2009
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PublicationArticle Intracellular levels of hydrogen peroxide and nitric oxide in oocytes at various stages of meiotic cell cycle and apoptosis(2009) Anima Tripathi; Sabana Khatun; A.N. Pandey; S.K. Mishra; Radha Chaube; T.G. Shrivastav; S.K. ChaubeThe objective was to find out the functional roles of hydrogen peroxide (H2O2) and nitric oxide (NO) during various stages of meiotic cell cycle and apoptosis in rat oocytes. For this purpose, 30 oocytes from each stage such as diplotene, metaphase-I (M-I), metaphase-II (M-II) and apoptosis were collected and intracellular H2O2, total nitrite level and inducible nitric oxide synthase (iNOS) expression were analysed. This study demonstrated that generation of a tonic level of H2O2 induces meiotic resumption in diplotene-arrested oocytes and further increase may lead to apoptosis. Conversely, reduction in iNOS expression and total nitrite level are associated with meiotic resumption in diplotene-arrested oocytes, but induce apoptosis in aged oocytes. These results suggest that generation of a tonic level of H2 O2, reduced iNOS expression and total nitrite level are associated with meiotic resumption, while more generation of H2O2 and sustained reduced total nitrite level are linked with oocyte apoptosis in rat.PublicationArticle Extracellular calcium protects against verapamil-induced metaphase-II arrest and initiation of apoptosis in aged rat eggs(2009) S.K. Chaube; Anima Tripathi; Sabana Khatun; S.K. Mishra; P.V. Prasad; T.G. ShrivastavNon-specific L-type calcium channel blockers, such as verapamil (≥50 μM), induce metaphase-II (M-II) arrest and apoptosis in aged rat eggs cultured in Ca2+-deficient medium. However, the effects of extracellular Ca2+ on verapamil-induced M-II arrest and apoptosis have not yet been reported. We have demonstrated that postovulatory aging induced exit from M-II arrest by extruding a second polar body, a morphological sign of spontaneous egg activation (SEA). Verapamil inhibited SEA and induced egg apoptosis in a dose-dependent manner in Ca2+-deficient medium. The initiation of apoptotic features was observed at 50 μM of verapamil. Extracellular Ca2+ (1.80 mM) reduced intracellular H2O2 level, bax protein expression, caspase-3 activity, DNA fragmentation and protected against 50 μM, but not higher concentrations of ≥100 μM in verapamil-induced egg apoptosis. These results suggest that extracellular Ca2+ ions have a role during SEA and protect against verapamil-induced apoptosis in aged rat eggs. © 2009 International Federation for Cell Biology.PublicationArticle A tumour stage-dependent evolution of drug resistant T cell lymphoma: Role of soluble mediators of tumour and host origin(2009) Vivek Singh; Sukh Mahendra SinghThe present investigation was carried out to investigate if soluble mediators present in tumour microenvironment and systemic circulation of a tumour-bearing host can regulate growth properties and response of the cells of a T cell lymphoma to chemotherapeutic drug: cisplatin, depending on the stage of tumour progression. In order to investigate this, tumour cells of a murine T cell lymphoma, designated as Dalton's lymphoma (DL), were incubated in vitro for 48 h in the presence of ascitic fluid and serum obtained from cisplatin treated or untreated tumour hosts at early or late tumour-bearing stages and cell survival was estimated. It was observed that tumour serum and ascitic fluid showed a tumour stage-dependent differential ability to regulate tumour cell survival and susceptibility of the tumour cells to the cytotoxic action of cisplatin. A tumour stage-dependent qualitative and quantitative difference in the profile of cell survival regulating cytokines: IL-1, IL-2, IFN-γ, TNF-α, VEGF and TGF-β in the ascitic fluid and serum of the tumour-bearing host was observed to be associated with a tumour stage-dependent differential regulation of survival of tumour cells by modulation in the expression of growth regulating proteins: IL-2R, p53, CAD, Hsp70 and Bcl-2. Further the result also showed that production of IL-1, TNF-α, and NO by macrophages could be implicated in the differential action of tumour sera on the altered survival responses of tumour cells depending on the stage of tumour growth. Possible mechanisms involved in the tumour stage-dependent differential survival response of tumour cells and evolution of drug resistance are discussed. The finding of this investigation will have clinical implications in designing of therapeutic strategies for T cell lymphoma based on manipulation of tumour growth regulatory mediators present in the tumour microenvironment. © 2008 Elsevier Ltd. All rights reserved.PublicationArticle Mutation in Rab11 results in abnormal organization of ommatidial cells and activation of JNK signaling in the Drosophila eye(2009) Anand K. Tiwari; Jagat K. RoyRab11mo, a P insertion line of Rab11 showed degenerated ommatidia and excess cell death in larval/pupal eyes. Here, we demonstrate that Rab11 is essential for normal organization of ommatidial cells and their survival in Drosophila, and a mutation in this gene results in cytoskeleton disruption and activation of JNK signaling in the eye. The spatial organization of various cell types in compound