However, early initiation of chelation has also been associated with DFO toxicity.
2
Herein, we clarify the effect and mechanism of action of DFO on angiogenesis.
3
The DFO must be selected from the ranks of SAA pilots.
4
None of the patients who attained final height had signs of DFO bone toxicity.
5
UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment.
1
Reduction of iron load, achieved by regular desferrioxamine infusion, resulted in normalisation of the urinary enzyme levels.
2
In the presence of desferrioxamine, adriamycin semiquinone does not disappear in the presence of hydrogen peroxide at a detectable rate.
3
No significant changes in the degree of IRI or AR were observed in the groups treated with desferrioxamine or melatonin.
4
In our study, treatment with the antioxidants melatonin or desferrioxamine before reperfusion had no effects on IRI damage or on AR frequency or severity.
1
Both NO inhibition and iron scavenging, using deferoxamine administration, reduced hydroxyl radical levels and neuronal cell death.
2
Likewise, depletion of iron by deferoxamine during induction of HO-1 by cobalt-protoporphyrin IX did not restore HCV replication.
3
DFE was 10 times more potent and more rapid in onset of effect than the clinically used iron chelator deferoxamine.
4
This increase was not significantly altered by SOD or deferoxamine, nor was it different from the mortality observed in air-exposed cells.
5
In patients previously exposed to aluminum, a deferoxamine test should be performed and a deferoxamine treatment started if the test is positive.