The effects of ecdysterone and enalapril on nitric oxide synthesis and the markers of oxidative stress in streptozotocin-induced diabetes in rats: a comparative study.

Cardiovascular functions in diabetes greatly depend on constitutive NOS (cNOS) activity. A comparative study of the effects of a steroid hormone ecdysterone and enalapril, an ACE inhibitor widely used to treat cardiac disorders on cNOS, inducible NOS (iNOS), xanthine oxidoreductase (XOR) activity, RNS, ROS, and lipid peroxidation in heart tissue in experimental diabetes was conducted. The rat model of diabetes was established by streptozotocin injection.

Diazoxide affects mitochondrial bioenergetics by the opening of mKATP channel on submicromolar scale.

Background: Cytoprotection afforded by mitochondrial ATP-sensitive K-channel (mK-channel) opener diazoxide (DZ) largely depends on the activation of potassium cycle with eventual modulation of mitochondrial functions and ROS production. However, generally these effects were studied in the presence of Mg∙ATP known to block K transport. Thus, the purpose of our work was the estimation of DZ effects on K transport, K cycle and ROS production in rat liver mitochondria in the absence of Mg∙ATP.

The Effect Of NO Donor on Calcium Uptake and Reactive Nitrogen Species Production in Mitochondria.

Background/aims: NO and reactive nitrogen species (RNS) are thought to be physiologically important effectors of mitochondrial calcium transport, but this issue was not studied in a living organism. According to literature, the modulation of Ca2+ uptake could influence RNS production via the action on mitochondrial NO synthase (mtNOS). The aim of this work was to study the effect of in vivo administration of NO donor nitroglycerine (NG) on matrix Ca2+ accumulation, RNS production and mtNOS activity.

The effect of atp-dependent potassium uptake on mitochondrial functions under acute hypoxia.

The opening of mitochondrial K(+) АТР-channel (mtK(+) АТР-channel) is supposed to be important in the modulation of mitochondrial functions under hypoxia, but the underlying mechanisms have not been clarified yet. The aim of this work was to study the effect of acute hypoxia on mtK(+) АТР-channel activity and to estimate the contribution of the channel in the modulation of mitochondrial functions. MtK(+) АТР-channel activity was assessed polarographically from the rate of State 4 respiration and by potentiometric monitoring of potassium efflux from deenergized mitochondria.