eye, viz., cone, photoreceptor, pigment and bristle cells, were disrupted in Rab11 mutants as revealed by immunostaining of F-actin and adherens and septate junction proteins. Genetic interaction studies indicated that mutation in Rab11 upregulates Drosophila apoptotic genes, rpr, hid and grim. In order to study the pathway that causes excessive cell death in Rab11 mutants, the JNK pathway was chosen and genetic interaction analyses were carried out between Rab11 and candidates of the JNK signaling pathway. A downregulation of JNK signaling rescued the phenotype in Rab11 mutant eyes significantly while overexpression of JNK in the eyes using UAS-eiger, UAS-dtak1 or EP(2)0578, resulted in enhancement of the eye phenotype indicating a link between Rab11 and the JNK signaling pathway. © 2009 Elsevier GmbH. All rights reserved.PublicationReview Apoptosis: Molecular mechanisms and pathogenicity(2009) Rajesh P. Rastogi; Richa; Rajeshwar P. SinhaApoptosis triggered by exogenous and endogenous stimuli such as ultraviolet radiation, oxidative stress, and genotoxic chemicals is a crucial phenomenon within biological systems. DNA damage activates and stabilizes p53 in nucleus and cytoplasm and regulates other proteins that stimulate intrinsic and extrinsic apoptotic pathways. Apoptosis is morphologically distinct from that of necrosis and both the phenomena depend on the types, developmental stages, physiological environment of tissues and the nature of death signal. Malfunctioning of apoptotic pathway may cause human diseases like cancer, neurodegenerative and autoimmune disorders. Recently, potent apoptosis-inducing compounds associated with human health have been recorded that prevent tumor promotion, progression, and the occurrence of cellular inflammatory responses. Certain photosensitizing drugs are being employed in photodynamic therapy to induce apoptosis for the treatment of cancer and non-cancerous cells. This review emphasizes the molecular mechanisms of apoptosis, associated diseases and certain therapeutic agents implicated in the elimination of malignant cells.PublicationArticle Curcumin induced cell death and inhibition of telomerase activity in mouse lymphoma P388D1 cells(2009) Vijendra Kumar Mishra; Ashok KumarTelomerase, a potential marker for tumorigenesis, has been found to be activated in more than 85-90% of human cancer. Curcumin is the major biologically active, yellow phytochemical compound of Curcuma longa (Zingiberaceae). The present study is aimed to investigate the capacity of curcumin on the regulation of telomerase activity and induction of apoptosis in P388D1 mouse lymphoma cells. Here, we demonstrate that curcumin at a concentration of 3.5 μM and an incubation period of 48h induces apoptosis and inhibits telomerase activity in the P388D1 cells. Curcumin induced apoptosis and telomerase activity in P388D1 lymphoma cells was confirmed by enumeration of apoptotic cells, % DNA fragmentation and RT-PCR. The culture supernatant of lymphoma cells treated with curcumin showed a higher level of nitric oxide content. RT-PCR analysis revealed over expression of TNF-α and IL-1β and inhibition of the antiapoptotic Bcl-2 and human catalytic subunit hTERT in the curcumin treated lymphoma cells as compared to untreated cells. Taken together the result shows that curcumin could significantly inhibit tumor proliferation and induce apoptosis in lymphoma cells. Thus, curcumin should be further tested as a possible antineoplastic agent.PublicationArticle Regression of Dalton's lymphoma in vivo via decline in lactate dehydrogenase and induction of apoptosis by a ruthenium(II)-complex containing 4-carboxy N-ethylbenzamide as ligand(2009) Raj K. Koiri; Surendra K. Trigun; Lallan Mishra; Kiran Pandey; Deobrat Dixit; Santosh K. DubeySummary: A novel ruthenium(II)-complex containing 4-carboxy N-ethylbenzamide (Ru(II)-CNEB) was found to interact with and inhibit M4-lactate dehydrogenase (M4-LDH), a tumor growth supportive enzyme, at the tissue level. The present article describes modulation of M4-LDH by this compound in a T-cell lymphoma (Dalton's Lymphoma: DL) vis a vis regression of the tumor in vivo. The compound showed a dose dependent cytotoxicity to DL cells in vitro. When a non toxic dose (10 mg/kg bw i.p.) of Ru(II)-CNEB was administered to DL bearing mice, it also produced a significant decline in DL cell viability in vivo. The DL cells from Ru(II)-CNEB treated DL mice showed a significant decline in the level of M4-LDH with a concomitant release of this protein in the cell free ascitic fluid. A significant increase of nuclear DNA fragmentation in DL cells from Ru(II)-CNEB treated DL mice also coincided with the release of mitochondrial cytochrome c in those DL cells. Importantly, neither blood based biochemical markers of liver damage nor the normal patterns of LDH isozymes in other tissues were affected due to the treatment of DL mice with the compound. These results were also comparable with the effects of cisplatin (an anticancer drug) observed simultaneously on DL mice. The findings suggest that Ru(II)-CNEB is able to regress Dalton's lymphoma in vivo via declining M4-LDH and inducing mitochondrial dysfunction-apoptosis pathway without producing any toxicity to the normal tissues. © 2008 Springer Science+Business Media, LLC.