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Activation of p38 and changes in mitochondria accompany autophagy to premature senescence-like phenotype switch upon chronic exposure to selenite in colon fibroblasts
E. Rudolf, K. Rezáčová, M. Cervinka,
Language English Country Netherlands
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Enzyme Activation MeSH
- Autophagy drug effects MeSH
- Cell Line MeSH
- Cell Cycle drug effects MeSH
- Time Factors MeSH
- Phenotype MeSH
- Fibroblasts drug effects enzymology pathology MeSH
- Colon drug effects enzymology pathology MeSH
- Humans MeSH
- DNA Methylation drug effects MeSH
- Mitochondria drug effects enzymology pathology MeSH
- p38 Mitogen-Activated Protein Kinases metabolism MeSH
- Oxidative Stress drug effects MeSH
- DNA Damage MeSH
- Cell Proliferation drug effects MeSH
- DNA Replication drug effects MeSH
- Sodium Selenite toxicity MeSH
- Signal Transduction drug effects MeSH
- Cellular Senescence drug effects MeSH
- Transfection MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Effects of chronic exposure to supranutritional sodium selenite (Se) were investigated in colonic fibroblasts. Initially, Se did not produce any gross changes in exposed cells; however, basal levels of autophagy were transiently increased and p38 activity was stimulated. From the 3rd week onwards, Se decreased cell proliferation, with corrensponding changes in cell cycle distribution. Also, in exposed cells oxidative stress and DNA damage slowly but gradually increased along with decreasing mitochondrial function and upon continued elevated activity of p38 kinase. Towards the end of the experiment, premature senescence features became more prominent in treated cells. Pharmacological inhibition as well as gene knockdown of these processes confirmed the involvement of p38 in balancing autophagy and premature senescence in cells exposed to Se and suggests that this element may in a given time frame compromise selected cell populations in digestive system.
References provided by Crossref.org
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- $a Effects of chronic exposure to supranutritional sodium selenite (Se) were investigated in colonic fibroblasts. Initially, Se did not produce any gross changes in exposed cells; however, basal levels of autophagy were transiently increased and p38 activity was stimulated. From the 3rd week onwards, Se decreased cell proliferation, with corrensponding changes in cell cycle distribution. Also, in exposed cells oxidative stress and DNA damage slowly but gradually increased along with decreasing mitochondrial function and upon continued elevated activity of p38 kinase. Towards the end of the experiment, premature senescence features became more prominent in treated cells. Pharmacological inhibition as well as gene knockdown of these processes confirmed the involvement of p38 in balancing autophagy and premature senescence in cells exposed to Se and suggests that this element may in a given time frame compromise selected cell populations in digestive system.
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