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The effect of cytokines on hepatocyt...

Duval, Dawn Louise.

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The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction./
Author:	Duval, Dawn Louise.
Description:	134 p.
Notes:	Source: Dissertation Abstracts International, Volume: 56-03, Section: B, page: 1282.
Contained By:	Dissertation Abstracts International56-03B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9524658

The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction.
Duval, Dawn Louise.

The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction. - 134 p.

Source: Dissertation Abstracts International, Volume: 56-03, Section: B, page: 1282.

Thesis (Ph.D.)--University of Nevada, Reno, 1994.

Tumor necrosis factor-Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction.
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008 130610s1994 eng d
035 $a (UnM)AAI9524658
035 $a AAI9524658
040 $a UnM $c UnM
100 1 $a Duval, Dawn Louise. $3 1908354
245 1 4 $a The effect of cytokines on hepatocytes: The role of reactive oxygen intermediates and glutathione in nitric oxide synthase induction.
300 $a 134 p.
500 $a Source: Dissertation Abstracts International, Volume: 56-03, Section: B, page: 1282.
500 $a Adviser: Ruth E. Billings.
502 $a Thesis (Ph.D.)--University of Nevada, Reno, 1994.
520 $a Tumor necrosis factor- $\ alpha $ (TNF $\ alpha $) is a macrophage-released cytokine identified for its tumor cytotoxic effects. However, cancer immunotherapy with TNF $\ alpha $ is limited by hepatotoxicity and hypotensive shock. TNF $\ alpha $ is a major cytotoxic mediator of inflammatory liver injury initiated by ischemia-reperfusion, sepsis, and chemical exposure. TNF $\ alpha $ treatment has been shown to promote oxidative stress, mitochondrial dysfunction, induction of proteins including nitric oxide synthase, liver regeneration, and apoptotic cell death.
520 $a The direct effects of TNF $\ alpha $ were explored in primary cultures of rat hepatocytes. Interferon $\ gamma $ (IFN $\ gamma $) was used to potentiate the effects of TNF $\ alpha $. This model was characterized by rapid increases in ATP, followed by a gradual increase in extracellular oxidized glutathione indicative of oxidative stress. Increased oxygen radical generation was measured in mitochondria isolated from treated hepatocytes. Cytotoxicity (as compared to reparable damage) was only induced in the presence of cycloheximide, a protein synthesis inhibitor, or actinomycin D, an inhibitor of transcription. TNF $\ alpha $ and IFN $\ gamma $ were potent inducers of nitric oxide synthase (NOS) in hepatocytes. While the release of nitric oxide into the extracellular environment may subsequently influence cytotoxicity, NOS did not directly contribute to (or protect hepatocytes from) cytotoxicity.
520 $a Hepatocyte NOS activity and induction were profiled. Hepatic induced nitric oxide synthase is a cytosolic enzyme with an activity profile similar to the macrophage nitric oxide synthase. While IFN $\ gamma $ and endotoxin were relatively ineffective inducers of nitric oxide synthase, TNF $\ alpha $ and interleukin-1 $\ beta $ (IL-1 $\ beta $) were potent stimulators. NOS induction by TNF $\ alpha $ and IFN $\ gamma $ was maximal by 10 hours and maintained through 24 hours.
520 $a The regulation of hepatocyte nitric oxide synthase mRNA, immunoreactive protein, and activity were examined. Both antioxidants and glutathione-depleting agents blocked TNF $\ alpha $ induction of NOS. This blockade indicated that NOS induction was dependent upon the generation of reactive oxygen intermediates (ROI) and cellular levels of reduced glutathione. Inhibition of NOS induction by the complex I inhibitor, rotenone, suggested that one source of ROI was the mitochondrial electron transport chain. The extracellular xanthine/xanthine oxidase superoxide generating system also induced NOS. These studies examine the induction of NOS by cytokines and link ROI generation and reduced glutathione levels with the induction of nitric oxide synthase by TNF $\ alpha $.
590 $a School code: 0139.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0433
690 $a 0379
690 $a 0419
710 2 0 $a University of Nevada, Reno. $3 626634
773 0 $t Dissertation Abstracts International $g 56-03B.
790 1 0 $a Billings, Ruth E., $e advisor
790 $a 0139
791 $a Ph.D.
792 $a 1994
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9524658