HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Scavenging system efficiency is crucial for cell resistance to ROS-mediated methylglyoxal injury.

Abstract
Methylglyoxal is a reactive dicarbonyl compound endogenously produced mainly from glycolytic intermediates. Recent research indicates that methylglyoxal is a potent growth inhibitor and genotoxic agent. The antiproliferative activity of methylglyoxal has been investigated for pharmacological application in cancer chemotherapy. However, various cells are not equally sensitive to methylglyoxal toxicity. Therefore, it would be important to establish the cellular factors responsible for the different cell-type specific response to methylglyoxal injury, in order to avoid the risk of failure of a therapy based on increasing the intracellular level of methylglyoxal. To this purpose, we comparatively evaluated the signaling transduction pathway elicited by methylglyoxal in human glioblastoma (ADF) and neuroblastoma (SH-SY 5Y) cells. Results show that methylglyoxal causes early and extensive reactive oxygen species generation in both cell lines. However, SH-SY 5Y cells show higher sensitivity to methylglyoxal challenge due to a defective antioxidant and detoxifying ability that, preventing these cells from an efficient scavenging action, elicits extensive caspase-9 dependent apoptosis. These data emphasize the pivotal role of antioxidant and detoxifying systems in determining the grade of sensitivity of cells to methylglyoxal.
AuthorsFernanda Amicarelli, Sabrina Colafarina, Franca Cattani, Annamaria Cimini, Carmine Di Ilio, Maria Paola Ceru, Michele Miranda
JournalFree radical biology & medicine (Free Radic Biol Med) Vol. 35 Issue 8 Pg. 856-71 (Oct 15 2003) ISSN: 0891-5849 [Print] United States
PMID14556850 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Free Radical Scavengers
  • NF-kappa B
  • Reactive Oxygen Species
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Pyruvaldehyde
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Thiolester Hydrolases
  • hydroxyacylglutathione hydrolase
  • Caspases
  • Lactoylglutathione Lyase
  • Glutathione Synthase
Topics
  • Apoptosis
  • Caspases (metabolism)
  • Catalase (metabolism)
  • Free Radical Scavengers
  • Glioblastoma (drug therapy, metabolism)
  • Glutathione Peroxidase (metabolism)
  • Glutathione Synthase (metabolism)
  • Humans
  • Lactoylglutathione Lyase (metabolism)
  • NF-kappa B (metabolism)
  • Neuroblastoma (drug therapy, metabolism)
  • Pyruvaldehyde (toxicity)
  • Reactive Oxygen Species (metabolism)
  • Receptors, Cytoplasmic and Nuclear (metabolism)
  • Signal Transduction
  • Superoxide Dismutase (metabolism)
  • Thiolester Hydrolases (metabolism)
  • Transcription Factors (metabolism)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: