Прегледај по Аутор "Milovanovic, Slobodan"

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    Fullerenol C60(OH)24 nanoparticles decrease relaxing effects of dimethyl sulfoxide on rat uterus spontaneous contraction
    (Springer, 2013) Slavic, Marija; Djordjevic, Aleksandar; Radojicic, Ratko; Milovanovic, Slobodan; Orescanin-Dusic, Zorana; Rakocevic, Zlatko; Spasic, Mihajlo B.; Blagojevic, Dusko
    Dimethyl sulfoxide (DMSO) is a widely used solvent and cryoprotectant that can cause impaired blood flow, reduction in intracranial pressure, tissue edema, inflammatory reactions, inhibition of vascular smooth muscle cell migration and proliferation, processes which can lead to atherosclerosis of the coronary, peripheral and cerebral circulation. Although the adverse effects are rare when DMSO is administered in clinically established concentrations, there is no safe antagonist for an overdose. In this work, we treated isolated spontaneous and calciuminduced contractile active rat uteri (Wistar, virgo intacta), with DMSO and fullerenol C60(OH)24 nanoparticle (FNP) in DMSO. FNP is a water-soluble derivative of fullerene C60. Its size is a 1.1 nm in diameter and is a very promising candidate for a drug carrier in nanomedicine. FNP also displays free radical scavenging activity. DMSO decreased both spontaneous and calcium-induced contractions. In contrast, FNP only decreased spontaneous contraction. FNP decreased copper–zinc superoxide dismutase activity and prevented the DMSO-induced increase in glutathione reductase activity. Atomic force microscopy detected that FNP aggregated with calcium ions. Our results indicate that FNP has properties that make it a good candidate to be a modulator of DMSO activity which could minimize side effects of the latter.
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    Reversible Oxidation ofMyometrial Voltage-Gated Potassium Channels with Hydrogen Peroxide
    (Hindawi, 2012) Appiah, Isabella; Nikolic-Kokic, Aleksandra; Orescanin-Dusic, Zorana; Radojicic, Ratko; Milovanovic, Slobodan; Spasic, Mihajlo; Blagojevic, Dusko
    The uteri, spontaneously active or Ca2+ (6mM) induced, were allowed to equilibrate, and to inhibit voltage-gated potassium (KV ) channels 1mM4-amino pyridine (4-AP) was applied for 15 min before addingH2O2 . H2O2 was added cumulatively: 2 μM, 20 μM, 200 μM, 400 μM, and 3mM. Average time for H2O2 concentrations (2, 20, 200, and 400) μM to reach its full effect was 15 min. H2O2 3mMhad a prolonged effect and therefore was left to act for 30 min. Two-way ANOVA showed significant differences in time dependency between spontaneous and Ca2+-induced rat uteri after applying 3mMH2O2 (type of contraction, P = 0.0280), but not 400 μMH2O2 (P = 0.9271). Our results indicate that H2O2 oxidises channel intracellular thiol groups and activates the channel, inducing relaxation. Cell antioxidative defence system quickly activates glutathione peroxidase (GSHPx) defence mechanism but not catalase (CAT) defence mechanism. Intracellular redox mechanisms repair the oxidised sites and again establish deactivation of KV channels, recuperating contractility. In conclusion, our results demonstrate that KV channels can be altered in a timedependent manner by reversible redox-dependent intracellular alterations.
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    The Effect of Potassium Channel Opener Pinacidil on the Non-Pregnant Rat Uterus
    (Wiley, 2007) Novakovic, Radmila; Milovanovic, Slobodan; Protic, Dragana; Djokic, Jelena; Heinle, Helmut; Gojkovic-Bukarica, Ljiljana
    The effects of the K+ channel opener, pinacidil on the spontaneous rhythmic contractions and contractions provoked by electrical field stimulation (50 Hz) or by oxytocin were investigated in the isolated uterus of the non-pregnant rat in oestrus. Pinacidil produced more potent inhibition of oxytocin-elicited contractions than of spontaneous rhythmic contractions or electrical field stimulation-induced contractions. Glibenclamide, a selective blocker of adenosine triphosphate (ATP)-sensitive K+ (KATP) channels, antagonized the pinacidil-induced inhibition of contractions elicited by oxytocin in a competitive manner. However, the pinacidil-induced inhibition of electrical field stimulation-elicited contractions and spontaneous rhythmic contractions was antagonized non-competitively by glibenclamide. In the uterine strips precontracted with 80 mM K+, the pinacidil-induced maximal relaxation was not affected. The present data show that pinacidil exhibits potent relaxant properties in the rat non-pregnant uterus in oestrus and therefore should be taken into account as a possible agent for treatment of dysmenorrhoea. Based on glibenclamide affinity, it appears that the inhibitory response to pinacidil involves KATP channels. We need further investigations to explain why the interaction between glibenclamide and pinacidil in this experimental model depends on the nature of contractions. The ability of pinacidil to completely relax the rat non-pregnant uterus pre-contracted with K+ -rich solution suggests that K+ channel-independent mechanism(s) also play a part in its relaxant effect.