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Background and objective: One of the reasons for thrombosis in chronic heart failure (CHF) might be reactive forms of oxygen activating platelets. The aim of this study was to evaluate the effect of oxidant hypochlorous acid (HOCl) on platelet aggregation and dityrosine concentration in CHF patients and healthy controls. Materials and Methods: CHF patients (n = 67) and healthy (n = 31) were investigated. Heart echoscopy, 6-min walking test, complete blood count, platelet aggregation, and dityrosine concentration were performed. Platelet aggregation and dityrosine concentration were measured in plasma samples after incubation with different HOCl concentrations (0.15, 0.0778, and 0.0389 mmol/L). Results: Platelet aggregation without oxidant was lower (p = 0.049) in CHF patients than in controls. The spontaneous platelet aggregation with oxidant added was higher in CHF patients (p = 0.004). Dityrosine concentration was also higher (p = 0.032) in CHF patients. Platelet aggregation was the highest in samples with the highest oxidant concentration in both healthy controls (p = 0.0006) and in CHF patients (p = 0.036). Platelet aggregation was higher in NYHA III group in comparison to NYHA II group (p = 0.0014). Concentration of dityrosine was significantly higher in CHF samples (p = 0.032). The highest concentration of dityrosine was obtained in NYHA IV group samples (p < 0.05). Intensity of platelet aggregation, analyzed with ADP, was correlated with LV EF (r = 0.42, p = 0.007). Dityrosine concentration was correlated with NYHA functional class (r = 0.27, p < 0.05). Conclusions: The increase in platelet aggregation in CHF and healthy controls shows the oxidant effect on platelets. The increase in dityrosine concentration in higher NYHA functional classes shows a higher oxidative stress in patients with worse condition.

Background and objective: An association between coronary artery disease (CAD) and agerelated macular degeneration (ARMD) has long been postulated, but exact mechanisms remain unclear. The global prevalence of CAD and ARMD increases and early biomarkers for early diagnosis of these diseases are necessary. The aim of this study was to investigate the plasma level of oxidative stress biomarker CML in patients with and without angiographic findings of atherosclerosis in the coronary arteries (CADath+ and CADath, respectively) and to assess if there was an association of CAD with ARMD. Materials and methods: The study enrolled 233 subjects. Based on cardiologic and ophthal- mologic examinations, the patients were divided into four subgroups: CADath+ARMD+, CADath+ARMD−, CADath−ARMD+, and CADath−ARMD−. The enzyme-linked immunosorbent assay was used for the measurement of plasma CML levels. Serum lipid levels were determined by an automatic analyzer using conventional enzymatic methods. Results: CADath+ patients had higher CML concentration compared to CADath subjects (1.04 ± 0.6 vs. 0.83 ± 0.4 ng/mL, P &lt, 0.001). The highest mean CML level (1.12 ± 0.7 ng/mL) was found in CADath+ARMD+ patients. The mean plasma CML concentration was higher in subjects with any of the analyzed diseases compared to CADath−ARMD− subjects. A significant positive association of CADath+ (OR = 2.50, 95% CI 1.60–3.90, P = 0.0001), ARMD (OR = 2.08, 95% CI 1.40–3.11, P = 0.0001) and both analyzed diseases (OR = 4.67, 95% CI 2.29– 9.53, P = 0.0001) with an increased level of plasma CML in a logistic regression model adjusting by age was identified. Conclusions: The level of CML, an oxidative stress biomarker, reflects the presence of atherosclerosis in coronary arteries and shows a possible link between ARMD and CADath+ via oxidative status.

Objective. To evaluate acute toxic effect of ibogaine and noribogaine on the survival of mice and determine median lethal doses of the substances mentioned. Material and methods. White laboratory mice were used for the experiments. Ibogaine and noribogaine were administered intragastrically to mice via a stomach tube. Control animals received the same volume of saline. The median lethal dose was calculated with the help of a standard formula. Results. To determine the median lethal dose of ibogaine, the doses of 100, 300, 400, and 500 mg/kg were administered intragastrically to mice. The survival time of mice after the drug administration was recorded, as well as the number of survived mice in each group. Upon administration of ibogaine at a dose of 500 mg/kg, all mice in this dose group died. Three out of four mice died in the group, which received 300 mg/kg of ibogaine. No mouse deaths were observed in the group, which received 100 mg/kg of ibogaine. The determined LD50 value of ibogaine equals to 263 mg/kg of body mass. In order to determine the median lethal dose of noribogaine, the doses of 300, 500, 700, and 900 mg/kg were administered to mice intragastrically. Noribogaine given at a dose of 500 mg/kg had no impact on the mouse survival. The increase of noribogaine dose to 700 mg/kg of mouse body mass led to the death of three out of four mice in the group. Upon administration of noribogaine at a dose of 900 mg/kg, all mice in this group died. The LD50 value of noribogaine in mice determined on the basis of the number of dead mice and the size of the doses used equals to 630 mg/kg of mouse body mass. The behavior of mice was observed upon administration of ibogaine or noribogaine. Low doses of ibogaine and noribogaine had no impact on the mouse behavior. External effects (convulsions, nervous behaviour, limb paralysis) were observed only when substances were administrated at higher doses. Conclusions. It has been determined that the median lethal dose of ibogaine and noribogaine equals to 263 mg and 630 mg/kg of mouse body mass, respectively. The toxicity of ibogaine is 2.4 times higher than that of noribogaine.