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How can hydrogen peroxide induce oxidative stress in hela cells?

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Hydrogen peroxide (H2O2) induces oxidative stress in HeLa cells through various mechanisms. H2O2 inhibits rDNA transcription, reduces RNA content, and causes nucleolar protein relocalization . It increases ROS levels, activates caspase-3, and induces apoptosis or necrosis, leading to mitochondrial membrane potential loss . Additionally, H2O2 can modulate aquaporin (AQP) permeability, facilitating H2O2 diffusion and increasing oxidative stress . Moreover, H2O2 can enhance hydrogen peroxide production by lactate dehydrogenase (LDH), contributing to cellular oxidative stress . Conversely, U. rigida ethanolic precipitate protects against H2O2-induced apoptosis by upregulating anti-apoptotic Bcl-xL and preventing MMP loss . Overall, H2O2 induces oxidative stress in HeLa cells by disrupting cellular processes, increasing ROS levels, and promoting apoptotic pathways.

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Open access•Journal Article•DOI Lactate dehydrogenases amplify reactive oxygen species in cancer cells in response to oxidative stimuli Hao Wu, Yuqi Wang, Minfeng Ying, Chengmeng Jin, Jiangtao Li, Xun Hu - Show less +5 more 28 Jun 2021-Signal Transduction and Targeted Therapy 19 Citations	Hydrogen peroxide induces oxidative stress in HeLa cells by being amplified by lactate dehydrogenases, particularly LDHA and LDHB, in response to oxidative stimuli, such as superoxide generated from mitochondria.
Open access•Journal Article•DOI Anti-apoptotic effect of caspase inhibitors on H2O2-treated HeLa cells through early suppression of its oxidative stress Woo Hyun Park 01 May 2014-Oncology Reports 20 Citations	Hydrogen peroxide induces oxidative stress in HeLa cells by increasing reactive oxygen species (ROS) levels, depleting glutathione (GSH), and activating caspases, leading to apoptosis or necrosis.
Open access•Journal Article•DOI Cerium Oxide Nanoparticles Regulate Oxidative Stress in HeLa Cells by Increasing the Aquaporin-Mediated Hydrogen Peroxide Permeability Giorgia Pellavio, Patrizia Sommi, Umberto Anselmi-Tamburini, Maria Paola Demichelis, Stefania Coniglio, Umberto Laforenza - Show less +5 more 01 Sep 2022-International Journal of Molecular Sciences 1 Citations	Hydrogen peroxide induces oxidative stress in HeLa cells by diffusing through aquaporins (AQP3, 6, 8) and increasing ROS levels, which can be regulated by cerium oxide nanoparticles.
Journal Article•DOI [Cytological analysis of the reaction of the nucleolar RNA and RNA-binding proteins to oxidative stress in HeLa cells] A. A. Mironova, A. A. Mironova, Natalia V. Barykina, Natalia V. Barykina, Olga V. Zatsepina - Show less +4 more 17 Dec 2014-Tsitologiia 4 Citations	Hydrogen peroxide induces oxidative stress in HeLa cells by inhibiting rDNA transcription, reducing total RNA content, diminishing 18S rRNA levels in nucleoli, and causing RNA-binding proteins to relocate.

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What is the definition and mechanism of oxidative stress?5 answersOxidative stress (OS) is characterized by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses. ROS, generated from endogenous and exogenous sources, induce DNA damage, inflammation, and cellular dysfunction, contributing to various diseases like cancer and respiratory conditions. In reproductive health, OS disrupts processes like spermatogenesis, folliculogenesis, and pregnancy, impacting fertility and sterility. Mitochondria play a crucial role in OS, as mitochondrial ROS contribute to aging and disease development. Antioxidants counteract OS effects, highlighting the importance of maintaining a balance between pro-oxidants and antioxidants for overall health. The intricate interplay between ROS, antioxidants, and cellular signaling pathways underscores the dual role of ROS as both a contributor to disease pathogenesis and a potential target for therapeutic interventions.

What is the effect of HSPB1 during oxidative stress induction in HeLA cells regarding intinsic apoptosis?4 answersDuring oxidative stress induction in HeLa cells, HSPB1 plays a crucial role in regulating intrinsic apoptosis. HSPB1 interacts with BIM, a pro-apoptotic protein, and modulates its stability. Additionally, HSPB1 can affect stress resistance and cell morphology by forming hetero-oligomeric complexes with other small heat shock proteins like HspB5. Furthermore, HSPB1 upregulation during oxidative stress promotes autophagy and inhibits apoptosis in renal tubular cells, highlighting its protective role against cell death. In H9c2 cells, HSPB1 enhances the reduced state of antioxidant pathways, including glutathione reductase and peroxiredoxin 1, ultimately improving the redox state of the cytoplasm. Overall, HSPB1's involvement in regulating apoptosis and autophagy during oxidative stress underscores its significance in cellular responses to stress conditions.

What are the factors that can increase oxidative stress in the skin?5 answersFactors that can increase oxidative stress in the skin include exposure to air pollution, water contamination, light-emitting diodes, electromagnetic frequencies, various yeast and fungi, parasitic infections, mold, heavy metal toxicity, solar ultraviolet, infrared and visible light, and psychological stress. Additionally, environmental stressors such as UV radiation, ionizing radiation, pollutants, and heavy metals, as well as xenobiotics like antiblastic drugs, can contribute to increased production of reactive oxygen species (ROS) and oxidative stress in the skin. Cigarette smoke exposure has also been shown to induce oxidative stress in the skin, leading to increased autofluorescence intensities.

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How oxidative stress disrupt cellular signaling pathway?2 answersOxidative stress disrupts cellular signaling pathways by modifying cell-signaling proteins, ion channels and transporters, and protein kinase and ubiquitination/proteasome systems. It can also lead to cell death through mitochondrial apoptotic pathways and activation of mitogen-activated protein kinases (MAPKs). Activation of the MEK5/ERK5 pathway, which is frequently involved in oxidative stress effects, plays a role in the anti-oxidative response. Additionally, oxidative stress can dysregulate the autophagy pathway, leading to non-canonical activation of the nuclear factor erythroid-2 (NF-E2)-related factor 2 (NRF2). NRF2 is a transcription factor that controls the expression of genes involved in counteracting oxidative stress. Dysregulation of NRF2 activation can have deleterious effects, highlighting the importance of controlled, canonical activation of NRF2 for cytoprotection.

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