scholarly journals Melatonin alleviates heat-induced damage of tomato seedlings by balancing redox homeostasis and modulating polyamine and nitric oxide biosynthesis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Mohammad Shah Jahan ◽  
Sheng Shu ◽  
Yu Wang ◽  
Zheng Chen ◽  
Mingming He ◽  
...  

Abstract Background Melatonin is a pleiotropic signaling molecule that plays multifarious roles in plants stress tolerance. The polyamine (PAs) metabolic pathway has been suggested to eliminate the effects of environmental stresses. However, the underlying mechanism of how melatonin and PAs function together under heat stress largely remains unknown. In this study, we investigated the potential role of melatonin in regulating PAs and nitric oxide (NO) biosynthesis, and counterbalancing oxidative damage induced by heat stress in tomato seedlings. Results Heat stress enhanced the overproduction of reactive oxygen species (ROS) and damaged inherent defense system, thus reduced plant growth. However, pretreatment with 100 μM melatonin (7 days) followed by exposure to heat stress (24 h) effectively reduced the oxidative stress by controlling the overaccumulation of superoxide (O2•−) and hydrogen peroxide (H2O2), lowering the lipid peroxidation content (as inferred based on malondialdehyde content) and less membrane injury index (MII). This was associated with increased the enzymatic and non-enzymatic antioxidants activities by regulating their related gene expression and modulating the ascorbate–glutathione cycle. The presence of melatonin induced respiratory burst oxidase (RBOH), heat shock transcription factors A2 (HsfA2), heat shock protein 90 (HSP90), and delta 1-pyrroline-5-carboxylate synthetase (P5CS) gene expression, which helped detoxify excess ROS via the hydrogen peroxide-mediated signaling pathway. In addition, heat stress boosted the endogenous levels of putrescine, spermidine and spermine, and increased the PAs contents, indicating higher metabolic gene expression. Moreover, melatonin-pretreated seedlings had further increased PAs levels and upregulated transcript abundance, which coincided with suppression of catabolic-related genes expression. Under heat stress, exogenous melatonin increased endogenous NO content along with nitrate reductase- and NO synthase-related activities, and expression of their related genes were also elevated. Conclusions Melatonin pretreatment positively increased the heat tolerance of tomato seedlings by improving their antioxidant defense mechanism, inducing ascorbate–glutathione cycle, and reprogramming the PAs metabolic and NO biosynthesis pathways. These attributes facilitated the scavenging of excess ROS and increased stability of the cellular membrane, which mitigated heat-induced oxidative stress.

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1871
Author(s):  
Karolina Chodkowska ◽  
Anna Ciecierska ◽  
Kinga Majchrzak ◽  
Piotr Ostaszewski ◽  
Tomasz Sadkowski

Gamma-oryzanol (GO) is a popular supplement for performance horses, dogs, and humans. Previous studies indicated that GO supplementation decreases creatine kinase activity and lactate level after exercise and may affect oxidative stress in Thoroughbred horses. GO may change genes expression in equine satellite cells (ESC). The purpose of this study was to evaluate the effect of GO on miRNA, gene expression, oxidative stress, and cell damage and viability in differentiating ESC pretreated with hydrogen peroxide (H2O2). ESCs were obtained from a young horse’s skeletal muscle. ESCs were pre-incubated with GO (24 h) and then exposed to H2O2 for one hour. For the microRNA and gene expression assessment, the microarray technique was used. Identified miRNAs and genes were validated using real time-quantitative polymerase chain reaction. Several tests related to cell viability, cell damage, and oxidative stress were performed. The microarray analysis revealed differences in 17 miRNAs and 202 genes between GO-treated and control ESC. The tests related to apoptosis, cell viability, and oxidative stress showed that GO affects these processes to varying degrees. Our results suggest that GO can change miRNA and gene expression and may impact the processes involved in tissue repairing after an injury.


2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Satinath Paul ◽  
Bela Keshan

The present study observed the effect of heat stress on ovarian development, fecundity, and vitellogenin gene expression in silkworm,Bombyx mori. The result showed that the heat shock treatment to spinning larvae and pupae at 39°C (1 h and 2 h) did not cause any adverse effect on the reproductive performance ofB. mori.However, the heat shock treatment at 42°C or above caused a decrease in the fecundity. The heat shock treatment to day 2 pupae for 2 h at 45°C caused a drastic effect on the development of ovary as measured by gonadosomatic index. The study thus showed that a brief exposure ofBombyxlarvae and pupae to a temperature of 42°C or higher, much prevalent in tropical countries like India, greatly affects the ovarian development and reproductive performance of this commercially important insect. The study further showed a developmental- and tissue-specific expression of vitellogenin mRNA in fat body and ovary upon heat shock. When heat shock treatment was done at 39°C and 42°C to spinning larvae, ovary showed an upregulation in the expression of vitellogenin mRNA, whereas fat body failed to do so. However, at 45°C, both fat body and ovary showed a downregulation. The heat shock treatment to day 2 pupae showed an upregulation in the vitellogenin mRNA expression in both fat body and ovary, even at 45°C. The upregulation in the expression of vitellogenin upon heat shock indicates its role in thermal protection ofBombyxlarvae and pupae.


