School Of Basic And Applied Sciences

Permanent URI for this communityhttps://kr.cup.edu.in/handle/32116/17

Browse

Has files: NoSubject: search.filters.subject.ROS

Search Results

Now showing 1 - 6 of 6
  • No Thumbnail Available
    Item
    Platelet-derived microvesicles activate human platelets via intracellular calcium mediated reactive oxygen species release
    (Academic Press Inc., 2022-08-28T00:00:00) Yadav, Pooja; Beura, Samir Kumar; Panigrahi, Abhishek Ramachandra; Bhardwaj, Taniya; Giri, Rajanish; Singh, Sunil Kumar
    Platelet-derived microvesicles (PMVs) are the most abundant microvesicles in circulation, originating from blood platelets via membrane blebbing. PMVs act as biological cargo carrying key molecules from platelets, including immunomodulatory molecules, growth factors, clotting molecules, and miRNAs that can regulate recipient cellular functions. Formation and release of PMVs play an essential role in the pathophysiology of vascular diseases such as hemostasis, inflammation, and thrombosis. Platelet activation is considered the critical event in thrombosis, and a growing number of evidence suggests that oxidative stress-mediated signaling plays a significant role in platelet activation. Ca2+ is a notable player in the generation of ROS in platelets. Reports have established that microvesicles exhibit dual nature in redox mechanisms as they possess both pro-oxidant and antioxidant machinery. However, the impact of PMVs and their ROS machinery on platelets is still a limited explored area. Here, we have demonstrated that PMVs mediate platelet activation via intracellular ROS generation. PMVs interacted with platelets and induced calcium-mediated intracellular ROS production via NADPH oxidase (NOX), leading to platelet activation. Our findings will open up new insights into the tangible relationship of PMVs with platelets and will further contribute to the therapeutic aspects of PMVs in vascular injury and tissue remodeling. � 2022
  • No Thumbnail Available
    Item
    Organophosphate-pesticides induced survival mechanisms and APE1-mediated Nrf2 regulation in non-small-cell lung cancer cells
    (John Wiley and Sons Inc, 2020-10-20T00:00:00) Thakur, Shweta; Sarkar, Bibekananda; Dhiman, Monisha; Mantha, Anil K.
    Epidemiological and molecular studies have indicated that environmental exposure to organophosphate pesticides (OPPs) is associated with increased cancer risk; however, the underlying molecular mechanisms still need to be explained. Increasing cancer incidence is linked�to OPPs-induced oxidative stress (OS). Our study evaluates monocrotophos (MCP) and chlorpyrifos (CP)-induced OS responses and apurinic/apyrimidinic endonuclease 1 (APE1) role in human non-small-cell lung cancer (NSCLC) cells. Our prior study has implicated OPPs-induced base excision repair (BER)-pathway dysregulation and APE1-mediated regulation of transcription factor (TF) c-jun in A549 cells. We further investigated the effects of MCP and CP on apoptosis, proliferation, and APE1's redox-regulation of nuclear factor-like 2 (Nrf2). Data demonstrates that MCP and CP at subtoxic concentrations induced reactive oxygen species generation and oxidative DNA base damage 8-oxo-dG lesions in NCI-H1299 cells. CP moderately upregulated�the apoptosis-inducing factor (AIF) in A549 cells, however, it did not trigger other pro-apoptotic factors viz. caspase-9 and caspase-3, suggesting early caspase-independent apoptosis. However, dose-dependent AIF-downregulation was observed for MCP treatment. Furthermore, CP and MCP treatments upregulated proliferating cell nuclear antigen levels. Immunofluorescent confocal imaging showed the colocalization of APE1 with Nrf2 in 10 �M CP- and MCP-treated NCI-H1299 cells. Immunoprecipitation confirmed that APE1 and Nrf2 physically interacted, indicating the role of APE1-mediated Nrf2 activation following OPPs treatment. This study suggests that low concentration MCP and CP exposure generates OS along with DNA damage, and modulates apoptosis, and APE1-mediated Nrf2 activation, which might be considered as the possible mechanism promoting lung cancer cell survival, suggesting that APE1 may have the potential to become a therapeutic target for the treatment of NSCLC. � 2020 Wiley Periodicals LLC
  • No Thumbnail Available
    Item
    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.
  • No Thumbnail Available
    Item
    Organophosphate-pesticides induced survival mechanisms and APE1-mediated Nrf2 regulation in non-small-cell lung cancer cells
    (John Wiley and Sons Inc, 2020-10-20T00:00:00) Thakur, Shweta; Sarkar, Bibekananda; Dhiman, Monisha; Mantha, Anil K.
    Epidemiological and molecular studies have indicated that environmental exposure to organophosphate pesticides (OPPs) is associated with increased cancer risk; however, the underlying molecular mechanisms still need to be explained. Increasing cancer incidence is linked�to OPPs-induced oxidative stress (OS). Our study evaluates monocrotophos (MCP) and chlorpyrifos (CP)-induced OS responses and apurinic/apyrimidinic endonuclease 1 (APE1) role in human non-small-cell lung cancer (NSCLC) cells. Our prior study has implicated OPPs-induced base excision repair (BER)-pathway dysregulation and APE1-mediated regulation of transcription factor (TF) c-jun in A549 cells. We further investigated the effects of MCP and CP on apoptosis, proliferation, and APE1's redox-regulation of nuclear factor-like 2 (Nrf2). Data demonstrates that MCP and CP at subtoxic concentrations induced reactive oxygen species generation and oxidative DNA base damage 8-oxo-dG lesions in NCI-H1299 cells. CP moderately upregulated�the apoptosis-inducing factor (AIF) in A549 cells, however, it did not trigger other pro-apoptotic factors viz. caspase-9 and caspase-3, suggesting early caspase-independent apoptosis. However, dose-dependent AIF-downregulation was observed for MCP treatment. Furthermore, CP and MCP treatments upregulated proliferating cell nuclear antigen levels. Immunofluorescent confocal imaging showed the colocalization of APE1 with Nrf2 in 10 �M CP- and MCP-treated NCI-H1299 cells. Immunoprecipitation confirmed that APE1 and Nrf2 physically interacted, indicating the role of APE1-mediated Nrf2 activation following OPPs treatment. This study suggests that low concentration MCP and CP exposure generates OS along with DNA damage, and modulates apoptosis, and APE1-mediated Nrf2 activation, which might be considered as the possible mechanism promoting lung cancer cell survival, suggesting that APE1 may have the potential to become a therapeutic target for the treatment of NSCLC. � 2020 Wiley Periodicals LLC
  • No Thumbnail Available
    Item
    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.
  • No Thumbnail Available
    Item
    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.