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Quinalphos or Ekalux, an organophosphate pesticide, is used in controlling the pests of a variety of crops. Quinalphos was studied on male Sprague-Dawley albino rats. The acute po LD50 of technical Ekalux was 19.95 mg/kg in males. Ekalux, produced several pathological changes in the kidney. A glomerulus demonstrated capillary lumina occluded by degenerated cellular debris. Basement membrane showed irregular wrinkling and branching. The proximal tubular cells showed damage such as dilation of endoplasmic reticulum, accumulation of glycogen granules, and pyknotic nucleus. The changes also included swelling of the mitochondria and reduction of the cristae up to total destruction. The distal tubular changes included electron lucency and vacuolation of cytoplasm. The distal convoluted tubule wall showed edematous epithelial cells, formation of blebs, and microvilli loss. These results suggest that subchronic exposure of rats to Ekalux causes ultrastructural changes in renal corpuscle and marked ultrastructural changes in proximal and distal tubules

Background: Depression is a severe mental disorder. Current antidepressants are effective in only one-half to one-third of the patients. Besides, these medications might bring about adverse effects. Therefore, the need for newer anti-depressant medications or complementary compounds is utterly felt. Objectives: We tested the hypothesis that geraniol (GE) attenuates anxiety and depression via the amelioration of oxidative stress and apoptosis in mice. Methods: In an experimental study, thirty-six BALB/c mice were randomly divided into three control, chronic restraint stress (CRS), and GE groups. CRS and GE groups underwent CRS for two weeks. Accordingly, the CRS group received normal saline (2 mL/kg, i.p.) whereas the GE group received GE (50 mg/kg, i.p.). The behavioral outcomes were assessed using the open-field test (OFT), elevated plus maze (EPM), and tail suspension test (TST). Moreover, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-px) activity, total antioxidant capacity (TAC), and reactive oxidative species (ROS) levels in the brain were assessed using the spectrophotometric method. The brain’s BAX, Bcl-2, and caspase-3 levels were measured usingWestern blotting. Results: CRS increased anxiety in stressed mice compared to the control group as indicated by OFT and EPM (P < 0.01 for both comparisons). Furthermore, CRS increased the immobility time in TST compared to control animals (P < 0.001). Biochemically, CRS decreased SOD activity (P < 0.01), GSH-px activity (P < 0.01), TAC level (P < 0.001), and ROS level (P < 0.001). It also increased the BAX/Bcl-2 ratio (P < 0.001) and caspase-3 level (P < 0.001) compared to the control group. GE reversed all the behavioral and biochemical changes in stressed mice compared to the CRS group. Conclusions: GE renders potent anxiolytic and antidepressant effects possibly through the modulation of oxidative stress and apoptosis in the mouse brain.

Ankaferd Blood Stopper (ABS) is a preparation of plant extracts originally used as a hemostatic agent. It has pleiotropic effects in many cellular processes such as cell cycle regulation, apoptosis, angiogenesis, signal transduction, inflammation, immunologic processes and metabolic pathways as well as hemostatic activity. This unique preparation has been widely investigated for its properties. However there are no studies investigating its action on leukemic cells. Aim of the study was to examine the ABS action on PAR1 and EPCR in leukemia cells. However, during the experiments, we observed the apoptotic effect of ABS on leukemic cells, particularly Jurkat cells. As a result the mechanism of apoptosis induced by ABS treatment was also explored in the study. Two leukemia cell lines, K-562 and Jurkat, were utilized for the study. Expression analyses of PAR1, EPCR and p21 upon ABS treatment were performed by quantitative real time PCR. Annexin V method was used for apoptosis detection. Our results demonstrated that ABS alters PAR1 and EPCR expression in K-562 and Jurkat cells in a time and dose dependent manner. Additionally it was found that ABS treatment induces apoptosis in leukemia cells. Possible involvement of PAR1 and p21 in this apoptotic process was observed in Jurkat cells. This study concludes that depending on the concentration and duration of the application, ABS causes apoptosis by regulating PAR1 and p53-independent p21 involvement in apoptosis stimulation in leukemia cells. The composition of ABS plant extracts might be responsible from the apoptotic effect that was observed. We think that our results could contribute to the development of new treatment for leukemia therapy.

