scholarly journals A trade-off between stress resistance and tolerance underlies the adaptive response to hydrogen peroxide

2021 ◽  
Author(s):  
Basile Jacquel ◽  
Audrey Matifas ◽  
Gilles Charvin

In response to environmental stress, cellular defense strategies may be divided into two categories: those, as in homeostatic systems, that seek to maintain cell proliferation by degrading the stressor (i.e., resistance); and those that ensure cell survival (i.e. tolerance), even if this is often at the expense of cell proliferation. In this study, we have explored the genetic bases of the antagonism between resistance and tolerance during the response to hydrogen peroxide (H2O2) in budding yeast. We show that inactivation of protein kinase A (PKA) by H2O2 signaling induces an abrupt transition from normal homeostatic function to a stress-tolerant state by protecting the growth machinery, hence maximizing cellular fitness in a changing environment. This model system paves the way for developing antiproliferative strategies that target both resistance and tolerance mechanisms to prevent relapse.

2007 ◽  
Vol 330-332 ◽  
pp. 131-134
Author(s):  
S. Yabe ◽  
Kanji Tsuru ◽  
Satoshi Hayakawa ◽  
Akiyoshi Osaka ◽  
Y. Yoshida ◽  
...  

Titania layer was fabricated on the titanium substrates with chemical treatment with 20ml or 40ml of hydrogen peroxide solution and subsequent heat treatment at 400°C, coded as CHT20 and CHT40, respectively. CHT20 spontaneously deposited apatite on the surface in a simulated body fluid (SBF), while CHT40 did not. TF-XRD patterns showed that the diffraction intensity of anatase of CHT20 was higher than that of CHT40. It was suggested that the thicker titania layer indicated in vitro apatite forming ability. The cell proliferation of CHT20 and CHT40 were lower than NT and HT. Since the surface of titania layers became hydrophobic after autoclaving, we can suppose that the cell proliferation on CHT20 and CHT40 were lower than NT and HT due to their surface hydrophobicity.


2017 ◽  
Vol 81 ◽  
pp. 103-109 ◽  
Author(s):  
Francine Benetti ◽  
João Eduardo Gomes-Filho ◽  
Luciana Louzada Ferreira ◽  
Edilson Ervolino ◽  
André Luiz Fraga Briso ◽  
...  

Author(s):  
Suriya Kumaresan ◽  
Rema Ramasamy ◽  
Philip Robinson Jayachandran

Objectives: Medicinal plants and herbs are used in combination in Ayurveda and folklore medicine as they exhibit good cytotoxic activity. In the present study, the antioxidant, phytochemical, and cell proliferation activity of the combined crude methanolic extract of Ficus religiosa and Ficus benghalensis leaves were investigated.Methods: Antioxidant activity was performed by 2, 2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) and hydrogen peroxide methods, and the presence of the phytochemicals was screened using the gas chromatography–mass spectrometry. The extract was further evaluated for its cell proliferation activity against cancer cells using the mitochondrial reduction assay. Antioxidant property of the extracts was measured using the DPPH, hydrogen peroxide, and ferric-reducing antioxidant power assay, respectively, using the UV spectrophotometer.Results: The combined extract exhibited strong antioxidant potential in DPPH assay by increase in the percentage of inhibition with the increase in concentration. Similarly, the IC50 value of the methanol extract in peroxidase scavenging activity was 49.85 μg/mL comparatively lower than the ascorbic acid used as standard. The phytochemical analysis of the methanol extract showed the presence of nine phytoconstituents, which exhibit antioxidant and anticancer property. Mitochondrial reduction assay performed to evaluate the cell proliferation activity of the combined leave extract showed that increase in the concentration of the extract decreased the cell proliferation in the HeLa cell line.Conclusion: The results of present study show a possible synergistic activity of leaves against human cervical cancer.


2009 ◽  
Vol 292 (8) ◽  
pp. 1107-1113 ◽  
Author(s):  
Ming Li ◽  
Li Zhao ◽  
Jun Liu ◽  
An-Ling Liu ◽  
Wei-Sen Zeng ◽  
...  

2014 ◽  
Vol 92 (5) ◽  
pp. 406-412 ◽  
Author(s):  
Fu-Xiang Yu ◽  
Yin-Yan Teng ◽  
Qian-Dong Zhu ◽  
Qi-Yu Zhang ◽  
Yin-He Tang

