Do parasites and antioxidant availability affect begging behaviour, growth rate and resistance to oxidative stress?

2018 ◽  
Vol 31 (6) ◽  
pp. 904-913 ◽  
Author(s):  
Lea Maronde ◽  
Sylvain Losdat ◽  
Heinz Richner
2019 ◽  
Vol 48 (3) ◽  
pp. 270-278
Author(s):  
Hediye Elif Kiliç ◽  
Hatice Tunca ◽  
Tuğba Ongun Sevindik ◽  
Ali Doğru

Abstract This study explores the activity of total superoxide dismutase (SOD), ascorbate peroxidase (APX) and glutathione reductase (GR), biomass accumulation and chlorophyll a content in Scenedesmus ellipsoideus Chodat grown under conditions of varying zinc (Zn) concentrations. In addition, the activity of different SOD isozymes (MnSOD, FeSOD and CuZnSOD) was measured separately to determine the intracellular extent of oxidative stress resulting from Zn toxicity. We found that the activity of FeSOD and MnSOD was induced by lower Zn concentration (2 μg ml−1 and 4 μg ml−1, respectively), whereas CuZnSOD activity was not affected, which indicates that chloroplasts are the first location in S. ellipsoideus cells where superoxide accumulation is accelerated by Zn toxicity. The activity of total SOD and APX was significantly increased by moderate Zn concentrations, probably due to some oxidative stress caused by Zn toxicity. The higher level of Zn application, however, led not only to the inhibition of total SOD and APX activity, but also to the reduction of biomass accumulation and chlorophyll a content. As a result, it can be concluded that the accumulation of superoxide radicals and H2O2 in S. ellipsoideus cells induced by Zn toxicity may be responsible for the reduced growth rate and the impairment of photosynthetic pigments.


2013 ◽  
Vol 26 (4) ◽  
pp. 431-441 ◽  
Author(s):  
Liangsheng Xu ◽  
Weidong Chen

Agrobacterium-mediated transformation (AMT) was used to identify potential virulence factors in Sclerotinia sclerotiorum. Screening AMT transformants identified two mutants showing significantly reduced virulence. The mutants showed growth rate, sclerotial formation, and oxalate production similar to that of the wild type. The mutation was due to a single T-DNA insertion at 212 bp downstream of the Cu/Zn superoxide dismutase (SOD) gene (SsSOD1, SS1G_00699). Expression levels of SsSOD1 were significantly increased under oxidative stresses or during plant infection in the wild-type strain but could not be detected in the mutant. SsSOD1 functionally complemented the Cu/Zn SOD gene in a Δsod1 Saccharomyces cerevisiae mutant. The SOD mutant had increased sensitivity to heavy metal toxicity and oxidative stress in culture and reduced ability to detoxify superoxide in infected leaves. The mutant also had reduced expression levels of other known pathogenicity genes such as endo-polygalacturanases sspg1 and sspg3. The functions of SsSOD1 were further confirmed by SsSOD1-deletion mutation. Like the AMT insertion mutant, the SsSOD1-deletion mutant exhibited normal growth rate, sclerotial formation, oxalate production, increased sensitivity to metal and oxidative stress, and reduced virulence. These results suggest that SsSOD1, while not being required for saprophytic growth and completion of the life cycle, plays critical roles in detoxification of reactive oxygen species during host–pathogen interactions and is an important virulence factor of Sclerotinia sclerotiorum.


2003 ◽  
Vol 375 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Renata SANTOS ◽  
Andrew DANCIS ◽  
David EIDE ◽  
Jean-Michel CAMADRO ◽  
Emmanuel LESUISSE

Analysis of Saccharomyces cerevisiae cell transcriptome revealed that iron deprivation/supplementation affects genes other than those of the iron regulon (controlled by Aft proteins). Several genes regulated by zinc (induced by zinc deprivation) were induced by iron. Cells lacking the yeast frataxin homologue Yfh1 accumulate large amounts of iron in their mitochondria. We have shown that the zinc metabolism of these cells is also impaired: zinc uptake and zinc accumulation were both much lower in Δyfh1 cells than in wild-type cells. Excess zinc in the growth medium also influenced the phenotypes of Δyfh1 cells. It prevented the accumulation of iron in the mitochondria of Δyfh1 cells and increased the growth rate of these cells and their resistance to oxidative stress. However, zinc did not restore the deficiency of Fe–S and haem proteins of Δyfh1 cells. Zinc inhibited mitochondrial respiration and protected Yah1p, the mitochondrial ferredoxin. These results suggest that zinc nutrition may be important in the aetiology of Friedreich's ataxia.


