Low oxygen and 1-MCP pretreatments delay superficial scald development by reducing reactive oxygen species (ROS) accumulation in stored ‘Granny Smith’ apples

2011 ◽  
Vol 62 (3) ◽  
pp. 295-304 ◽  
Author(s):  
Revital Sabban-Amin ◽  
Oleg Feygenberg ◽  
Eduard Belausov ◽  
Edna Pesis
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Superficial Scald ◽  
Ros Accumulation

scholarly journals Decitabine Induces Delayed Reactive Oxygen Species (ROS) Accumulation in Leukemia Cells and Induces the Expression of ROS Generating Enzymes

2014 ◽  
Vol 20 (5) ◽  
pp. 1249-1258 ◽  
Author(s):  
Tamer E. Fandy ◽  
Anchalee Jiemjit ◽  
Manjusha Thakar ◽  
Paulette Rhoden ◽  
Lauren Suarez ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Leukemia Cells ◽  
Oxygen Species ◽  
Ros Accumulation

scholarly journals Scavenging reactive oxygen species mimics the anoxic response in goldfish pyramidal neurons

2021 ◽  
Author(s):  
Varshinie Pillai ◽  
Leslie Buck ◽  
Ebrahim Lari
Keyword(s):  
Reactive Oxygen Species ◽  
Action Potential ◽  
Pyramidal Neurons ◽  
Reactive Oxygen ◽  
Severe Hypoxia ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Ros Scavenging ◽  
Patch Clamp Recording ◽  
Whole Cell

Goldfish are one of a few species able to avoid cellular damage during month-long periods in severely hypoxic environments. By suppressing action potentials in excitatory glutamatergic neurons, the goldfish brain decreases its overall energy expenditure. Co-incident with reductions in O2 availability is a natural decrease in cellular reactive oxygen species (ROS) generation, which has been proposed to function as part of a low oxygen signal transduction pathway. Therefore, using live-tissue fluorescence microscopy, we found that ROS production decreased by 10% with the onset of anoxia in goldfish telencephalic brain slices. Employing whole-cell patch-clamp recording, we found that like severe hypoxia the ROS scavengers N-acetyl cysteine (NAC) and MitoTEMPO, added during normoxic periods, depolarized membrane potential (severe hypoxia -73.6 to – 61.4 mV; NAC -76.6 to -66.2 mV; and MitoTEMPO -71.5 mV to -62.5 mV) and increased whole-cell conductance (severe hypoxia 5.7 to 8.0 nS; NAC 6 nS to 7.5 nS; and MitoTEMPO 6.0 nS to 7.6 nS). Also, in a subset of active pyramidal neurons these treatments reduced action potential firing frequency (severe hypoxia 0.18 Hz to 0.03 Hz; NAC 0.27 Hz to 0.06 Hz and MitoTEMPO 0.35 Hz to 0.08 Hz ). Neither severe hypoxia nor ROS scavenging impacted action potential threshold. The addition of exogenous hydrogen peroxide could reverse the effects of the antioxidants. Taken together, this supports a role for a reduction in [ROS] as a low oxygen signal in goldfish brain.

scholarly journals Post-stress bacterial cell death mediated by reactive oxygen species

2019 ◽  
Vol 116 (20) ◽  
pp. 10064-10071 ◽  
Author(s):  
Yuzhi Hong ◽  
Jie Zeng ◽  
Xiuhong Wang ◽  
Karl Drlica ◽  
Xilin Zhao
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Bacterial Resistance ◽  
Reactive Oxygen ◽  
Temperature Sensitive ◽  
Oxygen Species ◽  
Stress Genes ◽  
Primary Stress ◽  
Bacterial Cell Death ◽  
Ros Accumulation

