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The effects of diethyldithiocarbamat...

Mlockier-Audrain, Judith-Ariane.

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The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes./
Author:	Mlockier-Audrain, Judith-Ariane.
Description:	78 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1830.
Contained By:	Dissertation Abstracts International65-04B.
Subject:	Health Sciences, Toxicology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3129186
ISBN:	0496764462

The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes.
Mlockier-Audrain, Judith-Ariane.

The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes. - 78 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1830.

Thesis (Ph.D.)--St. John's University (New York), School of Pharmacy, 2004.

Diethyldithiocarbamate (DDC) is a carbamate derivative and potent metal chelator with documented neurotoxic properties. This may be due to its chelating ability resulting in increased concentrations of intracellular metals or forming disulfide linkages with essential proteins. The mechanism of toxicity of the thiocarbamates remains unknown. Glutathione (GSH) plays an important role in the anti-oxidant defense system. It has been shown that GSH post-treatment protects against DDC insult. In order to examine the effects of DDC and GSH on apoptosis, astrocytes were exposed for 1h to 35mug/ml and 350mug/ml DDC and allowed to recover by subsequent replenished plain media or media containing 10mM GSH. Apoptosis was assessed using various indicators. Results showed that both doses of DDC significantly decreased the cell viability at 24h, 48h and 72h. ELISA and TUNEL were performed at 48h post-treatment and confirmed the induction of apoptosis. Caspase-3, caspase-I (ICE) and c-myc were also significantly increased in the presence of DDC insult and protection was afforded by GSH post-treatment. Bcl-2 and p53 did not show any significant changes in the presence of DDC 24h post-treatment. When cells were post-treated with 10mM GSH, Bcl-2 was statistically significantly increased. We conclude that after an acute DDC insult, cells continue to deteriorate resulting in apoptosis. We further conclude that GSH post-treatment significantly protects against the DDC apoptotic event.

ISBN: 0496764462Subjects--Topical Terms:

1017752
Health Sciences, Toxicology.

The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes.
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100 1 $a Mlockier-Audrain, Judith-Ariane. $3 1900841
245 1 4 $a The effects of diethyldithiocarbamate (DDC) with or without glutathione (GSH) on apoptosis in rat hippocampal astrocytes.
300 $a 78 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1830.
500 $a Adviser: Louis D. Trombetta.
502 $a Thesis (Ph.D.)--St. John's University (New York), School of Pharmacy, 2004.
520 $a Diethyldithiocarbamate (DDC) is a carbamate derivative and potent metal chelator with documented neurotoxic properties. This may be due to its chelating ability resulting in increased concentrations of intracellular metals or forming disulfide linkages with essential proteins. The mechanism of toxicity of the thiocarbamates remains unknown. Glutathione (GSH) plays an important role in the anti-oxidant defense system. It has been shown that GSH post-treatment protects against DDC insult. In order to examine the effects of DDC and GSH on apoptosis, astrocytes were exposed for 1h to 35mug/ml and 350mug/ml DDC and allowed to recover by subsequent replenished plain media or media containing 10mM GSH. Apoptosis was assessed using various indicators. Results showed that both doses of DDC significantly decreased the cell viability at 24h, 48h and 72h. ELISA and TUNEL were performed at 48h post-treatment and confirmed the induction of apoptosis. Caspase-3, caspase-I (ICE) and c-myc were also significantly increased in the presence of DDC insult and protection was afforded by GSH post-treatment. Bcl-2 and p53 did not show any significant changes in the presence of DDC 24h post-treatment. When cells were post-treated with 10mM GSH, Bcl-2 was statistically significantly increased. We conclude that after an acute DDC insult, cells continue to deteriorate resulting in apoptosis. We further conclude that GSH post-treatment significantly protects against the DDC apoptotic event.
590 $a School code: 1377.
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650 4 $a Biology, Neuroscience. $3 1017680
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