2012 ◽  
Vol 16 (2) ◽  
pp. 365-376 ◽  
Author(s):  
Riadh Nciri ◽  
Frank Desmoulin ◽  
Mohamed Saleh Allagui ◽  
Jean-Claude Murat ◽  
Abdelfattah El Feki ◽  
...  

AbstractRecent studies suggest that lithium protects neurons from death induced by a wide array of neurotoxic insults, stimulates neurogenesis and could be used to prevent age-related neurodegenerative diseases. In this study, SH-SY5Y human neuronal cells were cultured in the absence (Con) or in the presence (Li+) of a low lithium concentration (0.5 mm Li2CO3, i.e. 1 mm lithium ion) for 25–50 wk. In the course of treatment, growth rate of Con and Li+ cells was regularly analysed using Alamar Blue dye. Resistance to oxidative stress was investigated by evaluating: (1) the adverse effects of high concentrations of lithium (4–8 mm) or glutamate (20–90 mm) on cell growth rate; (2) the levels of lipid peroxidation (TBARS) and total glutathione; (3) the expression levels of the anti-apoptotic Bcl-2 protein. In addition, glucose metabolism was investigated by analysing selected metabolites in culture media and cell extracts by 1H-NMR spectroscopy. As compared to Con, Li+ cells multiplied faster and were more resistant to stress, as evidenced by a lower dose-dependent decrease of Alamar Blue reduction and dose-dependent increase of TBARS levels induced by toxic doses of lithium and glutamate. Total glutathione content and Bcl-2 level were increased in Li+ cells. Glucose consumption and glycolytic activity were enhanced in Li+ cells and an important release of pyruvate was observed. We conclude that chronic exposure to lithium induces adaptive changes in metabolism of SH-SY5Y cells involving a higher cell growth rate and a better resistance to oxidative stress.


2021 ◽  
Author(s):  
Rongkang Hu ◽  
Ruiguo Cui ◽  
Qingqing Xu ◽  
Dongming Lan ◽  
Yonghua Wang

Abstract Methanol can be used by Pichia pastoris as the sole carbon source and inducer to produce recombinant proteins in high-cell-density fermentations, but also damages cells due to reactive oxygen species (ROS) accumulation from methanol oxidation. Here, we study the relationship between methanol feeding and ROS accumulation by controlling specific growth rate during the induction phase. A higher specific growth rate increased the level of ROS accumulation caused by methanol oxidation. While the cell growth rate was proportional to specific growth rate, but maximum total protein production and highest enzyme activity were achieved at a specific growth rate of 0.05 1/h as compared to that 0.065 1/h. Moreover, oxidative damage induced by over-accumulation of ROS in P. pastoris during the methanol induction phase caused cell death and reduced protein expression ability. ROS scavenging system analysis reveals that the higher specific growth rate, especially 0.065 1/h, resulted in increased intracellular catalase activity and decreased glutathione content significantly. Finally, Spearman's correlation analysis further reveals that the reduced glutathione might be beneficial for maintaining cell viability and increasing protein production under oxidative stress caused by ROS toxic accumulation. Our findings suggest an integrated strategy to control the feeding of the essential substrate based on analyzing its response to oxidative stress caused by ROS toxic accumulation, as well as develop a strategy to optimize fed-batch fermentation.


Processes ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 496
Author(s):  
Ignacio López Muñoz ◽  
Olivier Bernard

Dissolved oxygen plays a key role in microalgal growth at high density. This effect was so far rarely quantified. Here we propose a new model to represent the combined effect of light, oxygen concentration and temperature (LOT-model) on microalgae growth. The LOT-model introduces oxygen concentration in order to represent the oxidative stress affecting the cultures, adding a toxicity term in the expression of the net growth rate. The model was validated with experimental data for several species such as Chlorella minutissima, Chlorella vulgaris, Dunaliella salina, Isochrysis galbana. It successfully predicted experimental records with an average error lower than 5.5%. The model was also validated using dynamical data where oxygen concentration varies. It highlights a strong impact of oxygen concentration on productivity, depending on temperature. The model quantifies the sensitivity to oxidative stress of different species and shows, for example, that Dunaliella salina is much less affected than Chlorella vulgaris by oxidative stress. The modeling approach can support an optimization strategy to improve productivity, especially for managing high oxygen levels.


