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  • Genotoxic and cytotoxic effects induced by aluminum in the lymphocytes of the common carp (Cyprinus carpio). 20883821

    Few studies have been made in regard to the effect of aluminum on the molecular and cellular structure and function of aquatic organisms; therefore, in the present report we determined the genotoxic and cytotoxic effects induced by the metal on the lymphocytes of carp (Cyprinus carpio). Three groups of fish were exposed to 0.05, 120, and 239mg/L of aluminum (Al), respectively, by using Al(2) (SO(4))(3)·7H(2)O, and another group was included as control. The cells obtained were studied with the comet assay, flow cytometry, and the TUNEL method. With the first method we found a concentration and time dependent, significant increase in the amount of DNA damage induced by Al, and a higher damage when we evaluated the level of oxidized DNA. By applying flow cytometry we established that the metal induced a DNA content increase and ploidy modifications as well as apoptosis and disturbances of the cell cycle progression. With the last method we determined a significant increase in the amount of apoptotic cells, mainly in the 72-96h period. Our results established that Al caused deleterious DNA and cellular effects in the tested organism, and they suggested the pertinence of evaluating toxicity induced by the metal in organisms living in contaminated water bodies.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7100
    Nombre del producto:
    ApopTag® Peroxidase In Situ Apoptosis Detection Kit

  • Does furan affect the thymus in growing male rats? 22289615

    Furan has been identified in foods such as heat-treated foods, including coffee, canned meat, hazelnuts, and infant foods and formulas. Children may be exposed to furan via either consumption of these foods or their derivatives. We evaluated the effects of furan on the thymus of weaning male rats in the present study. Five separate groups containing male rats were used: control, oil control, and three furan-treated groups. Furan was given orally to rats in the treatment groups at doses of 2, 4, and 8 mg/kg/day for 90 days. At the end of the experiment, thymus of the rats were examined morphologically, histopathologically, and immunohistochemically. We observed that absolute and relative weights of thymus were decreased significantly in rats treated with 4- and 8-mg/kg/day doses of furan. In histopathological examination, enlargement of interstitial connective tissue between the thymic lobules, lymphocyte depletion, and hemorrhage were observed. We detected an increase in apoptotic cell counts in thymus of the treatment groups. In addition, we found significant differences in the distribution of fibronectin and transforming growth factor-beta in the thymus of the treatment groups. In conclusion, we suggest that furan has affected the thymus in growing male rats.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7101
    Nombre del producto:
    ApopTag® Plus Peroxidase In Situ Apoptosis Kit

  • Xenopus Bsx links daily cell cycle rhythms and pineal photoreceptor fate. 20308548

    In the developing central nervous system, the cell cycle clock plays a crucial role in determining cell fate specification. A second clock, the circadian oscillator, generates daily rhythms of cell cycle progression. Although these two clocks interact, the mechanisms linking circadian cell cycle progression and cell fate determination are still poorly understood. A convenient system to address this issue is the pineal organ of lower vertebrates, which contains only two neuronal types, photoreceptors and projection neurons. In particular, photoreceptors constitute the core of the pineal circadian system, being able to transduce daily light inputs into the rhythmical production of melatonin. However, the genetic program leading to photoreceptor fate largely remains to be deciphered. Here, we report a previously undescribed function for the homeobox gene Bsx in controlling pineal proliferation and photoreceptor fate in Xenopus. We show that Xenopus Bsx (Xbsx) is expressed rhythmically in postmitotic photoreceptor precursors, reaching a peak during the night, with a cycle that is complementary to the daily rhythms of S-phase entry displayed by pineal cells. Xbsx knockdown results in increased night levels of pineal proliferation, whereas activation of a GR-Xbsx protein flattens the daily rhythms of S-phase entry to the lowest level. Furthermore, evidence is presented that Xbsx is necessary and sufficient to promote a photoreceptor fate. Altogether, these data indicate that Xbsx plays a dual role in contributing to shape the profile of the circadian cell cycle progression and in the specification of pineal photoreceptors, thus acting as a unique link between these two events.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB5585