Antimicrobial efficacy, which is central to many aspects of medicine, is being rapidly eroded by bacterial resistance. Since new resistance can be induced by antimicrobial action, highly lethal agents that rapidly reduce bacterial burden during infection should help restrict the emergence of resistance. To improve lethal activity, recent work has focused on toxic reactive oxygen species (ROS) as part of the bactericidal activity of diverse antimicrobials. We report that whenEscherichia coliwas subjected to antimicrobial stress and the stressor was subsequently removed, both ROS accumulation and cell death continued to occur. Blocking ROS accumulation by exogenous mitigating agents slowed or inhibited poststressor death. Similar results were obtained with a temperature-sensitive mutational inhibition of DNA replication. Thus, bacteria exposed to lethal stressors may not die during treatment, as has long been thought; instead, death can occur after plating on drug-free agar due to poststress ROS-mediated toxicity. Examples are described in which (i) primary stress-mediated damage was insufficient to kill bacteria due to repair; (ii) ROS overcame repair (i.e., protection from anti-ROS agents was reduced by repair deficiencies); and (iii) killing was reduced by anti-oxidative stress genes acting before stress exposure. Enzymatic suppression of poststress ROS-mediated lethality by exogenous catalase supports a causal rather than a coincidental role for ROS in stress-mediated lethality, thereby countering challenges to ROS involvement in antimicrobial killing. We conclude that for a variety of stressors, lethal action derives, at least in part, from stimulation of a self-amplifying accumulation of ROS that overwhelms the repair of primary damage.

Survival in Hostile Environments: Strategies of Renal Medullary Cells

Physiology ◽  
2006 ◽  
Vol 21 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Wolfgang Neuhofer ◽  
Franz-X. Beck
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Renal Medulla ◽  
Extreme Conditions ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Oxygen Tensions ◽  
Hostile Environments ◽  
Medullary Cells

Cells in the renal medulla exist in a hostile milieu characterized by wide variations in extracellular solute concentrations, low oxygen tensions, and abundant reactive oxygen species. This article reviews the strategies adopted by these cells to allow them to survive and fulfill their functions under these extreme conditions.

scholarly journals Autophagy controls reactive oxygen species homeostasis in guard cells that is essential for stomatal opening

2019 ◽  
Vol 116 (38) ◽  
pp. 19187-19192 ◽  
Author(s):  
Shota Yamauchi ◽  
Shoji Mano ◽  
Kazusato Oikawa ◽  
Kazumi Hikino ◽  
Kosuke M. Teshima ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stomatal Closure ◽  
Reactive Oxygen ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Glycolate Oxidase ◽  
Oxygen Species ◽  
Ros Accumulation ◽  
Intracellular Ros ◽  
Ros Scavenger

Reactive oxygen species (ROS) function as key signaling molecules to inhibit stomatal opening and promote stomatal closure in response to diverse environmental stresses. However, how guard cells maintain basal intracellular ROS levels is not yet known. This study aimed to determine the role of autophagy in the maintenance of basal ROS levels in guard cells. We isolated the Arabidopsis autophagy-related 2 (atg2) mutant, which is impaired in stomatal opening in response to light and low CO2 concentrations. Disruption of other autophagy genes, including ATG5, ATG7, ATG10, and ATG12, also caused similar stomatal defects. The atg mutants constitutively accumulated high levels of ROS in guard cells, and antioxidants such as ascorbate and glutathione rescued ROS accumulation and stomatal opening. Furthermore, the atg mutations increased the number and aggregation of peroxisomes in guard cells, and these peroxisomes exhibited reduced activity of the ROS scavenger catalase and elevated hydrogen peroxide (H2O2) as visualized using the peroxisome-targeted H2O2 sensor HyPer. Moreover, such ROS accumulation decreased by the application of 2-hydroxy-3-butynoate, an inhibitor of peroxisomal H2O2-producing glycolate oxidase. Our results showed that autophagy controls guard cell ROS homeostasis by eliminating oxidized peroxisomes, thereby allowing stomatal opening.

scholarly journals Cross talk between increased intracellular zinc (Zn2+) and accumulation of reactive oxygen species in chemical ischemia

2017 ◽  
Vol 313 (4) ◽  
pp. C448-C459 ◽  
Author(s):  
Kira G. Slepchenko ◽  
Qiping Lu ◽  
Yang V. Li
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Ros Accumulation ◽  
Ischemic Stress

