scholarly journals Expression of death-related genes and reactive oxygen species production in Skeletonema tropicum upon exposure to the polyunsaturated aldehyde octadienal

2015 ◽  
Vol 6 (1/2) ◽  
Author(s):  
Alessandra A. Gallina ◽  
Chih-Ching Chung ◽  
Raffaella Casotti
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Marine Diatom ◽  
Ros Production ◽  
Oxygen Species ◽  
Diatom Population ◽  
Polyunsaturated Aldehydes ◽  
Species Production

<p>The effects of 4<em>E</em>/<em>Z</em>-octadienal (OCTA) on <em>ScDSP-1 </em>and <em>ScDSP-2 </em>gene expression and reactive oxygen species (ROS) production were investigated in the marine diatom <em>Skeletonema tropicum</em> (formerly <em>costatum</em>) using qRTPCR and flow cytometry. <em>ScDSP-1 </em>and <em>ScDSP-2 </em>genes have been previously shown to be involved in cell death in ageing cells and in response to photosynthetic stress. OCTA induced a differential, concentration-dependent <em>DSP</em> gene expression associated to ROS production, 821.6 and 97.7 folds higher for <em>ScDSP-1</em> and <em>ScDSP-2</em>, respectively. Among the concentrations tested, only 8 μM OCTA, which caused a reduction of 50% in cell concentrations at 24 h, was able to elicit an expression pattern consistent with a signalling role. Interestingly, only intermediate levels of reactive oxygen species (ROS) (<em>i.e</em>., 1.5±0.1 increase) were observed to be elicited by such concentration. These results suggest that ROS are key components of the molecular cascade triggered by polyunsaturated aldehydes (PUA) and leading to cell death. This could have implications for bloom final stages at sea, where PUA may act as effectors of diatom population dynamics through ROS acting as modulators.</p>

scholarly journals The Regulation of Reactive Oxygen Species Production during Programmed Cell Death

1998 ◽  
Vol 141 (6) ◽  
pp. 1423-1432 ◽  
Author(s):  
Shirlee Tan ◽  
Yutaka Sagara ◽  
Yuanbin Liu ◽  
Pamela Maher ◽  
David Schubert
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Glutamate Toxicity ◽  
Ros Production ◽  
Oxygen Species ◽  
Ht22 Cells

Reactive oxygen species (ROS) are thought to be involved in many forms of programmed cell death. The role of ROS in cell death caused by oxidative glutamate toxicity was studied in an immortalized mouse hippocampal cell line (HT22). The causal relationship between ROS production and glutathione (GSH) levels, gene expression, caspase activity, and cytosolic Ca2+ concentration was examined. An initial 5–10-fold increase in ROS after glutamate addition is temporally correlated with GSH depletion. This early increase is followed by an explosive burst of ROS production to 200–400-fold above control values. The source of this burst is the mitochondrial electron transport chain, while only 5–10% of the maximum ROS production is caused by GSH depletion. Macromolecular synthesis inhibitors as well as Ac-YVAD-cmk, an interleukin 1β–converting enzyme protease inhibitor, block the late burst of ROS production and protect HT22 cells from glutamate toxicity when added early in the death program. Inhibition of intracellular Ca2+ cycling and the influx of extracellular Ca2+ also blocks maximum ROS production and protects the cells. The conclusion is that GSH depletion is not sufficient to cause the maximal mitochondrial ROS production, and that there is an early requirement for protease activation, changes in gene expression, and a late requirement for Ca2+ mobilization.

scholarly journals Intradialytic granulocyte reactive oxygen species production: a prospective, crossover trial.

1993 ◽  
Vol 4 (2) ◽  
pp. 178-186 ◽  
Author(s):  
J Himmelfarb ◽  
K A Ault ◽  
D Holbrook ◽  
D A Leeber ◽  
R M Hakim
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Ros Production ◽  
Oxygen Species ◽  
Susceptibility To Infection ◽  
Flow Cytometric ◽  
Ros Formation ◽  
Dialysis Membranes ◽  
Species Production

By the use of flow cytometric techniques, this prospective, randomized crossover study was designed to analyze intradialytic granulocyte reactive oxygen species (ROS) formation in whole blood with complement-activating and noncomplement-activating hollow fiber membranes. Dialysis with a complement-activating membrane resulted in a 6.5-fold increase in granulocyte hydrogen peroxide production 15 min after dialysis initiation and remained significantly elevated (P < 0.01) through the first 30 min with this membrane in comparison to both predialysis values and simultaneous values with a noncomplement-activating membrane. Further studies demonstrated that blood obtained at 15 min with a complement-activating membrane generated significantly less granulocyte ROS production in response to Staphylococcus aureus incubation than blood obtained either predialysis or at the same time in dialysis with a noncomplement-activating membrane. Both complement-activating and noncomplement-activating dialysis membranes caused slightly decreased granulocyte responsiveness to phorbol myristate acetate. It was concluded that hemodialysis with complement-activating membranes results in increased granulocyte ROS production and decreased responsiveness to S. aureus challenge during the dialysis procedure. These results document the potential role of ROS in hemodialysis-associated pathology and susceptibility to infection.