  • Mu-opioid receptors modulate the stability of dendritic spines. 15659552

    Opioids classically regulate the excitability of neurons by suppressing synaptic GABA release from inhibitory neurons. Here, we report a role for opioids in modulating excitatory synaptic transmission. By activating ubiquitously clustered mu-opioid receptor (MOR) in excitatory synapses, morphine caused collapse of preexisting dendritic spines and decreased synaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. Meanwhile, the opioid antagonist naloxone increased the density of spines. Chronic treatment with morphine decreased the density of dendritic spines even in the presence of Tetrodotoxin, a sodium channel blocker, indicating that the morphine's effect was not caused by altered activity in neural network through suppression of GABA release. The effect of morphine on dendritic spines was absent in transgenic mice lacking MORs and was blocked by CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-ThrNH2), a mu-receptor antagonist. These data together with others suggest that endogenous opioids and/or constitutive activity of MORs participate in maintaining normal morphology and function of spines, challenging the classical model of opioids. Abnormal alteration of spines may occur in drug addiction when opioid receptors are overactivated by exogenous opiates.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7160
    Nombre del producto:
    ApopTag® Fluorescein Direct In Situ Apoptosis Detection Kit

  • Fcgamma receptors contribute to pyramidal cell death in the mouse hippocampus following local kainic acid injection. 20074624

    Recent studies have demonstrated the contribution of the gamma subunit of the Fc receptor of IgG (FcRgamma) to neuronal death following ischemic injury and Parkinson's disease. We examined the role of FcRgamma in hippocampal pyramidal cell death induced by kainic acid (KA). FcRgamma-deficient mice (FcRgamma-/-) and their FcRgamma+/+ littermates (wild type, B6) received an injection of KA into the dorsal hippocampus. Pyramidal cell death was quantified 24 and 72 h after the injection. The number of survived pyramidal cells was significantly larger in FcRgamma-/- mice than in B6 mice in both the CA1 and CA3. Immunohistochemical and immunofluorescent studies detected FcgammaRIIB protein in parvalbumin neurons, whereas FcgammaRIII and FcgammaRI proteins were detected in microglial cells. No activated microglial cells were detected 24 h after the KA injection in FcRgamma-/- mice, whereas many activated microglial cells were present in B6 mice. The production of nitrotyrosine as well as of the inducible nitric oxide synthase and cyclooxygenase-2 proteins, increased by 16 h after the KA injection in B6 mice. In addition, tissue plasminogen activator and metalloproteinase-2 proteins increased. By contrast, the magnitude of oxidative stress and the increase in protease expression were mild in FcRgamma-/- mice. Co-injection of a neutralizing antibody against FcgammaRll and FcgammaRlll with KA abolished pyramidal cell death and microglial activation. In addition, the neutralizing antibody reduced oxidative stress and expression of proteases. These observations suggested a role for FcgammaRllB in parvalbumin neurons as well as FcRgamma in microglia in pyramidal cell death. Copyright 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AP308F
    Nombre del producto:
    Goat Anti-Mouse IgG Antibody, (H+L) FITC conjugate

  • Toxicogenomics in the assessment of immunotoxicity. 17161310

    Microarray analysis is used for simultaneous measurement of expression of thousands of genes in a given sample and as such extends and deepens our understanding of biological processes. Application of the technique in toxicology is referred to as toxicogenomics. The examples of assessment of immunotoxicity by gene expression profiling presented and discussed here, show that microarray analysis is able to detect known and novel effects of a wide range of immunomodulating agents. Besides the elucidation of mechanisms of action, toxicogenomics is also applied to predict consequences of exposing biological systems to toxic agents. Successful attempts to classify compounds using signature gene expression profiles have been reported. These did, however, not specifically focus on immunotoxicity. Databases containing expression profiles can facilitate the applications of toxicogenomics. Platforms and methodologies for gene expression profiling may vary, however, hampering data compiling across different laboratories. Therefore, attention is paid to standardization of the generation, reporting, and management of microarray data. Obtained gene expression profiles should be anchored to pathological and functional endpoints for correct interpretation of results. These issues are also important when using toxicogenomics in risk assessment. The application of toxicogenomics in evaluation of immunotoxicity is thus not yet without challenges. It already contributes to the understanding of immunotoxic processes and the development of in vitro screening assays, though, and is therefore expected to be of value for mechanistic insight into immunotoxicity and hazard identification of existing and novel compounds.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7110
    Nombre del producto:
    ApopTag® Fluorescein In Situ Apoptosis Detection Kit

  • Apoptosis in transgenic mice expressing the P301L mutated form of human tau. 18368144

