A Small Dose of Hydrogen Peroxide Enhances Tumor Necrosis Factor-Alpha Toxicity in Inducing Human Vascular Endothelial Cell Apoptosis: Reversal with Propofol

2006 ◽  
Vol 103 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Tao Luo ◽  
Zhengyuan Xia
Keyword(s):  
Hydrogen Peroxide ◽  
Endothelial Cell ◽  
Tumor Necrosis ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Necrosis Factor Alpha ◽  
Human Vascular Endothelial Cell ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor-alpha augments pulmonary arterial transendothelial albumin flux in vitro

1990 ◽  
Vol 258 (2) ◽  
pp. L57-L67 ◽  
Author(s):  
S. E. Goldblum ◽  
W. L. Sun
Keyword(s):  
Endothelial Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Vascular Endothelial ◽  
Temperature Dependent ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Pulmonary Arterial ◽  
Necrosis Factor

Tumor necrosis factor-alpha (TNF alpha) has been implicated as a mediator of pulmonary vascular endothelial injury. We studied the effect of human recombinant TNF alpha (rTNF alpha) on transfer of 14C-labeled bovine serum albumin (BSA) across cultured bovine pulmonary arterial endothelial cell monolayers. rTNF alpha induced a dose-, time-, and temperature-dependent increment in transendothelial [14C]BSA flux. Only after an incubation time of greater than or equal to 4 h did rTNF alpha significantly (P less than 0.005) increase transendothelial albumin flux. rTNF alpha exposure times as brief as 5 min induced significantly (P less than 0.005) increased albumin transfer at 6 h. Although this initial rTNF alpha-endothelial interaction was not temperature dependent, the subsequent barrier dysfunction could only be generated at 37 degrees C. The rTNF alpha-induced changes could not be ascribed to endothelial cell cytotoxicity and was not blocked by protein synthesis inhibition. The effects of rTNF alpha on endothelial permeability were reversible and not specific for albumin transfer. Therefore, rTNF alpha may influence the movement of macromolecules across the pulmonary vascular endothelial barrier.

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