scholarly journals Preventive Effect of Daiokanzoto (TJ-84) on 5-Fluorouracil-Induced Human Gingival Cell Death through the Inhibition of Reactive Oxygen Species Production

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112689 ◽  
Author(s):  
Kaya Yoshida ◽  
Masami Yoshioka ◽  
Hirohiko Okamura ◽  
Satomi Moriyama ◽  
Kazuyoshi Kawazoe ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Preventive Effect ◽  
Species Production

scholarly journals The Characterization of TA-289, a Novel Antifungal from Fusarium sp.

2021 ◽  
Author(s):  
◽  
Natelle C H Quek
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Chemical Diversity ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
Oxygen Species ◽  
Wild Type

<p>Natural products offer vast structural and chemical diversity highly sought after in drug discovery research. Saccharomyces cerevisiae makes an ideal model eukaryotic organism for drug mode-of-action studies owing to ease of growth, sophistication of genetic tools and overall homology to higher eukaryotes. Equisetin and a closely related novel natural product, TA-289, are cytotoxic to fermenting yeast, but seemingly less so when yeast actively respire. Cell cycle analyses by flow cytometry revealed a cell cycle block at S-G2/M phase caused by TA-289; previously described oxidative stress-inducing compounds causing cell cycle delay led to further investigation in the involvement of equisetin and TA-289 in mitochondrial-mediated generation of reactive oxygen species. Chemical genomic profiling involving genome-wide scans of yeast deletion mutant strains for TA-289 sensitivity revealed sensitization of genes involved in the mitochondria, DNA damage repair and oxidative stress responses, consistent with a possible mechanism-of-action at the mitochondrion. Flow cytometric detection of reactive oxygen species (ROS) generation caused by TA-289 suggests that the compound may induce cell death via ROS production. The generation of a mutant strain resistant to TA-289 also displayed resistance to a known oxidant, H2O2, at concentrations that were cytotoxic to wild-type cells. The resistant mutant displayed a higher basal level of ROS production compared to the wild-type parent, indicating that the resistance mutation led to an up-regulation of antioxidant capacity which provides cell survival in the presence of TA-289. Yeast mitochondrial morphology was visualized by confocal light microscopy, where it was observed that cells treated with TA-289 displayed abnormal mitochondria phenotypes, further indicating that the compound is acting primarily at the mitochondrion. Similar effects observed with equisetin treatment suggest that both compounds share the same mechanism, eliciting cell death via ROS production in the mitochondrial respiratory chain.</p>

scholarly journals 2-Hydroxymelatonin, Rather Than Melatonin, Is Responsible for RBOH-Dependent Reactive Oxygen Species Production Leading to Premature Senescence in Plants

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1728
Author(s):  
Hyoung Yool Lee ◽  
Kyoungwhan Back
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Ion Leakage ◽  
Ros Production ◽  
Oxygen Species ◽  
Aba Signaling ◽  
Melatonin Treatment ◽  
Leaf Chlorosis ◽  
Leaf Necrosis ◽  
Species Production

Unlike animals, plants amply convert melatonin into 2-hydroxymelatonin (2-OHM) and cyclic 3-hydroxymelatonin (3-OHM) through the action of melatonin 2-hydroxylase (M2H) and melatonin 3-hydroxylase (M3H), respectively. Thus, the effects of exogenous melatonin treatment in plants may be caused by melatonin, 2-OHM, or 3-OHM, or some combination of these compounds. Indeed, studies of melatonin’s effects on reactive oxygen species (ROS) production have reported conflicting results. In this study, we demonstrated that 2-OHM treatment induced ROS production, whereas melatonin did not. ROS production from 2-OHM treatment occurred in old arabidopsis leaves in darkness, consistent with an ethylene-mediated senescence mechanism. Transgenic tobacco plants containing overexpressed rice M2H exhibited dwarfism and leaf necrosis of the upper leaves and early senescence of the lower leaves. We also demonstrated that 2-OHM-mediated ROS production is respiratory burst NADPH oxidase (RBOH)-dependent and that 2-OHM-induced senescence genes require ethylene and the abscisic acid (ABA) signaling pathway in arabidopsis. In contrast to melatonin, 2-OHM treatment induced senescence symptoms such as leaf chlorosis and increased ion leakage in arabidopsis. Senescence induction is known to begin with decreased levels of proteins involved in chloroplast maintenance, including Lhcb1 and ClpR1. Together, these results show that 2-OHM acts as a senescence-inducing factor by inducing ROS production in plants.

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