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  • Effect of fluoride intoxication on endometrial apoptosis and lipid peroxidation in rats: role of vitamins E and C. 17227693

    Fluoride is a strong, hard anion and cumulative toxic agent. The effect of fluoride intoxication on lipid peroxidation in endometrial tissue and the protective effects of combinations of vitamins E and C in rats were studied. Additionally, the apoptotic changes in endometrial tissue were examined. Experimental groups were as follows: control group; a group treated with 100 mg/l fluoride (F group); and a group treated with 100 mg/l fluoride plus vitamins E and C (F+Vit group). The F and F+Vit groups were treated orally with fluoride for 30 days. Vitamins E and C were injected simultaneously at doses of 50 mg/kg day i.m. and 20 mg/kg day body weight i.p. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick and labeling (TUNEL) method. Malondialdehyde (MDA) levels were determined in uterine tissue of rats. Fluoride caused a significant increase in MDA levels (an important marker of lipid peroxidation) in the fluoride group compared with the controls (p0.05). Vitamins E and C significantly reduced the fluoride-induced lipid peroxidation in the F+Vit group compared with the F group (p0.05). Diffuse apoptosis in glandular epithelium and stromal cells was found in endometrial tissues of F treated rats by TUNEL method. The severity of these lesions was reduced by the administration of vitamins. From these results, it can be concluded that subchronic fluoride administration causes endometrial apoptosis, and lipid peroxidation may be a molecular mechanism involved in fluoride-induced toxicity. Furthermore, treatment with a combination of vitamins E and C reduced endometrial apoptosis caused by fluoride.
    Document Type:
    Reference
    Product Catalog Number:
    S7101
    Product Catalog Name:
    ApopTag® Plus Peroxidase In Situ Apoptosis Kit

  • Intrinsic apoptotic pathway is subverted in mouse macrophages persistently infected by RSV. 21440589

    To persist, a virus must co-exist with the host that it infects, thus allowing the virus to survive and to subvert the programmed cell death of the host. In this study, we investigated whether the intrinsic pathway of the apoptotic process is suppressed in a previously reported macrophage cell line persistently infected with respiratory syncytial virus (RSV). To this end, after using staurosporine to induce apoptosis, we determined cell viability and the degree of annexin staining and DNA fragmentation between infected and mock-infected cells. RSV persistence leads to a subversion of apoptosis; whereas in mock-infected macrophages, apoptosis was evident. The cellular apoptotic pathway involve was searched by determining the activities of caspases and the expression of anti-apoptotic proteins. Although caspases-3 and -9 were expressed, their activities were altered; the activity of caspase-3 was reduced and that of caspase-9 could not be detected. Expression of anti-apoptotic proteins Bcl-2, Bcl-X, and XIAP was enhanced, with Bcl-X and XIAP being regulated post-transcriptionally; the induction of the anti-apoptotic factors and the reduced caspases activities might account for the subversion of apoptosis. The data implies that in our viral persistence model an anti-apoptotic program is induced relating alterations of caspases-3 and -9 activity and expression of anti-apoptotic proteins, suggesting that the intrinsic pathway is suppressed. These findings are of importance for understanding the intracellular genes involved in subversion of apoptosis by RSV persistence in macrophages.Copyright © 2011. Published by Elsevier B.V.
    Document Type:
    Reference
    Product Catalog Number:
    S7160
    Product Catalog Name:
    ApopTag® Fluorescein Direct In Situ Apoptosis Detection Kit

  • Anti-apoptotic and antioxidant effect of leptin on cCl(4)-induced acute liver injury in rats. 21607623

    The aim of this study is to investigate the effect of leptin in rats on carbon tetrachloride (CCl(4)) induced acute liver damage using immunohistochemical methods for apoptosis and biochemical parameters. In this experimental study, 18 Spraque-Dawley rats were divided into three groups viz; control, CCl(4) and CCl(4)+leptin treatment. 0.8 ml/kg olive oil was administered intraperitoneally (i.p.) to the control group and 0.8 ml/kg CCl(4) (1:1 dissolved in olive oil) was administered i.p. to the CCl(4) and CCl(4)+leptin treatment groups, respectively. After 6 h of administrating CCl(4), CCl(4)+leptin treatment group was given i.p. leptin (10 μg/kg). Twenty-four hours after administrating CCl(4) all of the groups were euthanized. Biochemical assessments were performed using serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), plasma tumor necrosis factor alpha (TNF-α) levels and tissue malondialdehyde (MDA), and TNF-α levels. Histological assessments were then performed using Hematoxylin&Eosin (H&E) staining in light microscope and apoptosis assessment using Terminal Transferase dUTP Nick End Labeling (TUNEL)-staining. Serum AST, ALT, ALP and plasma TNF-α levels, tissue MDA and TNF-α levels had all increased in CCl(4) group, but were found to be significantly decreased in CCl(4)+leptin treatment group. Moreover, TUNEL-positive cell counts in liver had significantly increased in CCl(4) group, but decreased in CCl(4)+leptin treatment group (P < 0.05). The results of our study the biochemical, histological and TUNEL-staining showed that leptin has treatment effects on liver CCl(4) induced injury. It plays a role as a potent free radical scavenger, a powerful antioxidant and it also has anti-apoptotic effects.
    Document Type:
    Reference
    Product Catalog Number:
    S7101
    Product Catalog Name:
    ApopTag® Plus Peroxidase In Situ Apoptosis Kit

  • Neuregulin-1 is neuroprotective in a rat model of organophosphate-induced delayed neuronal injury. 22583949