Both zinc (Zn2+) and reactive oxygen species (ROS) have been shown to accumulate during hypoxic-ischemic stress and play important roles in pathological processes. To understand the cross talk between the two of them, here we studied Zn2+ and ROS accumulation by employing fluorescent probes in HeLa cells to further the understanding of the cause and effect relationship of these two important cellular signaling systems during chemical-ischemia, stimulated by oxygen and glucose deprivation (OGD). We observed two Zn2+ rises that were divided into four phases in the course of 30 min of OGD. The first Zn2+ rise was a transient, which was followed by a latent phase during which Zn2+ levels recovered; however, levels remained above a basal level in most cells. The final phase was the second Zn2+ rise, which reached a sustained plateau called Zn2+ overload. Zn2+ rises were not observed when Zn2+ was removed by TPEN (a Zn2+ chelator) or thapsigargin (depleting Zn2+ from intracellular stores) treatment, indicating that Zn2+ was from intracellular storage. Damaging mitochondria with FCCP significantly reduced the second Zn2+ rise, indicating that the mitochondrial Zn2+ accumulation contributes to Zn2+ overload. We also detected two OGD-induced ROS rises. Two Zn2+ rises preceded two ROS rises. Removal of Zn2+ reduced or delayed OGD- and FCCP-induced ROS generation, indicating that Zn2+ contributes to mitochondrial ROS generation. There was a Zn2+-induced increase in the functional component of NADPH oxidase, p47phox, thus suggesting that NADPH oxidase may mediate Zn2+-induced ROS accumulation. We suggest a new mechanism of cross talk between Zn2+ and mitochondrial ROS through positive feedback processes that eventually causes excessive free Zn2+ and ROS accumulations during the course of ischemic stress.

Effects of Low Oxygen Condition on the Generation of Reactive Oxygen Species and the Development in Mouse Embryos Culturedin vitro

1999 ◽  
Vol 25 (5) ◽  
pp. 359-366 ◽  
Author(s):  
Hyuck-Chan Kwon ◽  
Hyun-Won Yang ◽  
Kyung-Joo Hwang ◽  
Jung-Hyun Yoo ◽  
Myung-Sin Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mouse Embryos ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Oxygen Condition

Induction ofPseudomonas aeruginosafhpandfhpRby reactive oxygen species

2009 ◽  
Vol 55 (6) ◽  
pp. 657-663 ◽  
Author(s):  
Taija S. Koskenkorva-Frank ◽  
Pauli T. Kallio
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Promoter Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Butyl Hydroperoxide ◽  
Tert Butyl Hydroperoxide ◽  
Oxygen Conditions

In Pseudomonas aeruginosa , flavohemoglobin (Fhp) and its cognate regulator FhpR (PA2665) form a protective regulatory circuit, which responds to reactive nitrogen species and is also capable of protecting cells against nitrosative stress. Recently, it has been shown that the expression of the fhp promoter is regulated not only by FhpR, but also by two new regulators, PA0779 and PA3697. It has also been suggested that the bacterial flavohemoglobins (flavoHbs) could play a crucial role in the protection of cells against reactive oxygen species (ROS). Therefore, the role and function of the Fhp/FhpR system during oxidative stress were studied by assessing the viability and membrane integrity of P. aeruginosa cells and by analyzing the promoter activities of fhp and fhpR upon exposure to paraquat, hydrogen peroxide, and tert-butyl hydroperoxide, under both aerobic and low-oxygen conditions. The results showed that under aerobic conditions, both fhp and fhpR promoters are induced by ROS generated by the stressors. Thus, the Fhp/FhpR system is implicated in the oxidative stress response. ROS-induced fhp promoter activity was dependent on FhpR, PA0779, and PA3697 regulators. Tert-butyl hydroperoxide-induced fhpR promoter activity was found to be highly repressed by PA0779, and FhpR showed negative autoregulation of its own promoter. Under low-oxygen conditions, the activity of the fhp promoter was not inducible by ROS, but fhpR promoter activity was induced by paraquat, and hydrogen peroxide was repressed in both cases by the regulators PA0779 and PA3697.

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