Objective To evaluate the role of soluble Fas (sFas) and soluble Fas ligand (sFasL) in the pathogenesis of distal symmetrical polyneuropathy (DSPN) in patients with type 2 diabetes mellitus, and to analyze the relationship between these apoptotic markers with clinical parameters and electrophysiologic profile of DSPN, as well as with different diabetic factors among those patients. Patients and methods The study included 60 Egyptians with type 2 diabetes mellitus. All patients were evaluated clinically for DSPN by using Michigan Neuropathy Screening Instrument. Electrophysiological diagnosis of DSPN was based on the criteria suggested by the European Standardized Telematic tool to Evaluate Electrodiagnostic Methods group. Diabetic patients were divided into two groups according to the electrophysiological findings: group A included patients with DSPN (N=42), and group B included patients without DSPN (N=18). The severity of DSPN among group A patients was assessed clinically using Toronto Clinical Neuropathy Score and electrophysiologically by the severity score proposed by Hidasi and colleagues. The study also included 30 healthy volunteers as a control group. Serum levels of sFas and sFasL were assessed in all the studied groups. Results Serum level of sFas was significantly elevated in diabetic patients with DSPN compared with diabetics without DSPN and nondiabetic control (P=0.029 and 0.000). Receiver operating characteristic (ROC) curve analysis detected that sFas was statistically significant in discriminating between diabetic patients with DSPN from those patients without DSPN with an accuracy of 66%. The cutoff point that has the highest sensitivity (61%) and specificity (62%) was 33.3 ng/ml. Serum level of sFas showed a positive significant correlation with the electrophysiological severity of DSPN (P=0.020). Serum level of sFasL did not show statistically significant difference between all the studied groups. Conclusion Fas-mediated apoptosis has an important role in the development of diabetic DSPN and is correlated with its electrophysiological severity.

Titanium complexes have been synthesized by the reaction between titanium tetrachloride (TiCl4), respective bidentate ligand [4,4′ -dimethoxy-2,2′ -bipyridine (bpome), 6,6′-dimethyl-2,2′-bipyridine (dpme), 1,2-diaminocyclohexane (dach), 1,10-phenanthroline (phen), and benzoylacetone (bzac)], and adamantylamine (ada) in 1 : 2 : 2 molar ratios, respectively. The structure of synthesized complexes was confirmed using elemental analysis, FTIR, UV-visible, 1H NMR, and mass spectrometry techniques. The nanocrystalline nature of complexes was confirmed by powder XRD study. The complexes were evaluated for cytotoxic potential in HeLa (cervical), C6 (glioma), and CHO (Chinese hamster ovarian) cell lines. The complex E was found to be more effective cytotoxic agent against HeLa cell line with an IC50 value of 4.06 µM. Furthermore, the effect of synthesized complexes was studied on different stages of the cell cycle in CHO cells. All complexes exhibited the dose dependent increase in cytotoxicity. The results have shown an increase in sub-G0 population with increase in concentration which is an indicative measure of apoptosis.