2021 ◽  
Author(s):  
Rongkang Hu ◽  
Ruiguo Cui ◽  
Qingqing Xu ◽  
Dongming Lan ◽  
Yonghua Wang

Abstract Methanol can be used by Pichia pastoris as the sole carbon source and inducer to produce recombinant proteins in high-cell-density fermentations, but also damages cells due to reactive oxygen species (ROS) accumulation from methanol oxidation. Here, we study the relationship between methanol feeding and ROS accumulation by controlling specific growth rate during the induction phase. A higher specific growth rate increased the level of ROS accumulation caused by methanol oxidation. While the cell growth rate was proportional to specific growth rate, but maximum total protein production and highest enzyme activity were achieved at a specific growth rate of 0.05 1/h as compared to that 0.065 1/h. Moreover, oxidative damage induced by over-accumulation of ROS in P. pastoris during the methanol induction phase caused cell death and reduced protein expression ability. ROS scavenging system analysis reveals that the higher specific growth rate, especially 0.065 1/h, resulted in increased intracellular catalase activity and decreased glutathione content significantly. Finally, Spearman's correlation analysis further reveals that the reduced glutathione might be beneficial for maintaining cell viability and increasing protein production under oxidative stress caused by ROS toxic accumulation. Our findings suggest an integrated strategy to control the feeding of the essential substrate based on analyzing its response to oxidative stress caused by ROS toxic accumulation, as well as develop a strategy to optimize fed-batch fermentation.


2020 ◽  
Vol 367 (23) ◽  
Author(s):  
Romina Frare ◽  
Margarita Stritzler ◽  
Cecilia Pascuan ◽  
Karen Liebrenz ◽  
Luisa Galindo-Sotomonte ◽  
...  

ABSTRACT Nitrogen is a most important nutrient resource for Escherichia coli and other bacteria that harbor the glnKamtB operon, a high-affinity ammonium uptake system highly interconnected with cellular metabolism. Although this system confers an advantage to bacteria when growing under nitrogen-limiting conditions, little is known about the impact of these genes on microbial fitness under nutrient-rich conditions. Here, the genetically tractable E. coli BW25113 strain and its glnKamtB-null mutant (JW0441) were used to analyze the impact of GlnK-AmtB on growth rates and oxidative stress tolerance. Strain JW0441 showed a shorter initial lag phase, higher growth rate, higher citrate synthase activity, higher oxidative stress tolerance and lower expression of serA than strain BW25113 under nutrient-rich conditions, suggesting a fitness cost to increase metabolic plasticity associated with serine metabolism. The overexpression of serA in strain JW0441 resulted in a decreased growth rate and stress tolerance in nutrient-rich conditions similar to that of strain BW25113, suggesting that the negative influence on bacterial fitness imposed by GlnK-AmtB can be traced to the control of serine biosynthesis. Finally, we discuss the potential applications of glnKamtB mutants in bioproduction processes.


2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Haixia Zhou ◽  
Liang Han ◽  
Han Wang ◽  
Jun Wei ◽  
Zhigang Guo ◽  
...  

Objective. Chidamide has a broad spectrum of antitumor activity but its function on glioma remains unknown. The increase of reactive oxygen species (ROS) and reactive nitrogen species (RNS) may control glioma risk by promoting its apoptosis and necrosis. Hedgehog pathway is crucial to glioma cell proliferation and controls ROS production. We aimed to explore the effects of chidamide on the levels of miR-338-5p (glioma cell inhibitor), which may regulate Hedgehog signaling, resulting in the changes of RNS. Materials and Methods. Migration and invasion activities of glioma cells were measured by using the Transwell chamber assay. The expression levels of Sonic Hedgehog (Shh), Indian Hedgehog (Ihh), Desert Hedgehog (Dhh), miR-338-5p, and related molecules were detected by using real-time PCR (RT-PCR) and or Western Blot in U87 and HS683 glioma cells. The effects of chidamide on these molecules were measured by using the miR-338-5p inhibitor or mimics in U87 and HS683 glioma cell lines. ROS and RNS were measured by DCF DA and DAF-FM DA fluorescence. Biomarkers of oxidative stress were measured by using a corresponding kit. Apoptosis and necrosis rates were measured by using flow cytometry. Results. Chidamide inhibited the growth rate, migration, and invasion of human malignant glioma cells and increased the level of miR-338-5p. miR-338-5p inhibitor or mimics increased or inhibited the growth rate of U87 and HS683 glioma cells. Chidamide inhibited the levels of Shh, Ihh, migration protein E-cadherin, and invading protein MMP-2. The increase in the level of Shh and Ihh led to the reduction in the ROS and RNS levels. miR-338-5p inhibitor or mimics also showed a promoting or inhibitory function for the levels of Shh and Ihh. Furthermore, miR-338-5p mimics and inhibitor inhibited or promoted the migration and invasion of the glioma cells (P<0.05). Evaluated levels of miR-338-5p increased oxidative stress level and apoptosis and necrosis rate by regulating the levels of biomarkers of oxidative stress (P<0.05). Conclusion. Chidamide inhibits glioma cells by increasing oxidative stress via the miRNA-338-5p regulation of Hedgehog signaling. Chidamide may be a potential drug in the prevention of glioma development.


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