Abstract
Ischemic and reperfusion injury leads to necrosis and apoptosis. Mitochondrial enzymes and antiapoptotic gene plays an important role in necrosis and apoptosis. The aim of this study was to investigate the role of Bcl-2 expression in alternations in mitochondrial energy regulation during hepatic ischemia and reperfusion and role in necrosis and apoptosis. Total 12 Wistar rats were divided into sham-operated control group (I) and ischemia and reperfusion group (II). Mitochondrial tri carboxylic acid cycles marker enzymes, respiratory marker enzymes, apoptotic cells, necrotic cells and Bcl-2 expression was measured. Number of necrotic and apoptotic cells were increased in ischemic and reperfusion group with reducing tri carboxylic acid cycles marker enzymes, respiratory marker enzymes and decreasing of Bcl-2 expression. On the basis of our findings it may be concluded that suppression of Bcl-2 gene, inhibition of tri carboxylic acid cycles and respiration rate, adenosine tri phosphate production in mitochondria is a pathophysiological consequences which provides a clue for necrosis and apoptosis in hepatic ischemic and reperfusion injury.
Highlights
Bcl-2 is an antiapoptotic gene that was originally found in over expression of B-cell lymphoma[1]
Oxidant stress-induced cytotoxicity is mediated through oxidation of pyridine nucleotides, mitochondrial calcium overload, generation of superoxide radicals, formation of membrane permeability transition pores leading to breakdown of the mitochondrial membrane potential[5]
There are no reports on the relationship between the mitochondrial tri carboxyl pathway (TCA) pathway and apoptosis in ischemia followed by reperfusion injury; in addition, there is a lack of information to correlate Bcl-2 gene expression with TCA pathway during ischemia followed by reperfusion injury
Summary
Bcl-2 is an antiapoptotic gene that was originally found in over expression of B-cell lymphoma[1]. Oxidant stress-induced cytotoxicity is mediated through oxidation of pyridine nucleotides, mitochondrial calcium overload, generation of superoxide radicals, formation of membrane permeability transition pores leading to breakdown of the mitochondrial membrane potential[5]. It has During ischemia, when lack of oxygen inhibits mitochondrial electron transport and mitochondrial generation of ATP, the F F -ATP can in reverse. - August 2010 www.ijpsonline.com obtain insight into between the relations with ischemia -reperfusion induced necrosis and apoptosis specific overexpression of Bcl-2 suppresses cell death as well as well as potential mechanisms by which Bcl-2 might modulate cellular metabolism
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