Hepatic stellate cells (HSCs) play an important role in the process of liver fibrosis. In this study, we investigated the inhibitory effects of capsaicin on HSCs and liver fibrosis. Cultured HSCs were incubated with various concentrations of capsaicin. Cell proliferation was examined using a cell counting kit. Production of hydrogen peroxide was determined using a 2′,7′-dichlorofluorescin diacetate (DCFH-DA) assay. The mRNA and protein expression of target genes was analyzed by reverse transcription PCR and Western blot analysis, respectively. Cell apoptosis was evaluated by annexin V-FITC and propidium iodide (PI) costaining followed by flow cytometric analysis. A CCl4 rat liver fibrosis model was used to assess in vivo effects of capsaicin by histological examination and measurement of liver fibrosis markers, including hydroxyproline content, serum type III collagen, and hyaluronic acid (HA) levels. Our results show that capsaicin dose-dependently inhibited cell proliferation, suppressed cell activation, and decreased hydrogen peroxide production in cultured HSCs. Capsaicin reduced the mRNA levels of tissue inhibitors of metalloproteinase 1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in HSCs. Moreover, capsaicin-induced cell apoptosis was associated with increased expression of Bax, cytochrome c (cyt c), and caspase-3, but reduced levels of Bcl-2. The animal studies further revealed that capsaicin efficiently reduced the extent of liver fibrosis, inhibited HSC proliferation, and promoted cell apoptosis. Our findings suggest that capsaicin might inhibit fibrogenesis by inhibiting the activities of HSCs.


Microbiology ◽  
2006 ◽  
Vol 152 (6) ◽  
pp. 1671-1677 ◽  
Author(s):  
Andrei L. Brioukhanov ◽  
Alexander I. Netrusov ◽  
Rik I. L. Eggen

Methanosarcina barkeri is a strictly anaerobic methanogenic archaeon, which can survive oxidative stress. The oxidative stress agent paraquat (PQ) suppressed growth of M. barkeri at concentrations of 50–200 μM. Hydrogen peroxide (H2O2) inhibited growth at concentrations of 0.4–1.6 mM. Catalase activity in cell-free extracts of M. barkeri increased about threefold during H2O2 stress (1.3 mM H2O2, 2–4 h exposure) and nearly twofold during superoxide stress (160 μM PQ, 2 h exposure). PQ (160 μM, 2–4 h exposure) and H2O2 (1.3 mM, 2 h exposure) also influenced superoxide dismutase activity in cell-free extracts of M. barkeri. Dot-blot analysis was performed on total RNA isolated from H2O2- and PQ-exposed cultures, using labelled internal DNA fragments of the sod and kat genes. It was shown that H2O2 but not PQ strongly induced up-regulation of the kat gene. PQ and to a lesser degree H2O2 induced the expression of superoxide dismutase. The results indicate the regulation of the adaptive response of M. barkeri to different oxidative stresses.


2014 ◽  
Vol 197 (3) ◽  
pp. 431-440 ◽  
Author(s):  
Lu Zhang ◽  
James R. Alfano ◽  
Donald F. Becker

The oxidation ofl-proline to glutamate in Gram-negative bacteria is catalyzed by the proline utilization A (PutA) flavoenzyme, which contains proline dehydrogenase (PRODH) and Δ1-pyrroline-5-carboxylate (P5C) dehydrogenase domains in a single polypeptide. Previous studies have suggested that aside from providing energy, proline metabolism influences oxidative stress resistance in different organisms. To explore this potential role and the mechanism, we characterized the oxidative stress resistance of wild-type andputAmutant strains ofEscherichia coli. Initial stress assays revealed that theputAmutant strain was significantly more sensitive to oxidative stress than the parental wild-type strain. Expression of PutA in theputAmutant strain restored oxidative stress resistance, confirming that depletion of PutA was responsible for the oxidative stress phenotype. Treatment of wild-type cells with proline significantly increased hydroperoxidase I (encoded bykatG) expression and activity. Furthermore, the ΔkatGstrain failed to respond to proline, indicating a critical role for hydroperoxidase I in the mechanism of proline protection. The global regulator OxyR activates the expression ofkatGalong with several other genes involved in oxidative stress defense. In addition tokatG, proline increased the expression ofgrxA(glutaredoxin 1) andtrxC(thioredoxin 2) of the OxyR regulon, implicating OxyR in proline protection. Proline oxidative metabolism was shown to generate hydrogen peroxide, indicating that proline increases oxidative stress tolerance inE. colivia a preadaptive effect involving endogenous hydrogen peroxide production and enhanced catalase-peroxidase activity.


1999 ◽  
Vol 190 (1) ◽  
pp. 53-64 ◽  
Author(s):  
Carla Miller ◽  
Jack A. Ragheb ◽  
Ronald H. Schwartz

Recombinant-activating gene 2 (RAG-2−/−) T cell receptor–transgenic mice repeatedly injected with the superantigen staphylococcal enterotoxin A entered a tolerant state in which splenic CD4+ T cells produced little interleukin (IL)-2, interferon γ, or IL-4. This state resulted from a combination of both clonal anergy and cytokine-mediated immunosuppression. The anergy persisted for at least 3 wk and could be distinguished from the suppression by a decrease in IL-2 production per cell, a block in the activation of early response kinases, and a failure to be reversed with anti–transforming growth factor (TGF)-β. Full suppression lasted for only 1 wk and involved both IL-10 and TGF-β, but required additional unknown molecules for optimal effect. These experiments show that complex in vivo interactions of multiple peripheral tolerance mechanisms can now be dissected at both the cellular and molecular levels.


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