Chronic lymphocytic leukemia (CLL) develops due to an imbalance between apoptosis and proliferation of B lymphocytes. Chrysin induced apoptosis in leukemia cell lines such as U937, MO7e, THP-1 and HL-60, but there has not yet been data demonstrating the apoptotic effect of chrysin on CLL cells. Therefore, in our investigation we examined the cytotoxicity of chrysin against two leukemia cell lines, MOLT-4 and JVM-13, peripheral blood lymphocytes isolated from B-CLL patients and peripheral blood mononuclear cells (PBMC) from healthy individuals in vitro. The effect of chrysin on viability of MOLT-4 and JVM-13 cell lines, B-CLL cells derived from 28 patients and PBMC from 16 healthy subjects was determined by MTT assay. The type of cell death induced by chrysin was verified by Annexin V/7AAD assay and acridine orange and ethidium bromide (AO/EB) staining assay. Intracellular localisation and endogenic expression of apoptotic proteins including Bax, Bcl-2, cytochrome c and caspase-3 were determined by flow cytometry and fluorescent microscopy. Our results demonstrated that exposure of MOLT-4, JVM-13 cell lines and B-CLL cells to the concentration of chrysin of 10μM and higher selectively decreased viability of cells in this cell population, but not in the PBMC derived from healthy subjects; LC50 values of chrysin for B-CLL cells were 51μM for 24 hours and 32μM for 48 hours of incubation, respectively. Our findings demonstrated that chrysin induces the activation of proapoptotic Bax and decreases the expression of antiapoptotic Bcl-2 protein, releases cytochrome c from mitochondria into cytosol and cleavages/activates caspase-3, subsequently leading to the activation of apoptosis of B-CLL cells. Together, these findings suggest that chrysin selectively induces apoptosis of peripheral blood lymphocytes isolated from human chronic lymphocytic leukemia patients via mitochondrial pathway in vitro and that it might have a promising role as a potential future antileukemic remedy.

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.

IntroductionEndometrial hyperplasia is a condition that occurs as a result of hormonal imbalance between estrogen and progesterone. Morphological disturbance of endometrial cells occurs consequently leading towards endometrial cancer. In therapy of endometrial hyperplasia SERMs are used to supress effects of locally high estrogen level in uterus. There is strong evidence suggesting that estrogen could be involved in cell death – apoptosis. There are no experimental data demstrating the direct apoptotic effect of both raloxifene and estrogen on the ThESC cell line. The aim of our study wa sto investigate both cytotoxic and apototic mechanism of raloxifene and estrogen – induced death in the ThESC cell line.Material and methodsIn order to determine their cytotoxic and apoptotic effects, various doses of raloxifene and estrogen were applied to the ThESC cell line for 24 h. After the treatment MTT assay, FACS analysis and immunofluoroscence method were conducted.ResultsThe results of this study for the first time demonstrated the cytotoxic and apoptotic effects of raloxifene and estrogen on human endometrial stromal cell line suggesting the involvement of the inner, mitochondrial apoptotic pathway.ConclusionsOur results demonstrated apoptotic effects of investigated drugs in the ThESC cell line through increasing the Bax/Bcl-2 ratio and activation of caspase 3.

Gingival tissue destruction caused by inflammatory process leads to significant changes in collagen density and population of resident connective tissue cells. Although inflammatory cells dominated with the disease advancing, a high variation within the same investigated groups suggests fluctuation of the pathological process.

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