2000
DOI: 10.1016/s0039-128x(00)00183-5
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In vitro effects of different steroid hormones on superoxide anion production of human neutrophil granulocytes

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Cited by 100 publications
(36 citation statements)
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“…The lucigenin chemiluminescence measurement showed that ACh-induced formation of superoxide anion was greater in segments from orchidectomized than control rats. This result agrees with a study carried out in mesenteric artery and with previous studies showing the antioxidant properties of androgens (Békési et al 2000, Yorek et al 2002.…”
Section: Discussionsupporting
confidence: 93%
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“…The lucigenin chemiluminescence measurement showed that ACh-induced formation of superoxide anion was greater in segments from orchidectomized than control rats. This result agrees with a study carried out in mesenteric artery and with previous studies showing the antioxidant properties of androgens (Békési et al 2000, Yorek et al 2002.…”
Section: Discussionsupporting
confidence: 93%
“…However, tempol induced slight or strong increase in the vasodilator response to SNP respectively in arteries from control or orchidectomized rats. These results indicate a higher NO metabolism in arteries from orchidectomized rats, as we have found in mesenteric artery and reinforced the described antioxidant properties of androgens (Békési et al 2000, Yorek et al 2002. Additionally, the lack of effect of exogenous SOD would indicate that the predominant isoform involved in this effect would be the cytosolic Cu/Zn-SOD.…”
Section: Discussionsupporting
confidence: 86%
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“…In addition, we observed that superoxide anion negatively modulates the vasodilator response to ACh only in arteries from orchidectomized rats, since SOD, a superoxide anion scavenger, or tempol, a membrane-permeable mimetic of endogenous SOD, increased the relaxation to ACh only in arteries from these rats. These results indicate a greater NO metabolism in arteries from orchidectomized rats and are in line with reports describing the antioxidant properties of androgens (Békési et al 2000, Yorek et al 2002, Martín et al 2005. Additionally, these results also indicate that the localization of the SOD involved in this effect would be predominantly extracellular.…”
Section: Discussionsupporting
confidence: 92%
“…Oxidative stress could be a mechanism involved in progression of cardiovascular disease, in part for the oxidation of LDL-cholesterol [16], and in part for the activation of neutrophils, that contribute to ROS production through NADPH oxidase activation and release of myeloperoxidase, with a vicious circle inducing more toxic oxidant species. This mechanism can be counteracted by testosterone [17].…”
Section: Discussionmentioning
confidence: 99%