2014 ◽  
Vol 75 (2) ◽  
pp. 503-509 ◽  
Author(s):  
Dan Wu ◽  
Hongye Chu ◽  
Lixiu Jia ◽  
Kunming Chen ◽  
Liqun Zhao

2011 ◽  
Vol 23 (1) ◽  
pp. 218
Author(s):  
M. Nichi ◽  
R. P. Bertolla ◽  
T. B. Soler ◽  
C. N. M. Cortada ◽  
R. M. Zuge ◽  
...  

Previous studies have indicated that semen of heat-stressed bulls shows impaired mitochondrial activity and high levels of oxidative stress, which may cause structural damage to biomolecules, DNA, lipids, carbohydrates and proteins, as well as other cellular components (Nichi et al. 2006 Theriogenology 66, 822–828). Disruption of the sperm mitochondria could have a potential damaging effect not only on an individual sperm cell but also on the surrounding cells, especially regarding the sperm membrane, possibly due to the release of a high amount of reactive oxygen species (ROS) produced in this environment (rich in electrons) that would then lead to oxidative stress. To test this hypothesis, semen samples of 11 Simmental bulls kept in tropical environments were collected during the summer months. Semen was evaluated as follows: the 3-3′ diaminobenzidine stain (DAB) as an index of mitochondrial activity, the hypo-osmotic swelling test (HOST) as an index of membrane integrity, measurement of thiobarbituric acid reactive substances (TBARS) as an index of lipid peroxidation, and measurement of the enzymatic antioxidants superoxide dismutase, catalase and glutathione peroxidase activities. For correlation analysis, the Pearson test was used (variables were transformed when necessary), and for nonparametric variables, the Spearman rank test was used. A high positive correlation was found between sperm cells with highly active mitochondria (DAB class I) and the percentage of cells with intact membrane by HOST (r = 0.93; P < 0.05), and a negative correlation between the latter and the percentage of inactive mitochondria (r = –0.91; P < 0.05), indicating that the higher the percentage of cells showing impaired mitochondrial activity, the higher the percentage of cells with damaged membrane. There was also a positive correlation between TBARS and the percentage of cells with disrupted mitochondria (r = 0.86; P < 0.05), indicating that the higher the percentage of sperm with impaired mitochondrial activity, the higher the oxidative stress. No correlation existed between the enzymatic antioxidants and any of the variables studied. The results indicate that heat stress may lead to an increase in testicular ROS levels, overcoming the seminal antioxidant protection. This, in turn, may cause damage of the mitochondria and a subsequent release of more pro-oxidative substances, and an exponential increase of oxidative stress. Understanding these mechanisms may lead to more tailored antioxidant therapies in the future. The authors thank FAPESP for the scholarship and financial support.


1998 ◽  
Vol 9 (6) ◽  
pp. 1339-1349 ◽  
Author(s):  
Kazuhiro Shiozaki ◽  
Mitsue Shiozaki ◽  
Paul Russell

Fission yeast Spc1/StyI MAPK is activated by many environmental insults including high osmolarity, oxidative stress, and heat shock. Spc1/StyI is activated by Wis1, a MAPK kinase (MEK), which is itself activated by Wik1/Wak1/Wis4, a MEK kinase (MEKK). Spc1/StyI is inactivated by the tyrosine phosphatases Pyp1 and Pyp2. Inhibition of Pyp1 was recently reported to play a crucial role in the oxidative stress and heat shock responses. These conclusions were based on three findings: 1) osmotic, oxidative, and heat stresses activate Spc1/StyI in wis4 cells; 2) oxidative stress and heat shock activate Spc1/StyI in cells that express Wis1AA, in which MEKK consensus phosphorylation sites were replaced with alanine; and 3) Spc1/StyI is maximally activated in Δpyp1 cells. Contrary to these findings, we report: 1) Spc1/StyI activation by osmotic stress is greatly reduced in wis4 cells; 2)wis1-AA and Δwis1 cells have identical phenotypes; and 3) all forms of stress activate Spc1/StyI inΔpyp1 cells. We also report that heat shock, but not osmotic or oxidative stress, activate Spc1 in wis1-DDcells, which express Wis1 protein that has the MEKK consensus phosphorylation sites replaced with aspartic acid. Thus osmotic and oxidative stress activate Spc1/StyI by a MEKK-dependent process, whereas heat shock activates Spc1/StyI by a novel mechanism that does not require MEKK activation or Pyp1 inhibition.


2019 ◽  
Vol 5 (02) ◽  
pp. 78-83
Author(s):  
Rajesh Kumar Tewari

Nitric oxide is reported to alleviate Fe-deficiency effects, possibly by enhancing the functional Fe status of plants. Study describes changes in leaf tissue Fe status and consequent modulation of oxidative stress and antioxidant defense in Fe-deficient maize (Zea mays L.) plants supplied with NO. Supply of sodium nitroprusside (SNP), but not of sodium ferrocyanide (SF), caused regreening of leaves, syntheses of chlorophylls and carotenoids and increased activities of hydrogen peroxide-scavenging heme-Fe enzymes and lipid peroxidation, decreased SOD activity and hydrogen peroxide concentration. Though SNP or SF appears to donate Fe and increase leaf active Fe, the later did not induce increases in chlorophyll and carotenoids, and therefore NO appears to have a role in Fe nutrition irrespective of total or active Fe status of plants.


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