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Contribution of reactive oxygen spec...
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University of the Sciences in Philadelphia.
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Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Contribution of reactive oxygen species to para-aminophenol-induced cytotoxicity./
作者:
Foreman, Brooke D.
面頁冊數:
88 p.
附註:
Adviser: Joan Tarloff.
Contained By:
Masters Abstracts International45-05.
標題:
Biology, Cell. -
電子資源:
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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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.
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