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Evaluation of oxidative damage and r...

The University of Texas School of Public Health., Environmental & Occupational Health Sciences.

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Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane./
Author:	Piskac, Amanda L.
Description:	84 p.
Notes:	Adviser: Mary Ann Smith.
Contained By:	Dissertation Abstracts International68-12B.
Subject:	Health Sciences, Occupational Health and Safety. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3295611
ISBN:	9780549404125

Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane.
Piskac, Amanda L.

Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane. - 84 p.

Adviser: Mary Ann Smith.

Thesis (Ph.D.)--The University of Texas School of Public Health, 2007.

Lindane, or gamma-hexachlorocyclohexane, is a chlorinated hydrocarbon pesticide that was banned from U.S. production in 1976, but until recently continued to be imported and applied for occupational and domestic purposes. Lindane is known to cause central nervous system (CNS), immune, cardiovascular, reproductive, liver, and kidney toxicity. The mechanism for which lindane interacts with the CNS has been elucidated, and involves antagonism of the gamma-aminobutyric acid/benzodiazepine (GABAA/BZD) receptor. Antagonism of this receptor results in the inhibition of Cl- channel flux, with subsequent convulsions, seizures, and paralysis. This response makes lindane a desirable defense against arthropod pests in agriculture and the home. However, formulation and application of this compound can contribute to human toxicity. In conjunction with this exposure scenario, workers may be subject to both heat and physical stress that may increase their susceptibility to pesticide toxicity by altering their cellular stress response. The kidneys are responsible for maintaining osmotic homeostasis, and are exposed to agents that undergo urinary excretion. The mechanistic action of lindane on the kidneys is not well understood. Lindane, in other organ systems, has been shown to cause cellular damage by generation of free radicals and oxidative stress. Previous research in our laboratory has shown that lindane causes apoptosis in distal tubule cells, and delays renal stress response under hypertonic stress. Characterizing the mechanism of action of lindane under conditions of physiologic stress is necessary to understand the potential hazard cyclodiene pesticides and other organochlorine compounds pose to exposed individuals under baseline conditions, as well as under conditions of physiologic stress. We demonstrated that exposure to lindane results in oxidative damage and dysregulation of glutathione response in renal distal tubule (MDCK) cells. We showed that under conditions of hypertonic stress, lindane-induced oxidative stress resulted in early onset apoptosis and corresponding down-regulated expression of the anti-apoptotic protein, Bcl-xL. Thus, the interaction of lindane with renal peripheral benzodiazepine receptors (PBR) is associated with attenuation of cellular protective proteins, making the cell more susceptible to injury or death.

ISBN: 9780549404125Subjects--Topical Terms:

1017799
Health Sciences, Occupational Health and Safety.

Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane.
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100 1 $a Piskac, Amanda L. $3 1021719
245 1 0 $a Evaluation of oxidative damage and renal distal tubule cell stress response following exposure to lindane.
300 $a 84 p.
500 $a Adviser: Mary Ann Smith.
500 $a Source: Dissertation Abstracts International, Volume: 68-12, Section: B, page: 7975.
502 $a Thesis (Ph.D.)--The University of Texas School of Public Health, 2007.
520 $a Lindane, or gamma-hexachlorocyclohexane, is a chlorinated hydrocarbon pesticide that was banned from U.S. production in 1976, but until recently continued to be imported and applied for occupational and domestic purposes. Lindane is known to cause central nervous system (CNS), immune, cardiovascular, reproductive, liver, and kidney toxicity. The mechanism for which lindane interacts with the CNS has been elucidated, and involves antagonism of the gamma-aminobutyric acid/benzodiazepine (GABAA/BZD) receptor. Antagonism of this receptor results in the inhibition of Cl- channel flux, with subsequent convulsions, seizures, and paralysis. This response makes lindane a desirable defense against arthropod pests in agriculture and the home. However, formulation and application of this compound can contribute to human toxicity. In conjunction with this exposure scenario, workers may be subject to both heat and physical stress that may increase their susceptibility to pesticide toxicity by altering their cellular stress response. The kidneys are responsible for maintaining osmotic homeostasis, and are exposed to agents that undergo urinary excretion. The mechanistic action of lindane on the kidneys is not well understood. Lindane, in other organ systems, has been shown to cause cellular damage by generation of free radicals and oxidative stress. Previous research in our laboratory has shown that lindane causes apoptosis in distal tubule cells, and delays renal stress response under hypertonic stress. Characterizing the mechanism of action of lindane under conditions of physiologic stress is necessary to understand the potential hazard cyclodiene pesticides and other organochlorine compounds pose to exposed individuals under baseline conditions, as well as under conditions of physiologic stress. We demonstrated that exposure to lindane results in oxidative damage and dysregulation of glutathione response in renal distal tubule (MDCK) cells. We showed that under conditions of hypertonic stress, lindane-induced oxidative stress resulted in early onset apoptosis and corresponding down-regulated expression of the anti-apoptotic protein, Bcl-xL. Thus, the interaction of lindane with renal peripheral benzodiazepine receptors (PBR) is associated with attenuation of cellular protective proteins, making the cell more susceptible to injury or death.
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773 0 $t Dissertation Abstracts International $g 68-12B.
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790 1 0 $a Smith, Mary Ann, $e advisor
790 1 0 $a Waller, Kim $e committee member
791 $a Ph.D.
792 $a 2007
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