    Current medical countermeasures against organophosphate (OP) nerve agents are effective in reducing mortality, but do not sufficiently protect the CNS from delayed brain damage and persistent neurological symptoms. In this study, we examined the efficacy of neuregulin-1 (NRG-1) in protecting against delayed neuronal cell death following acute intoxication with the OP diisopropylflurophosphate (DFP). Adult male Sprague-Dawley rats were pretreated with pyridostigmine (0.1 mg/kg BW, i.m.) and atropine methylnitrate (20 mg/kg BW, i.m.) prior to DFP (9 mg/kg BW, i.p.) intoxication to increase survival and reduce peripheral signs of cholinergic toxicity but not prevent DFP-induced seizures or delayed neuronal injury. Pretreatment with NRG-1 did not protect against seizures in rats exposed to DFP. However, neuronal injury was significantly reduced in most brain regions by pretreatment with NRG-1 isoforms NRG-EGF (3.2 μg/kg BW, i.a) or NRG-GGF2 (48 μg/kg BW, i.a.) as determined by FluroJade-B labeling in multiple brain regions at 24 h post-DFP injection. NRG-1 also blocked apoptosis and oxidative stress-mediated protein damage in the brains of DFP-intoxicated rats. Administration of NRG-1 at 1h after DFP injection similarly provided significant neuroprotection against delayed neuronal injury. These findings identify NRG-1 as a promising adjuvant therapy to current medical countermeasures for enhancing neuroprotection against acute OP intoxication.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple

  • Protective effects of dispersive viscoelastics on corneal endothelial damage in a toxic anterior segment syndrome animal model. 22899758

    Purpose. We evaluated whether viscoelastics have protective effects on the corneal endothelial cell damage in a toxic anterior segment syndrome (TASS) animal model depending on the types of viscoelastics. Methods. A TASS animal model was established with an injection of 0.1 mL o-phthaldehyde solution (0.14%) into the anterior chamber of New Zealand white rabbits. One of two different viscoelastics, 1% sodium hyaluronate (cohesive group) or a 1:3 mixture of 4% chondroitin sulfate and 3% sodium hyaluronate (dispersive group), was injected into the anterior chamber. After five minutes, it was removed using a manual I/A instrument, and then 0.1 mL of o-phthaldehyde solution (0.14%) was injected into the anterior chamber. Damage to corneal endothelial cells was compared between the two groups. Results. The corneal thickness increased quickly in both groups after the disinfectant injection. However, the dispersive group showed relatively mild corneal edema compared to the cohesive group. The mean corneal haze score in the dispersive group also was lower than that of the cohesive group. These partial protective effects of the dispersive viscoelastic were demonstrated by the different findings of a live/dead cell assay, TUNEL staining, and scanning electron microscopy between the two groups. Conclusions. The TASS animal model seems to be a useful means to evaluate corneal endothelial cell damage caused by toxic substances to find ways to protect or reduce endothelial cell damage. Dispersive viscoelastics were shown to have partial protective effects against corneal endothelial cell damage caused by a toxic disinfectant.
    Document Type:
    Reference
    Product Catalog Number:
    S7165
    Product Catalog Name:
    ApopTag® Red In Situ Apoptosis Detection Kit

  • Cell-in-cell Structures Formed between Human Cancer Cell Lines and the Cytotoxic Regulatory T-cell Line HOZOT. 20348186

    We previously established a novel cell line, termed HOZOT, derived from umbilical cord blood mononuclear cells that is characterized as a human cytotoxic regulatory T (Treg) cell line with a FOXP3(+)CD4(+)CD8(+)CD25(+) phenotype. Here, we describe a new property of HOZOT cells: they actively penetrate into a variety of human cancer cell lines, but not into normal cell lines, and form apparent cell-in-cell structures. In the process of cell penetration, we observed that HOZOT cells adhered to target cells seemed to first insert their nuclei into the cytoplasm of target cells, distinct from the process of phagocytosis. In addition, blocking experiments showed that major histocompatibility complex class I is one of the target cell recognition molecules for HOZOT cells. Furthermore, we propose that cell-in-cell structures between HOZOT cells and target cancer cells could be one of the cytotoxic mechanisms of HOZOT cells.
    Document Type:
    Reference
    Product Catalog Number:
    S7101
    Product Catalog Name:
    ApopTag® Plus Peroxidase In Situ Apoptosis Kit

  • Alterations in lung mast cell populations in patients with chronic obstructive pulmonary disease. 19926870

    Rationale: Mast cells have important roles in innate immunity and tissue remodeling but have remained poorly studied in inflammatory airway diseases like chronic obstructive pulmonary disease (COPD). Objectives: To perform a detailed histological characterization of human lung mast cell populations at different severities of COPD, comparing with smoking and never-smoking control subjects. Methods: Mast cells were analyzed in lung tissues from patients with mild to very severe COPD, GOLD I-IV (n = 25, 10 of whom were treated with corticosteroids). Never-smokers and smokers served as controls. The density, morphology, and molecular characteristics of mucosal and connective tissue mast cells (MC(T) and MC(TC), respectively) were analyzed in several lung regions. Measurements and Main Results: In all compartments of COPD lungs, especially at severe stages, the MC(TC) population increased in density, whereas the MC(T) population decreased. The net result was a reduction in total mast cell density. This phenomenon was paralleled by increased numbers of luminal mast cells, whereas the numbers of terminal transferase dUTP nick end labeling (TUNEL)(+) apoptotic mast cells remained unchanged. In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin. Statistically significant correlations were found between several COPD-related mast cell alterations and lung function parameters. Conclusions: As COPD progresses to its severe stages, the mast cell populations in the lung undergo changes in density, distribution, and molecular expression. In COPD lungs, these novel histopathological features were found to be correlated to lung function and they may thus have clinical consequences.
    Document Type:
    Reference
    Product Catalog Number:
    S7110
    Product Catalog Name:
    ApopTag® Fluorescein In Situ Apoptosis Detection Kit
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