Background : PI3K / AKT pathway plays major roles in regulating cardiomyocyte metabolism. The roles of PI3K / AKT pathway and FOXO3a in mediating high glucose-induced apoptosis in cardiomyocytes remain unclear. Objectives : In this experimental study, we investigated the mechanisms of the PI3K / AKT pathway and FOXO3a in mediating hyperglycemia-induced apoptosis in neonatal rat ventricular myocytes (NRVMs). Materials and Methods : NRVMs were adopted as the cell model to investigate the roles of PI3K / AKT and FOXO3a in mediating hyperglycemia-induced apoptosis in cardiomyocytes. Annexin-V-FITC staining and PI staining were used to evaluate the apoptosis in NRVMs under indicated conditions of serum starvation, high glucose exposure, and pharmacological or genetic manipulations on the expressions of PI3K / AKT and FOXO3a. Western blotting was conducted to evaluate the cytoplasmic / nuclear localization of FOXO3a in NRVMs exposed to high glucose. FOXO3a transcriptional activity was measured by luciferase reporter assay. Results : High glucose (30 mM) induced significant apoptosis in serum-starved NRVMs as compared with normal glucose (5 mM) control (12.01 ± 0.76 % vs. 2.86 ± 0.55 % ; P < 0.001). Treatment with IGF1 attenuated hyperglycemia-induced apoptosis by 68 % (3.23 ± 0.76% vs. 9.97 ± 1.29 % ; P < 0.001 ; n = 3) in comparison with the non-treated control. Treatment with PI3K inhibitor LY294002 enhanced hyperglycemia-induced apoptosis by 109 % (20.83 ± 1.87 % vs. 9.97 ± 1.29 % ; P < 0.001 ; n = 3) in comparison with the non-treated control. Over-expression of AKT by transduction with CA-AKT attenuated hyperglycemia-induced apoptosis by 47 % (5.48 ± 0.35 % vs.10.31 ± 0.94 % ; P < 0.001 ; n = 3) in comparison with the empty-vector control. Transduction with DN-AKT enhanced high glucose-induced apoptosis by 105 % (21.13 ± 1.11 % vs. 10.31 ± 0.94 % ; P < 0.001 ; n = 3) in comparison with the empty-vector control. Western blotting showed that high glucose induced a significant increase in FOXO3a nuclear localization. Luciferase reporter assay showed that high glucose induced a significant increase of 310 % (P < 0.001 ; n = 3) in FOXO3a transcriptional activity against Fas ligand when NRVMs were transducted with TM-FOXO3a in comparison with the empty-vector control. Conclusions : The PI3K / AKT pathway mediated hyperglycemia-induced apoptosis of NRVMs through the translocation of FOXO3a to nuclei and the resultant enhanced transcriptional activity of FOXO3.

It is hypothesized that Down syndrome (DS) patients are associated with abnormalities of the immune system. Accordingly, this study was conducted to measure replicative aging and apoptosis in lymphocytes, which play an important role in the immune system, before and after being biostimulated with He:Ne laser. Replicative aging was measured in terms of telomerase activity, and ETS-2 gene relative expression. Apoptosis was measured in terms of DNA fragmentation and apoptosis genes (Fas, FasL and Bax) and antiapoptotic Bcl-2 protein. Results showed that Telomerase activity, ETS-2 mRNA expression, plasma DNA fragmentation, Fas and FasL were significantly higher among DS patients compared to controls: Telomerase activity (1.5±0.5 vs. 0.9±0.4, p<0.001); ETS2 mRNA expression (0.6±0.1 vs. 0.43±0.04, p<0.0001); plasma DNA fragmentation (0.45%±0.12 vs. 0.2%±0.1, p<0.0001); Fas protein (5.3±1.2 vs. 2.3±0.2, p<0.0001); FasL mRNA relative expression (0.37±0.05 vs. 0.24±0.01, p<0.001); Bax mRNA relative expression (0.9±0.1 vs. 0.5±0.1, p<0.00001). Bcl-2 protein was significantly low in DS patients compared to controls (8.6±1.3 vs. 10±2.1, p<0.01). He:Ne laser biostimulation applied to evaluate lymphocytes’ response significantly increased the former parameters in DS patients compared to their level before irradiation, except for Bcl-2, which was significantly decreased. In conclusion: increased telomerase activity associated with increased activity and overexpression of ETS-2 on chromosome 21 in DS patients may contribute to the increased rate of early senescence in circulating lymphocytes, which consequently contributes to the abnormalities of the immune system observed in DS. Increased apoptosis is due to increased oxidative stress, which induces an increase in the apoptotic genes Bax, Fas and FasL accompanied by a decrease in the antiapoptotic gene Bcl-2.