Mechanism and atomic structure of superoxide dismutase. [1991]

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2018-12-25
Mechanism and atomic structure of superoxide dismutase
Mechanism and atomic structure of superoxide dismutase. [1991];_WJD_2018-1225_V001R01_IR93_
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/1649094
Info cited on 2018-12-25-WD2 (資訊引用於 中華民國107年12月25日) by 湯偉晉 (WeiJin Tang)
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Free Radic Res Commun. 1991;12-13 Pt 1:269-78.
Mechanism and atomic structure of superoxide dismutase.

Mechanism and atomic structure of superoxide dismutase.

Mechanism and atomic structure of superoxide dismutase.
Roberts VA1, Fisher CL, Redford SM, McRee DE, Parge HE, Getzoff ED, Tainer JA.
Author information
1
Department of Molecular Biology, Research Institute of Scripps Clinic, La Jolla, California 92037.
Abstract
The active site Cu ion in Cu,Zn superoxide dismutase is alternately oxidized and reduced during the enzymatic dismutation of superoxide to hydrogen peroxide and molecular oxygen. For oxidized Cu,Zn superoxide dismutase, an atomic structure has been determined for the human enzyme at 2.5 A resolution. The resolution of the bovine enzyme structure has been extended to 1.8 A. Atomic resolution data has been collected for reduced and inhibitor-bound Cu,Zn superoxide dismutases, and the interpretation of the electron density difference maps is in progress. The geometry and molecular surfaces of the active sites in these structures, together with biochemical data, suggest a specific model for the enzyme mechanism. Similarities in the active site geometry of the Mn and Fe superoxide dismutases with the Cu,Zn enzyme suggest that dismutation in these enzymes may follow a similar mechanism.

PMID: 1649094
[Indexed for MEDLINE]
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The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_

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The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_
The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_.docx
The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_

The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_

The effect of aging on glutathione and cysteine levels in different regions of the mouse brain. [1989];_WJD_2018-0102_V001R01_IR93_
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2018-01-02
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/2928355/
Info cited on 2018-01-02-WD2 (資訊引用於 中華民國107年1月2日) by 湯偉晉 (WeiJin Tang)
#

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Proc Soc Exp Biol Med. 1989 Apr;190(4):399-402.
The effect of aging on glutathione and cysteine levels in different regions of the mouse brain.

The effect of aging on glutathione and cysteine levels in different regions of the mouse brain.

The effect of aging on glutathione and cysteine levels in different regions of the mouse brain.
Chen TS1, Richie JP Jr, Lang CA.
Department of Pharmacology, University of Louisville, Kentucky 40292.

Abstract
A general glutathione (GSH) deficiency occurs in many tissues of the aging mouse. However, there is no information on GSH in the aging brain even though it has been involved in a number of neurobiologic reactions. To this end, C57BL/6 mice, 3-31 months old, representing the growth, maturation, and aging periods of the life-span were studied. Brain cortex, hippocampus, and stem samples were dissected, processed, and analyzed specifically for reduced and oxidized glutathione (GSH, GSSG) and cyst(e)ine using high performance liquid chromatography with dual electrochemical detection. The GSH content of each brain region varied in the order brain cortex greater than brain hippocampus greater than brainstem. However, the GSH profiles of all regions were the same through the life-span, namely, high values during growth dropping to a maturation plateau and then decreasing 30% during aging. In contrast to GSH, the order of cysteine levels was brain cortex less than brain hippocampus less than brainstem and no life-span changes occurred in any region. In addition, the brain GSSG and cystine contents of all regions were very low and did not change during the life-span. Thus, the GSH loss was not accountable by oxidation to GSSG or degradation to cyst(e)ine. Altogether these results demonstrated a GSH deficiency in brain tissues of aging mice like that found previously in other tissues. These findings suggest an increased susceptibility of the aging brain to oxidative damage.

PMID: 2928355
[Indexed for MEDLINE]

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