposition. Liposomes incubated with FeSO(,4) and linoleate hydroperoxide peroxidized more rapidly than when FeSO(,4) alone was present, indicative of a propagating role for the alkoxy radical. Addition of EDTA completely inhibited lipid peroxidation. In contrast to linoleate hydroperoxide, the decomposition of hydrogen peroxide by FeSO(,4) did not stimulate liposomal peroxidation, thus negating a role for hydroxyl radical as an initiator of lipid peroxidation.
590 $a School code: 0188.
650 4 $a Health Sciences, Pharmacology. $3 1017717
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710 2 0 $a University of Rochester. $3 515736
773 0 $t Dissertation Abstracts International $g 42-04B.
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791 $a Ph.D.
792 $a 1981
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8122381