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Paper Information

Title: 

THE CELLULAR MECHANISMS INVOLVED IN GLUTAMATE-INDUCED APOPTOTIC CELL DEATH IN NEURONAL CELLS AND ANTI-APOPTOTIC EFFECTS OF EQUINE ESTROGENS IN THIS PROCESS

Type: POSTER
Author(s): CHERAGHI J.,TAATI M.,ROSTAMZADEH A.,KABOUTARI KATAJ J.,ZENDEHDEL KHEYBARI M.,AFKHAMI GOLI A.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Glutamate-induced apoptotic cell death is associated with regulation of genes such as Bcl-2, Bax, and/or caspase-3 and mitochondrial cytochrome c. It is known that glutamate induces cytochrome c release from the mitochondria into the cytoplasm where it activates caspase-3 and causes apoptotic cell death in primary cortical cells via a caspase-dependent pathway. High concentrations (mM) of the excitatory neurotransmitter glutamate can accumulate in the brain and are thought to be involved in the etiology of a number of neurodegenerative disorders including Alzheimer's disease. A number of invitro studies indicate that at high concentrations, glutamate is a potent neurotoxin capable of destroying neurons by apoptosis. Glutamate toxicity appears to involve a rapid Ca2+ influx into neurons and these high levels of intracellular Ca2+ are cytotoxic. Ca2+ can activate several key enzymes, including nitric oxide synthase (NOS) and proteases such as calpains and can also result in mitochondrial dysfunction. Numbers of studies have demonstrated that estrogens are potent antioxidants that can inhibit some of the neurotoxic effects of oxidative stress. Others have reported that estrogens can increase cell survival; indicate that estrogens prevent glutamate-induced cell death by reducing the upregulation and/or translocation of AIF from the mitochondria into the cytosol as well as by attenuating activity of calpain and caspase-3 in primary cortical cells.

 
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