Figure 1532

The importance of the cytosolic phospholipase A2 in oxidant injury. A, Time-dependent release of arachidonic acid (AA) from LLC-PKj cells exposed to hydrogen peroxide (0.5 mM). B and C, The concentration-dependent effects of hydrogen peroxide on LLC-PKj cell death (using lactate dehydrogenase [LDH] release as marker) after 3 hours' exposure. Cells were transfected with 1) the cytosolic PLA2 (LLC-cPLA2), 2) the secretory PLA2 (LLC-sPLA2), 3) vector (LLC-vector), or 4) were not transfected (LLC-PKj). Cells transfected with cytosolic PLA2 exhibited greater AA release and cell death in response to oxidant exposure than cells transfected with the vector or secretory PLA2 or not transfected. These results suggest that activation of cytosolic PLA2 during oxidant injury contributes to cell injury and death. (From Sapirstein et al. [15]; with permission.)

Inhibitor 1 is IL-1ß converting enzyme inhibitor 1 (YVAD-CHO) and inhibitor II is CPP32/apopain inhibitor (DEVD-CHO). These results suggest that caspases are activated after mitochondrial inhibition and that caspases may contribute to antimycin A-induced DNA damage and cell death. (From Kaushal et al. [16]; with permission.)

Potential role of caspases in cell death in LLC-PK1 cells exposed to antimycin A. A, Time-dependent effects of antimycin A treatment on caspase activity in LLC-PKj cells. B, C, The effect of two capase inhibitors on antimycin A-induced DNA damage and cell death, respectively. Antimycin A is an inhibitor of mitochondrial electron transport.

Inhibitor 1 is IL-1ß converting enzyme inhibitor 1 (YVAD-CHO) and inhibitor II is CPP32/apopain inhibitor (DEVD-CHO). These results suggest that caspases are activated after mitochondrial inhibition and that caspases may contribute to antimycin A-induced DNA damage and cell death. (From Kaushal et al. [16]; with permission.)

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