Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Borovic, S; Cipak, A; Meinitzer, A; Kejla, Z; Perovic, D; Waeg, G; Zarkovic, N.
Differential sensitivity to 4-hydroxynonenal for normal and malignant mesenchymal cells.
Redox Rep. 2007; 12(1): 50-54.
Doi: 10.1179/135100007X162194
Web of Science
PubMed
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- Co-Autor*innen der Med Uni Graz
- Meinitzer Andreas
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- Abstract:
- Normal and malignant cells of various origin differ in their sensitivity to oxidative stress. Therefore, we used normal and malignant mesenchymal cells--human osteosarcoma cells (HOS and 143B), human fibroblasts (WI38) and two primary cultures of normal human osteoblasts to test sensitivity to reactive aldehyde 4-hydroxynonenal (HNE), known as a second messenger of free radicals and a signaling molecule. Upon HNE-treatment, decrease in cell viability (by Trypan-blue), apoptosis induction (by TiterTACS TUNEL assay), HNE-protein binding (by HNE-His ELISA) were higher in malignant than in normal cells, while glutathione content was higher in normal cells. These results indicate that HNE affects the growth of malignant mesenchymal cells more than normal and that this effect was mainly related to lower glutathione concentration and higher binding of HNE to the cellular proteins. We thus assume that HNE and GSH homeostasis play an important role in the growth regulation of normal and malignant mesenchymal cells.
- Find related publications in this database (using NLM MeSH Indexing)
- Aldehydes - toxicity
- Apoptosis - drug effects
- Bone Neoplasms - pathology
- Cell Line, Tumor - pathology
- Cell Survival - drug effects
- Fibroblasts - drug effects
- Humans - drug effects
- Mesoderm - drug effects
- Neoplasm Proteins - drug effects
- Osteosarcoma - pathology
- Proteins - drug effects
- Reference Values - drug effects
- Find related publications in this database (Keywords)
- 4-hydroxynonenal
- mesenchymal cells
- human osteosarcoma
- human osteoblasts
- apoptosis
- HNE-His ELISA
- glutathione