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Contribution of reactive oxygen spec...

University of the Sciences in Philadelphia.

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Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity./
Author:	Foreman, Brooke D.
Description:	88 p.
Notes:	Adviser: Joan Tarloff.
Contained By:	Masters Abstracts International45-05.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1442974

Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity.
Foreman, Brooke D.

Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity. - 88 p.

Adviser: Joan Tarloff.

Thesis (M.S.)--University of the Sciences in Philadelphia, 2007.

Para-aminophenol (PAP) causes nephrotoxicity, however, its biochemical mechanism is undetermined. PAP can undergo non-enzymatic oxidation to form reactive intermediates, which in turn may potentiate toxicity through redox cycling. By incorporating several scavengers of reactive oxygen species (ROS), this study investigated the role they may play in PAP toxicity in LLC-PK 1 cells. The presence of ROS was seen following treatment with PAP. Several scavengers were then chosen to determine the identity of the ROS. Toxicity was substantially reduced with catalase treatment, while potentiation of toxicity occurred with superoxide dismutase (SOD). These data suggest superoxide anion and hydrogen peroxide are the likely radicals leading to ROS-induced toxicity. In addition, tiron, pyruvate, bathocuproine and 1,10-phenathroline were able to reduce ROS; however, little improvement in cell viability was observed. These data suggest ROS play a role in PAP toxicity; however, these species are not the predominant cause of cellular injury.Subjects--Topical Terms:

1017686
Biology, Cell.

Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity.
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005 20100629
008 100629s2007 ||||||||||||||||| ||eng d
035 $a (UMI)AAI1442974
035 $a AAI1442974
040 $a UMI $c UMI
100 1 $a Foreman, Brooke D. $3 1017851
245 1 0 $a Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity.
300 $a 88 p.
500 $a Adviser: Joan Tarloff.
500 $a Source: Masters Abstracts International, Volume: 45-05, page: 2483.
502 $a Thesis (M.S.)--University of the Sciences in Philadelphia, 2007.
520 $a Para-aminophenol (PAP) causes nephrotoxicity, however, its biochemical mechanism is undetermined. PAP can undergo non-enzymatic oxidation to form reactive intermediates, which in turn may potentiate toxicity through redox cycling. By incorporating several scavengers of reactive oxygen species (ROS), this study investigated the role they may play in PAP toxicity in LLC-PK 1 cells. The presence of ROS was seen following treatment with PAP. Several scavengers were then chosen to determine the identity of the ROS. Toxicity was substantially reduced with catalase treatment, while potentiation of toxicity occurred with superoxide dismutase (SOD). These data suggest superoxide anion and hydrogen peroxide are the likely radicals leading to ROS-induced toxicity. In addition, tiron, pyruvate, bathocuproine and 1,10-phenathroline were able to reduce ROS; however, little improvement in cell viability was observed. These data suggest ROS play a role in PAP toxicity; however, these species are not the predominant cause of cellular injury.
590 $a School code: 1379.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Toxicology. $3 1017752
690 $a 0379
690 $a 0383
710 2 $a University of the Sciences in Philadelphia. $3 1017850
773 0 $t Masters Abstracts International $g 45-05.
790 $a 1379
790 1 0 $a Tarloff, Joan, $e advisor
791 $a M.S.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1442974