2013
DOI: 10.1016/j.toxlet.2013.02.003
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JNK and p38 MAPK regulate oxidative stress and the inflammatory response in chlorpyrifos-induced apoptosis

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Cited by 171 publications
(97 citation statements)
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“…A previous study demonstrated that various stress stimuli, including the oxidative stress caused by ROS, may induce potential activation of MAPK signaling pathways (24). In addition, the activation of JNK contributes to stress-induced apoptosis (25). p38 MAPK has been demonstrated to either promote apoptosis or enhance cell survival depending on the cell type and stimulus (26,27).…”
Section: Discussionmentioning
confidence: 99%
“…A previous study demonstrated that various stress stimuli, including the oxidative stress caused by ROS, may induce potential activation of MAPK signaling pathways (24). In addition, the activation of JNK contributes to stress-induced apoptosis (25). p38 MAPK has been demonstrated to either promote apoptosis or enhance cell survival depending on the cell type and stimulus (26,27).…”
Section: Discussionmentioning
confidence: 99%
“…COX-2 drives the inflammatory response and is implicated in some mechanisms of cell death. 35 Amfenac amide is a prodrug that is converted to amfenac by intraocular hydrolases. Amfenac inhibits both cyclooxygenase COX-1 and COX-2 activity.…”
Section: Discussionmentioning
confidence: 99%
“…Zhou et al [16] showed that the disruption of intestinal epithelial cell was closely related to apoptosis and oxidative damage in rats. Studies revealed that the gene expression of TJs, apoptosis and antioxidant capacity could be regulated by myosin light chain kinase (MLCK) [17], c-Jun N-terminal protein kinase (JNK) [18] and NF-E2-related factor 2 (Nrf2) [19] in humans, respectively. However, no study has addressed the effects of dietary proteins on the intestinal physical barriers and its possible mechanism in fish.…”
Section: Introductionmentioning
confidence: 99%