[A study of the acting mechanism of aspirin for resistance to oxidative damage].
OBJECTIVE
To explore the mechanism of aspirin for resistance to oxidative damage in endothelial cells.


METHODS
Using cultured endothelial cells, we measured the levels of aspirin induced ferritin expression on resistance to hydrogen peroxide toxicity toward cells in the presence of the iron chelator desferrioxamine added to FeCl3.


RESULTS
Aspirin at low concentration (0.1 mmol/L) induced significant increase of ferritin expression in a time- and concentration-dependent fashion up to 25% over basal levels(P < 0.05). Preincubating the cells for 8 h with aspirin (0.1 mmol/L) reduced lactate dehydrogenase(LDH) release rate by 50%, toxicity reduction by 40%, and significant decrease of malondialdehyde (MDA) production. Aspirin induced cytoprotection from H2O2 damage was also in a concentration- and time-dependent fashion. However, in the presence of the iron chelator desferrioxamine, aspirin enhanced ferritin synthesis was abrogated, in contrast, FeCl3 increased aspirin induced ferritin synthesis in cells.


CONCLUSIONS
The study suggested that the antioxidation of aspirin was brought into action by affecting the cellular iron metabolism pathway to induce ferritin synthesis.
He
Z
Z
Department of Pediatrics, Second Affiliated Hospital, WCUMS, Chengdu 610041, China.
Liao
Q
Q
Xu
X
X
Luo
C
C
Zhou
T
T
Li
Q
Q
Li
F
F
D000975:Antioxidants / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000166:cytology* / Q000378:metabolism; D005293:Ferritins / Q000378:metabolism*; D006801:Humans; D008315:Malondialdehyde / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology
D000975:Antioxidants; D016861:Cyclooxygenase Inhibitors; D008315:Malondialdehyde; D005293:Ferritins; D001241:Aspirin