[New antioxidants as neuroprotective agents for the treatment of ischemic brain injury and neurodegenerative diseases].

Central nervous system disorders are the leading cause of mortality and disability in the world. Unfortunately, the possibility of pathogenetic therapy is limited and it is important to search for new drugs with neuroprotective mechanism of action. One of the most promising groups of drugs are antioxidants--substances that can neutralize free radicals and reduce oxidative stress.

[Intravenous injection of coenzyme Q10 increases its level in rat brain].

It is established that intravenous injection of solubilized coenzyme Q10 provides quick and lasting increase in its level in the brain as compared to control intact rats and those with cerebral ischemia. These new data provide a basis for studying the efficacy of coenzyme Q10 as a neuroprotective agent in ischemic stroke.

[Effect of coenzyme Q10 on rat myocardiumin the acute stage of experimental infarction].

The influence of coenzyme Q10 (CoQ10) on early ischemic deterioration was studied on Wistar rats with experimental myocardial infarction. CoQ10 (30 mg/kg) was injected intravenously 10 min after coronary artery occlusion, and morphometric analysis was performed for 72 h after the onset of ischemia. CoQ10-treated rats had restricted total myocardial damage (by 52%), including areas of necrosis (by 84%) and areas of cellular inflammatory infiltration (by 38%) as compared to saline-treated rats (p < 0.

[Coenzyme Q10 single intravenous infusion protects rat myocardium against subsequent ischemia/reperfusion].

Cardioprotective effects of coenzyme Q10 (CoQ10) injected intravenously 30 min before coronary artery occlusion were assessed on the model of myocardial ischemia/reperfusion in Wistar rats. Rats treated with CoQ10 after 30 min of ischemia and 120 min of reperfusion exhibited smaller (by 35%, p < 0.01) size of irreversibly damaged myocardium, shorter duration and decreased number of arrhythmias during reperfusion, and increased content of myocardial CoQ10 (by 210%, p < 0.

[Depression as a side effect of alpha-interferon: mechanisms of development and criteria for experimental evaluation].

Possible mechanisms of the development of depression as a side effect of the a-interferon are reviewed. Methods used for the characterization of depressive states in experiment are considered.