الفهرس 
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Abstract
For long time ischemic renal injury had been considered as a necrotic form of cell death.recently,it has been shown that another type of cell death namely programmed cell death may contribute to ischemic renal injury.apoptosis or programmed cell death is a process in which the cell actively participates in its own demise and is considered operationally,morphologically and biochemically distict from necrotic cell death the present study developed and in-vitro model of ischemic renal injury by exposure of renal tubular epithelial cells(LLC-PK1)to chemical hypoxia.this model was used to examine the role of endonuclease activation,considered a characteristic feature of apoptosis.several scavengers of reactive oxygen metabolites and modulators of extracellular and intracellular calcium were sed to evaluate the role of reactive oxygen metabolites and calcium in DNA damage and cell death during hypoxic injury to LIC-PK1.