Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis
In this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 μmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 μmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-t...
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Series: | Oxidative Medicine and Cellular Longevity |
Online Access: | http://dx.doi.org/10.1155/2013/516051 |
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doaj-650d8ea7f2604356b2da8b591dc2f72e2020-11-24T23:07:06ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942013-01-01201310.1155/2013/516051516051Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell ApoptosisZhang Yiran0Jiang Chenyang1Wang Jiajing2Yuan Yan3Gu Jianhong4Bian Jianchun5Liu Xuezhong6Liu Zongping7College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaCollege of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, ChinaIn this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 μmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 μmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-terminal kinases) inhibitor (SP600125), and extracellular signal-regulated kinase (ERK) inhibitor (U0126) for 30 min, and then treated with 20 μmol/L Cd for 12 h. Cd decreased cell viability, SOD, and GSH-Px activity in a concentration-dependent manner. Increased MDA level, ROS generation, nuclear condensation, shrinkage, and fragmentation in cell morphology were inhibited by NAC. Cd-induced apoptosis was attenuated by pretreatment with SB203580, SP600125, and U0126. The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation. Cd treatment elevated the mRNA levels of Bax and decreased the mRNA levels of Bcl-2, respectively. The same effect was found in their protein expression levels. These results suggest that oxidative stress and MAPK pathways participate in Cd-induced apoptosis and that the balance between pro- and antiapoptotic genes (Bax and Bcl-2) is important in Cd-induced apoptosis.http://dx.doi.org/10.1155/2013/516051 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Zhang Yiran Jiang Chenyang Wang Jiajing Yuan Yan Gu Jianhong Bian Jianchun Liu Xuezhong Liu Zongping |
spellingShingle |
Zhang Yiran Jiang Chenyang Wang Jiajing Yuan Yan Gu Jianhong Bian Jianchun Liu Xuezhong Liu Zongping Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis Oxidative Medicine and Cellular Longevity |
author_facet |
Zhang Yiran Jiang Chenyang Wang Jiajing Yuan Yan Gu Jianhong Bian Jianchun Liu Xuezhong Liu Zongping |
author_sort |
Zhang Yiran |
title |
Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis |
title_short |
Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis |
title_full |
Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis |
title_fullStr |
Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis |
title_full_unstemmed |
Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis |
title_sort |
oxidative stress and mitogen-activated protein kinase pathways involved in cadmium-induced brl 3a cell apoptosis |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2013-01-01 |
description |
In this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 μmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 μmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-terminal kinases) inhibitor (SP600125), and extracellular signal-regulated kinase (ERK) inhibitor (U0126) for 30 min, and then treated with 20 μmol/L Cd for 12 h. Cd decreased cell viability, SOD, and GSH-Px activity in a concentration-dependent manner. Increased MDA level, ROS generation, nuclear condensation, shrinkage, and fragmentation in cell morphology were inhibited by NAC. Cd-induced apoptosis was attenuated by pretreatment with SB203580, SP600125, and U0126. The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation. Cd treatment elevated the mRNA levels of Bax and decreased the mRNA levels of Bcl-2, respectively. The same effect was found in their protein expression levels. These results suggest that oxidative stress and MAPK pathways participate in Cd-induced apoptosis and that the balance between pro- and antiapoptotic genes (Bax and Bcl-2) is important in Cd-induced apoptosis. |
url |
http://dx.doi.org/10.1155/2013/516051 |
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1725620120350359552 |