    The rTg4510 mouse is a tauopathy model, characterized by massive neurodegeneration in Alzheimer's disease (AD)-relevant cortical and limbic structures, deficits in spatial reference memory, and progression of neurofibrillary tangles (NFT). In this study, we examined the role of apoptosis in neuronal loss and associated tau pathology. The results showed that DNA fragmentation and caspase-3 activation are common in the hippocampus and frontal cortex of young rTg4510 mice. These changes were associated with cleavage of tau into smaller intermediate fragments, which persist with age. Interestingly, active caspase-3 was often co-localized with cleaved tau. In vitro, fibrillar Abeta(1-42) resulted in nuclear fragmentation, caspase activation, and caspase-3-induced cleavage of tau. Notably, incubation with the antiapoptotic molecule tauroursodeoxycholic acid abrogated apoptosis-mediated cleavage of tau in rat cortical neurons. In conclusion, caspase-3-cleaved intermediate tau species occurred early in rTg54510 brains and preceded cell loss in Abeta-exposed cultured neurons. These results suggest a potential role of apoptosis in neurodegeneration.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB5430
    Nombre del producto:
    Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421)

  • Protection against cisplatin-induced ovarian damage by the antioxidant sodium 2-mercaptoethanesulfonate (mesna) in female rats. 18395042

    OBJECTIVE: The hypothesis was that the administration of the antioxidant mesna (sodium 2-mercaptoethanesulfonate) during chemotherapy would protect ovaries against follicular damage. STUDY DESIGN: Sprague-Dawley rats were treated with saline solution, mesna-plus-cisplatin, or cisplatin. Immunohistochemistry was used to evaluate the Müllerian inhibiting substance (MIS) positive follicles. Serum and ovarian MIS were measured with enzyme-linked immunosorbent assay and Western blot analysis, respectively. Apoptosis in ovaries was studied by terminal deoxynucleotidyl transfer biotin-d UTP nick end labeling (TUNEL) assay. RESULT: Immunofluorescence staining for MIS was higher in preantral follicles in the mesna-plus-cisplatin group. The ovarian and serum MIS levels were higher in the mesna-plus-cisplatin than in the cisplatin alone group. There were no differences statistically in the TUNEL and the ovarian cyst analyses. CONCLUSION: Mesna, which was used at the time of cisplatin administration, protected ovaries against damage. The data that are presented challenge the existing clinical paradigm that gonadotropin-releasing hormone agonists represent the only medical method for the protection of ovaries during chemotherapy. Alternative medical means to protect ovaries during chemotherapy may be achievable.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7111
    Nombre del producto:
    ApopTag® Plus In Situ Apoptosis Fluorescein Detection Kit

  • APOPTAG® Stop/Wash Buffer

    Tipo de documento:
    Certificado de análisis
    Número de lote:
    3010199
    Referencia del producto:
    S7108
    Nombre del producto:
    ApopTag® Stop/Wash Buffer

  • Protein kinase Cepsilon inhibits UVR-induced expression of FADD, an adaptor protein, linked to both Fas- and TNFR1-mediated apoptosis. 19194472

    Protein kinase C (PKC)epsilon overexpression in FVB/N transgenic mice sensitized skin to UVR-induced development of squamous cell carcinomas and suppressed formation of sunburn cells, which are DNA-damaged keratinocytes undergoing apoptosis. Here, we elucidated the mechanisms associated with the inhibition of UVR-induced appearance of sunburn cells in PKCepsilon transgenic mice. We found that the inhibition of UVR-induced sunburn cell formation in PKCepsilon transgenic mice may be the result of the inhibition of the expression of Fas, Fas ligand, and the mammalian death adaptor protein termed Fas-associated with death domain (FADD). The adaptor protein FADD is the key component of the death-inducing signaling complex of both Fas and tumor necrosis factor receptor 1. A decreased expression of epidermal FADD was observed after a single UVR exposure. However, a complete loss of FADD expression was found after four (Monday, Wednesday, Friday, and Monday) repeated UVR exposures. FADD transmits apoptotic signals from death receptors to the downstream initiator caspase-8 and connects to the mitochondrial intrinsic apoptotic signal transduction pathway by the cleavage of Bid, a Bcl-2 family member. PKCepsilon-mediated loss of FADD expression inhibited UVR signals to the activation of both extrinsic and intrinsic apoptotic pathways.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7111
    Nombre del producto:
    ApopTag® Plus In Situ Apoptosis Fluorescein Detection Kit