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Oxidant and redox-dependent apoptosi...

Pias, Erin Kathleen.

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Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model./
作者:	Pias, Erin Kathleen.
面頁冊數:	214 p.
附註:	Director: Tak Yee Aw.
Contained By:	Dissertation Abstracts International63-05B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3053159
ISBN:	0493687882

Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model.
Pias, Erin Kathleen.

Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model. - 214 p.

Director: Tak Yee Aw.

Thesis (Ph.D.)--Louisiana State University Health Sciences Center - Shreveport, 2002.

It is known that oxidative stress can induce apoptosis under various circumstances and that reactive oxygen species (ROS) can contribute to this stress. Less is known about how redox imbalance affects apoptosis, either directly or through a ROS intermediate. Also, the role of the overexpression of the superoxide dismutase enzymes (SODS) in apoptosis and its effect on redox balance is analyzed. Thus, the objective of this dissertation is to characterize an oxidant and redox-induced apoptosis in a pheochromocytoma (PC12) cell model, and to compare and contrast this to a second model with either manganese SOD (MnSOD) or copper zinc SOD (CuZnSOD) ovexpressors.

ISBN: 0493687882Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model.
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245 1 0 $a Oxidant and redox-dependent apoptosis and the role of SOD-overexpression in a PC12 cell model.
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500 $a Source: Dissertation Abstracts International, Volume: 63-05, Section: B, page: 2143.
502 $a Thesis (Ph.D.)--Louisiana State University Health Sciences Center - Shreveport, 2002.
520 $a It is known that oxidative stress can induce apoptosis under various circumstances and that reactive oxygen species (ROS) can contribute to this stress. Less is known about how redox imbalance affects apoptosis, either directly or through a ROS intermediate. Also, the role of the overexpression of the superoxide dismutase enzymes (SODS) in apoptosis and its effect on redox balance is analyzed. Thus, the objective of this dissertation is to characterize an oxidant and redox-induced apoptosis in a pheochromocytoma (PC12) cell model, and to compare and contrast this to a second model with either manganese SOD (MnSOD) or copper zinc SOD (CuZnSOD) ovexpressors.
520 $a The first series of studies assessed the effect of oxidant-dependent apoptosis using tert-butyl hydroperoxide (TBH). The results showed an initial early surge in GSSG and caspase-3 and caspase-9 dependent apoptosis that was mediated through numerous mitochondrial sites. The second study exemplified that redox imbalance alone without ROS generation can initiate a surge in oxidized glutathione (GSSG) that subsequently leads to caspase-3 dependent apoptosis. A further exacerbation of redox imbalance with lower glucose increased the kinetics of death and decreased the pool of the essential NADPH cofactor.
520 $a The final study addressed the role of SOD overexpression in TBH-induced apoptosis showing that MnSOD overexpression attenuated TBH-dependent apoptosis while CuZnSOD overexpression exacerbated apoptosis in both stable and transient transfectants. This differential control of apoptosis was mediated by decreased ROS in MnSOD PC12 cells and by increased kinetics of cell death (caspase activation) in CuZnSOD overexpressors. The total glutathione pool in both SOD overexpressors showed an increase in baseline glutathione of stable transfectants, but transiently transfectants showed no such increase. Together, these data imply that SOD isoforms differentially affect apoptosis in PC12 cells, with MnSOD protecting at the ROS level and CuZnSOD inducing death at the caspase and BAX/Bcl-2 level without modifying TBH-induced ROS generation. We deduce that in stable SOD transfectants, apoptosis is independent of glutathione status. Physiologically, it must also be considered that chronic SOD overexpression will have a different effect on glutathione pools than transient SOD upregulation.
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773 0 $t Dissertation Abstracts International $g 63-05B.
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790 1 0 $a Aw, Tak Yee, $e advisor
791 $a Ph.D.
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