Ruthenium(II) complexes offer the potential for lower toxicity compared to platinum(II) complexes. Our study aimed to compare cardiotoxicity of [Ru(Cl-tpy)(en)Cl][Cl], [Ru(Cl-tpy)(dach)Cl][Cl], [Ru(Cl-tpy)(bpy)Cl][Cl], cisplatin and saline through assessment of redox status and relative expression of apoptosis-related genes. A total of 40 Wistar albino rats were divided into five groups. Ruthenium groups received intraperitoneally single dose of complexes (4 mg/kg/week) for 4-weeks period; cisplatin group received cisplatin (4 mg/kg/week) and control group received saline (4 mL/kg/week) in the same manner as ruthenium groups. In collected blood and heart tissue samples, spectrophotometrically determination of oxidative stress biomarkers was performed. The relative expression of apoptosis-related genes (Bcl-2, Bax, and caspase-3) in hearts was examined by RT-PCR. Our results showed that systemic and cardiac pro-oxidative markers (TBARS and NO2-) were significantly lower in ruthenium groups compared to cisplatin group, while concentrations of antioxidative parameters (CAT, SOD, and GSSG) were significantly higher. Ruthenium administration led to significantly lower gene expression of Bax and caspase-3 compared to cisplatin-treated rats, while Bcl-2 remained unchanged. Applied ruthenium complexes have less pronounced potential for induction of oxidative stress-mediated cardiotoxicity compared to cisplatin. These findings may help for future studies that should clarify the mechanisms of cardiotoxicity of ruthenium-based metallodrugs.

In recent decades, steroid abuse has become very popular and widespread among professional and recreational athletes. The aim of this study was to examine the chronic effects of training combined with high doses of nandrolone decanoate on cardiac muscle tissue. The study included 32 Wistar albino rats divided into 4 groups: control (T-N-), steroid (T-N+), exercisetraining (T+N-) and exercise plus steroid (T+N+) groups. The T+N- and T+N+ group swam for 4 weeks, 1 hour per day, 5 days per week. The N+ (nandrolone positive groups) received nandrolone decanoate (20 mg/kg) once per week, subcutaneously. After 4 weeks of training, the rats were sacrificed. Heart biopsy specimens were routinely fixed and embedded in paraffin. Fivemicrometre thick sections were stained with haematoxylin and eosin (H/E) and Masson-Trichrome dyes. Captured microscopic images were processed by special software for image analysis to quantify results. Our results showed that the combination of nandrolone and training causes left ventricular wall thickening of 30%. Average cardiac muscle cell longitudinal diameter was increased by 6% in the T-N+ group, by 16% in the T+N- group and by 25% in the T+N+ group. The cross sectional muscle cell area was increased in the T+N+ group by 33%. Heart collagen content was increased in the nandrolone group compared to the control group by 261%. Collagen content was decreased in the T+N+ group by 34%. High doses of AAS induced left ventricle hypertrophy and excessive heart collagen deposition.

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Due to existing evidence regarding antioxidant and anti-inflammatory effects of Melissa officinalis extracts (MOEs), this study was aimed at investigating the potential of ethanolic MOE to prevent the development of myocarditis and its ability to ameliorate the severity of experimental autoimmune myocarditis (EAM) by investigating MOE effects on in vivo cardiac function, structure, morphology, and oxidative stress parameters. A total of 50 7-week-old male Dark Agouti rats were enrolled in the study and randomly allocated into the following groups: CTRL, nontreated healthy rats; EAM, nontreated rats with EAM; MOE50, MOE100, and MOE200, rats with EAM treated with either 50, 100, or 200 mg/kg of MOE for 3 weeks per os. Myocarditis was induced by immunization of the rats with porcine myocardial myosin (0.5 mg) emulsion on day 0. Cardiac function and dimensions of the left ventricle (LV) were assessed via echocardiography. Additionally, the blood pressure and heart rate were measured. On day 21, rats were sacrificed and the hearts were isolated for further histopathological analyses (H/E and Picrosirius red staining). The blood samples were collected to determine oxidative stress parameters. The EAM group characteristically showed greater LV wall thickness and lower ejection fraction ( 50.33 ± 7.94 % vs. 84.81 ± 7.74 %) and fractional shortening compared to CTRL ( p < 0.05 ). MOE significantly improved echocardiographic parameters (EF in MOE200 81.44 ± 5.51 %) and also reduced inflammatory infiltrate (by 88.46%; p < 0.001 ) and collagen content (by 76.39%; p < 0.001 ) in the heart tissues, especially in the MOE200 group compared to the EAM group. In addition, MOEs induced a significant decrease of prooxidants production (O2-, H2O2, and TBARS) and improved antioxidant defense system via increase in GSH, SOD, and CAT compared to EAM, with medium and high dose being more effective than low dose ( p < 0.05 ). The present study suggests that ethanolic MOEs, especially in a 200 mg/kg dose, improve cardiac function and myocardial architecture, possibly via oxidative stress mitigation, thus preventing heart remodeling, development of dilated cardiomyopathy, and subsequent heart failure connected with EAM. MOEs might be considered as a potentially helpful adjuvant therapy in patients with autoimmune myocarditis.

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