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Inhibition of human neutrophil oxidative burst by pyrazolone derivatives

Title
Inhibition of human neutrophil oxidative burst by pyrazolone derivatives
Type
Article in International Scientific Journal
Year
2006
Authors
Costa, D
(Author)
Other
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Marques, AP
(Author)
Other
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Reis, RL
(Author)
Other
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Fernandes, E
(Author)
FFUP
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Journal
Vol. 40 No. 4
Pages: 632-640
ISSN: 0891-5849
Publisher: Elsevier
Scientific classification
FOS: Medical and Health sciences > Clinical medicine
Other information
Authenticus ID: P-004-N8V
Abstract (EN): The risk of agranulocytosis associated with the use of pyrazolone drugs at therapeutical doses and for short periods of time has been considered to be very low. However, little or no attention at all has been devoted to the possible hindrance of neutrophil burst and scavenging of neutrophil-generated reactive oxygen species (ROS) by these compounds. Such an effect could be beneficial in the case of overactivation of neutrophils but could also be highly detrimental if the number of circulating neutrophils is already decreased. Thus, the aim of the present study was to evaluate the putative inhibitory effect of the pyrazolones dipyrone, aminopyrine, isopropylantipyrine, and antipyrine against human neutrophil burst and their scavenging activity against O-2(center dot-), H2O2, HO center dot, ROO center dot, and HOCl. The obtained results showed that dipyrone and aminopyrine prevent phorbol-12-myristate-13-acetate-induced neutrophil burst with high efficiency, while isopropylantipyrine had little effect and antipyrine had no effect at all. Dipyrone and aminopyrine were highly potent scavengers of HO center dot and HOCl, while, in accordance with the neutrophil burst results, isopropylantipyrine had little effect and antipyrine had no effect at all against these two ROS. None of the studied pyrazolones was capable of scavenging O2(center dot-) or H2O2, while dipyrone was shown to be the most reactive against ROO center dot.
Language: English
Type (Professor's evaluation): Scientific
Contact: egracas@ff.up.pt
No. of pages: 9
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