Botany - Research Publications

Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/32

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    Abiotic stress in algae: response, signaling and transgenic approaches
    (Springer Science and Business Media B.V., 2022-05-02T00:00:00) Kaur, Manpreet; Saini, Khem Chand; Ojah, Hiramoni; Sahoo, Rajalakshmi; Gupta, Kriti; Kumar, Adesh; Bast, Felix
    High salinity, nutrient deficiency, heavy metals, desiccation, temperature fluctuations, and ultraviolet radiations are major abiotic stress factors considered inhospitable to algal growth and development in natural and artificial environments. All these stressful conditions cause effects on algal physiology and thus biochemical functioning. For instance, long-term exposure to hyper/hypo salinity conditions inhibits cell differentiation and reduces growth. Photosynthesis is completely blocked in algae's dehydrated state, resulting in photoinhibition or photodamage. The limitation of nutrients in aquatic environments inhibits primary production via regulating phytoplankton community development and structure. Hence, in response to these stressful conditions, algae develop plenty of cellular, physiological, and morphological defences to survive and thrive. The conserved and generalized defence responses in algae include the production of secondary metabolites, desaturation of membrane lipids, activation of reactive species scavengers, and accumulation of compatible solutes. Moreover, a well-coordinated and timely response to such stresses involves signal perception and transduction mainly via phytohormones that could sustain algae growth under abiotic stress conditions. In addition, the combination of abiotic stresses and plant hormones could further elevate the biosynthesis of metabolites and enhance the ability of algae to tolerate abiotic stresses. This review aims to present different kinds of stressful conditions confronted by algae and their physiological and biochemical responses, the role of phytohormones in combatting these conditions, and, last, the future transgenic approaches for improving abiotic stress tolerance in algae. � 2022, The Author(s), under exclusive licence to Springer Nature B.V.
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    Abiotic stress in algae: response, signaling and transgenic approaches
    (Springer Science and Business Media B.V., 2022-05-02T00:00:00) Kaur, Manpreet; Saini, Khem Chand; Ojah, Hiramoni; Sahoo, Rajalakshmi; Gupta, Kriti; Kumar, Adesh; Bast, Felix
    High salinity, nutrient deficiency, heavy metals, desiccation, temperature fluctuations, and ultraviolet radiations are major abiotic stress factors considered inhospitable to algal growth and development in natural and artificial environments. All these stressful conditions cause effects on algal physiology and thus biochemical functioning. For instance, long-term exposure to hyper/hypo salinity conditions inhibits cell differentiation and reduces growth. Photosynthesis is completely blocked in algae's dehydrated state, resulting in photoinhibition or photodamage. The limitation of nutrients in aquatic environments inhibits primary production via regulating phytoplankton community development and structure. Hence, in response to these stressful conditions, algae develop plenty of cellular, physiological, and morphological defences to survive and thrive. The conserved and generalized defence responses in algae include the production of secondary metabolites, desaturation of membrane lipids, activation of reactive species scavengers, and accumulation of compatible solutes. Moreover, a well-coordinated and timely response to such stresses involves signal perception and transduction mainly via phytohormones that could sustain algae growth under abiotic stress conditions. In addition, the combination of abiotic stresses and plant hormones could further elevate the biosynthesis of metabolites and enhance the ability of algae to tolerate abiotic stresses. This review aims to present different kinds of stressful conditions confronted by algae and their physiological and biochemical responses, the role of phytohormones in combatting these conditions, and, last, the future transgenic approaches for improving abiotic stress tolerance in algae. � 2022, The Author(s), under exclusive licence to Springer Nature B.V.
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    Antioxidant potential of ganoderic acid in Notch-1 protein in neuroblastoma
    (Springer New York LLC, 2019) Gill B.S.; Navgeet; Kumar S.
    Neuroblastoma is a childhood tumor arising from developing a sympathetic nervous system and causes around 10% of pediatric tumors. Despite advancement in the use of sophisticated techniques in molecular biology, neuroblastoma patient's survivability rate is very less. Notch pathway is significant in upholding cell maintenance and developmental process of organs. Notch-1 proteins are a ligand-activated transmembrane receptor which decides the fate of the cell. Notch signaling leads to transcription of genes which indulged in numerous diseases including tumor progression. Ganoderic acid, a lanosterol triterpene, isolated from fungus Ganoderma lucidum with a wide range of medicinal values. In the present study, various isoforms of the ganoderic acid and natural inhibitors were docked by molecular docking using Maestro 9 in the Notch-1 signaling pathway. The receptor-based molecular docking exposed the best binding interaction of Notch-1 with ganoderic acid A with GScore (? 8.088), kcal/mol, Lipophilic EvdW (? 1.74), Electro (? 1.18), Glide emodel (? 89.944) with the active participation of Arg 189, Arg 199, Glu 232 residues. On the other hand natural inhibitor, curcumin has GScore (? 7.644), kcal/mol, Lipophilic EvdW (? 2.19), Electro (? 0.73), Glide emodel (? 70.957) with Arg 75 residues involved in docking. The ligand binding affinity of ganoderic acid A in Notch-1 is calculated using MM-GBSA (? 76.782), whereas curcumin has (? 72.815) kcal/mol. The QikProp analyzed the various drug-likeness parameters such as absorption, distribution, metabolism, excretion, and toxicity (ADME/T) and isoforms of ganoderic acid require some modification to fall under Lipinski rule. The ganoderic acid A and curcumin were the best-docked among different compounds and exhibits downregulation in Notch-1 mRNA expression and inhibits proliferation, viability, and ROS activity in IMR-32 cells.
