These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: The presence of calbindin in rat cortical neurons protects in vitro from oxydative stress. Author: Hugon J, Hugon F, Esclaire F, Lesort M, Diop AG. Journal: Brain Res; 1996 Jan 29; 707(2):288-92. PubMed ID: 8919307. Abstract: Free radicals are highly reactive chemicals containing an unpaired electron and are normally produced by the cellular metabolism. The oxydative stress is defined as a lack of balance between the production of free radicals and the activity of antioxydant metabolites. It induces cellular damages to lipids, proteins and membranes. Abnormal calcium metabolism can be a consequence of oxydative stress leading to increased intracellular concentrations. Calbindin D28K is a calcium binding protein which could have a neuroprotective action against various cellular insults. In this study rat cortical cell cultures were exposed during various times and at different concentrations to the couple Xanthine/Xanthine oxydase (XA/XO), which produces the superoxyde radical O2-.. Neuronal survival revealed that XA/XO is toxic for cortical cell cultures. The Calbindin D28K immunocytochemical study shows that the percentages of Calbindin positive cells are greater in surviving neurons following the XA/XO exposure compared to controls. There is a time-dependent and a dose-dependent relation between the number of surviving neurons and the percentage of Calbindin positive neurons. These results suggest that the presence of cytosolic neuronal Calbindin D28k is associated with a greater resistance to oxydative stress.[Abstract] [Full Text] [Related] [New Search]