• Rasheedunnisa Begum

      Articles written in Journal of Biosciences

    • Invitro culturedSpodoptera frugiperda insect cells: Model for oxidative stress-induced apoptosis

      Seyed E Hasnain Tarvinder K Taneja Nand K Sah Manjari Mohan Niteen Pathak Sudhir Sahdev Mohammad Athar Satish M Totey Rasheedunnisa Begum

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      Cellular imbalance in the levels of antioxidants and reactive oxygen species (ROS) is directly associated with a number of pathological states and results in programmed cell death or apoptosis. We demonstrate the use ofin vitro culturedSpodoptera frugiperda (sf9) insect cells as a model to study oxidative stress induced programmed cell death. Apoptosis ofin vitro cultured sf9 cells was induced by the exogenous treatment of H2O2 to cells growing in culture. The AD50 (concentration of H2O2 inducing about 50% apoptotic response) varied with the duration of treatment, batch to batch variation of H2O2 and the physiological state of cells. At 24 h post-treatment with H2O2 AD50 was about 475 Μm. Apoptosis could also be induced byin situ generation of H2O2 by the inhibition of catalase activity upon hydroxylamine treatment. Hydroxylamine acted synergistically with H2O2 with an AD50 of 2.2 mM. DMSO, a free radical scavenger, inhibited H2O2-induced apoptosis thereby confirming the involvement of reactive oxygen species. Exposure of cells to UV radiation (312 nm) resulted in a dose-dependent induction of apoptosis. These results provide evidence on the novel use of insect cells as a model for oxidative stress-induced apoptosis.

    • Biochemical basis of the high resistance to oxidative stress inDictyostelium discoideum

      Bandhana Katoch Rasheedunnisa Begum

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      Aerobic organisms experience oxidative stress due to generation of reactive oxygen species during normal aerobic metabolism. In addition, several chemicals also generate reactive oxygen species which induce oxidative stress. Thus oxidative stress constitutes a major threat to organisms living in aerobic environments. Programmed cell death or apoptosis is a physiological mechanism of cell death, that probably evolved with multicellularity, and is indispensable for normal growth and development.Dictyostelium discoideum, an eukaryotic developmental model, shows both unicellular and multicellular forms in its life cycle and exhibits apparent caspase-independent programmed cell death, and also shows high resistance to oxidative stress. An attempt has been made to investigate the biochemical basis for high resistance ofD. discoideum cell death induced by different oxidants. Dose-dependent induction of cell death by exogenous addition of hydrogen peroxide (H2O2),in situ generation of H2O2 by hydroxylamine, and nitric oxide (NO) generation by sodium nitroprusside treatment inD. discoideum were studied. The AD50 doses (concentration of the oxidants cusing 50% of the cells to die) after 24 h of treatment were found to be 0.45 mM, 4 mM and 1 mM, respectively. Studies on enzymatic antioxidant status ofD. discoideum when subjected to oxidative stress, NO and nutrient stress reveal that superoxide dismutase and catalase were unchanged; a significant induction of glutathione peroxidase was observed. Interestingly, oxidative stress-induced lipid membrane peroxidative damage could not be detected. The results shed light on the biochemical basis for the observed high resistance to oxidative stress inD. discoideum.

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      Forthcoming Special issue.

    • To trigger further research on plant mitochondria, the Journal of Biosciences is bringing out a special issue titled "Plant Mitochondria: Properties and Interactions with Other Organelles".

      Plant mitochondria are quite distinct and have unique features, such as a cyanide-insensitive alternate pathway. They also interact with chloroplasts to optimize photosynthetic carbon assimilation.

      Submissions are welcome until 30 July 2023. The contributions can be original articles, short communications, reviews, or mini-reviews on any topic related to plant mitochondria.

      Authors can submit their articles online at https://www.editorialmanager.com/jbsc/default2.aspx

      Posted on April 12, 2023
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