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    Antioxidant potential of ganoderic acid in Notch-1 protein in neuroblastoma
    (Springer, 2018) Gill, Balraj Singh; Navgeet; Kuamr, Sanjeev
    Neuroblastoma is a childhood tumor arising from developing a sympathetic nervous system and causes around 10% of pediatric tumors. Despite advancement in the use of sophisticated techniques in molecular biology, neuroblastoma patient's survivability rate is very less. Notch pathway is significant in upholding cell maintenance and developmental process of organs. Notch-1 proteins are a ligand-activated transmembrane receptor which decides the fate of the cell. Notch signaling leads to transcription of genes which indulged in numerous diseases including tumor progression. Ganoderic acid, a lanosterol triterpene, isolated from fungus Ganoderma lucidum with a wide range of medicinal values. In the present study, various isoforms of the ganoderic acid and natural inhibitors were docked by molecular docking using Maestro 9 in the Notch-1 signaling pathway. The receptor-based molecular docking exposed the best binding interaction of Notch-1 with ganoderic acid A with GScore (- 8.088), kcal/mol, Lipophilic EvdW (- 1.74), Electro (- 1.18), Glide emodel (- 89.944) with the active participation of Arg 189, Arg 199, Glu 232 residues. On the other hand natural inhibitor, curcumin has GScore (- 7.644), kcal/mol, Lipophilic EvdW (- 2.19), Electro (- 0.73), Glide emodel (- 70.957) with Arg 75 residues involved in docking. The ligand binding affinity of ganoderic acid A in Notch-1 is calculated using MM-GBSA (- 76.782), whereas curcumin has (- 72.815) kcal/mol. The QikProp analyzed the various drug-likeness parameters such as absorption, distribution, metabolism, excretion, and toxicity (ADME/T) and isoforms of ganoderic acid require some modification to fall under Lipinski rule. The ganoderic acid A and curcumin were the best-docked among different compounds and exhibits downregulation in Notch-1 mRNA expression and inhibits proliferation, viability, and ROS activity in IMR-32 cells.
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    Metformin inhibits human breast cancer cell growth by promoting apoptosis via a ROS-independent pathway involving mitochondrial dysfunction: pivotal role of superoxide dismutase (SOD)
    (Springer, 2018) Sharma, Prateek; Kumar, Sanjeev
    Purpose Despite a growing body of evidence indicating a potential efficacy of the anti-diabetic metformin as anti-cancer agent, the exact mechanism underlying this efficacy has remained largely unknown. Here, we aimed at assessing putative mechanisms associated with the ability of metformin to reduce the proliferation and migration of breast cancer cells. Methods A battery of in vitro assays including MTT, colony formation, NBT and scratch wound healing assays were performed to assess the viability, proliferation, anti-oxidative potential and migration of breast cancer-derived MCF-7, MDA-MB-231 and T47D cells, respectively. Reactive oxygen species (ROS) assays along with fluorescence microscopy were used to assess apoptotic parameters. Quantification of SOD, Bcl-2, Bax, MMPs, miR-21 and miR-155 expression was performed using qRT-PCR. Results We found that metformin inhibited the growth, proliferation and clonogenic potential of the breast cancer-derived cells tested. ROS levels were found to be significantly reduced by metformin and, concomitantly, superoxide dismutase (SOD) isoforms were found to be upregulated. Mitochondrial dysfunction was observed in metformin treated cells, indicating apoptosis. In metastatic MDA-MB-231 cells, migration was found to be suppressed by metformin through deregulation of the matrix metalloproteinases MMP-2 and MMP-9. The oncogenic microRNAs miR-21 and miR-155 were found to be downregulated by metformin, which may be correlated with the suppression of cell proliferation and/or migration. Conclusions Our data indicate that metformin may play a pivotal role in modulating the anti-oxidant system, including the SOD machinery, in breast cancer-derived cells. Our observations were validated by in silico analyses, indicating a close interaction between SOD and metformin. We also found that metformin may inhibit breast cancer-derived cell proliferation through apoptosis induction via the mitochondrial pathway. Finally, we found that metformin may modulate the pro-apoptotic Bax, anti-apoptotic Bcl-2, MMP-2, MMP-9, miR-21 and miR-155 expression levels. These findings may be instrumental for the clinical management and/or (targeted) treatment of breast cancer.