The variation of reactive oxygen species scavenging enzymes and related gene expressions during occurrence and recovery of rubber tree tapping panel dryness

2021 ◽  
Author(s):  
Kun Yuan ◽  
Jing He ◽  
Yiyu Hu ◽  
Chengtian Feng ◽  
Zhenhui Wang
Keyword(s):  
Reactive Oxygen Species ◽  
Rubber Tree ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Related Gene ◽  
Gene Expressions ◽  
Tapping Panel Dryness ◽  
Scavenging Enzymes

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

scholarly journals Non-lethal exposure to H2O2 boosts bacterial survival and evolvability against oxidative stress

2019 ◽  
Author(s):  
Alexandro Rodríguez-Rojas ◽  
Joshua Jay Kim ◽  
Paul Johnston ◽  
Olga Makarova ◽  
Murat Eravci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Time Lapse ◽  
Oxygen Species ◽  
Bacterial Survival ◽  
Phenotypic Resistance ◽  
Subsequent Exposure ◽  
Scavenging Enzymes ◽  
Multicellular Organisms

AbstractUnicellular organisms have the prevalent challenge to survive under oxidative stress of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2). ROS are present as by-products of photosynthesis and aerobic respiration. These reactive species are even employed by multicellular organisms as potent weapons against microbes. Although bacterial defences against lethal and sub-lethal oxidative stress have been studied in model bacteria, the role of fluctuating H2O2 concentrations remains unexplored. It is known that sub-lethal exposure of Escherichia coli to H2O2 results in enhanced survival upon subsequent exposure. Here we investigate the priming response to H2O2 at physiological concentrations. The basis and the duration of the response (memory) were also determined by time-lapse quantitative proteomics. We found that a low level of H2O2 induced several scavenging enzymes showing a long half-life, subsequently protecting cells from future exposure. We then asked if the phenotypic resistance against H2O2 alters the evolution of resistance against oxygen stress. Experimental evolution of H2O2 resistance revealed faster evolution and higher levels of resistance in primed cells. Several mutations were found to be associated with resistance in evolved populations affecting different loci but, counterintuitively, none of them was directly associated with scavenging systems. Our results have important implications for host colonisation and infections where microbes often encounter reactive oxygen species in gradients.

Syringic acid triggers reactive oxygen species–mediated cytotoxicity in HepG2 cells

2019 ◽  
Vol 38 (6) ◽  
pp. 694-702 ◽  
Author(s):  
S Gheena ◽  
D Ezhilarasan
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Line ◽  
Hepg2 Cell ◽  
Hepg2 Cells ◽  
Cytotoxic Effect ◽  
Reactive Oxygen ◽  
Syringic Acid ◽  
Oxygen Species ◽  
Hepg2 Cell Line ◽  
Gene Expressions

Hepatocellular carcinoma is the second most common cause of cancer death in the world and its incidence has dramatically increased worldwide in the past two decades. Syringic acid (SA) has been studied for its hepatoprotective, anti-inflammatory, immunomodulatory, free radical scavenging, and antioxidant activities. We aimed to evaluate the cytotoxic effect of SA against human hepatoma HepG2 cell line. Cytotoxicity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. HepG2 cells were treated with SA at concentration ranges of 25, 50, and 100 µM for 24 h. Reactive oxygen species (ROS) expression was investigated by dichlorofluorescein staining assay. Morphological changes of SA-treated HepG2 cells were evaluated by acridine orange (AO) and ethidium bromide (EB) dual staining. Apoptotic marker gene expressions were evaluated by qPCR. SA treatment caused significant cytotoxicity and liberation of ROS in HepG2 cells. AO and EB staining showed membrane blebbing and distortion in SA-treated cells. Apoptotic markers such as caspases 3 and 9, cytochrome c, Apaf-1, Bax, and p53 gene expressions were significantly increased upon SA treatment indicating the possibility of apoptosis induction in HepG2 cells. This treatment also caused significant downregulation of Bcl-2 gene expression. SA has a cytotoxic effect on human HepG2 cell line, and this might be a promising agent in anticancer research.

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