17-ß-estradiol Decreases Neutrophil Superoxide Production through Rac1.

Neutrophil granulocytes form the biggest free radical producing system of the human body. The importance of this system in atherosclerotic plaque formation and other free radical mediated disorders is confirmed by both in vivo and in vitro studies. Estrogen's effect on free radical production involves multiple estrogen receptors and occurs both on transcriptional and on protein phosphorylational level. Estrogen decreases the superoxide production of neutrophil granulocytes in such a short time frame it is unlikely to be mediated by transcription regulation. We investigated the underlying mechanism through which the mentioned estrogen effect takes place using an immunabsorption-based method. Phosphorylation data of 43 different messenger proteins were used for pathway analysis. The newly identified pathway involved largely second messengers from previously described non-genomic estrogen effects and affected superoxide production via Rac1 - an important regulator of free radical production and chemotaxis. Selective inhibition of the participating second messengers altered superoxide production in the predicted direction confirming that this pathway is at least partly responsible for the effect of 17-ß-estradiol on chemoattractant induced superoxide production.

Increased total scavenger capacity in rats fed corticosterone and cortisol on lipid-rich diet.

BACKGROUND: In our earlier studies both corticosterone and cortisol had antioxidant effect in vitro. OBJECTIVES: Our aim was to clarify whether corticosterone and cortisol oral administration results in beneficial antioxidant changes in Sprague-Dawley adult male rats in vivo. METHODS: Experimental animals were fed a lipid rich diet and treated with corticosterone or cortisol in the drinking fluid. Control group was fed only lipid rich diet with untreated drinking water. The untreated group was feda normal diet with untreated water. Total scavenger capacity (TSC) was measured before and after 4 weeks of treatment in blood samples using a chemiluminometric assay. RESULTS: Both corticosterone and cortisol treatment caused increased TSC. The control group and the untreated group showed no significant changes in TSC. CONCLUSION: Our results support the hypothesis that corticosterone and cortisol administration can improve the antioxidant status not only in vitro but also in vivo.