Reactive oxygen species generation and antioxidant systems in plant mitochondria

2007 ◽  
Vol 129 (1) ◽  
pp. 185-195 ◽  
Author(s):  
Nicolas Navrot ◽  
Nicolas Rouhier ◽  
Eric Gelhaye ◽  
Jean-Pierre Jacquot
Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 277 ◽  
Author(s):  
Swati Sachdev ◽  
Shamim Akhtar Ansari ◽  
Mohammad Israil Ansari ◽  
Masayuki Fujita ◽  
Mirza Hasanuzzaman

Climate change is an invisible, silent killer with calamitous effects on living organisms. As the sessile organism, plants experience a diverse array of abiotic stresses during ontogenesis. The relentless climatic changes amplify the intensity and duration of stresses, making plants dwindle to survive. Plants convert 1–2% of consumed oxygen into reactive oxygen species (ROS), in particular, singlet oxygen (1O2), superoxide radical (O2•–), hydrogen peroxide (H2O2), hydroxyl radical (•OH), etc. as a byproduct of aerobic metabolism in different cell organelles such as chloroplast, mitochondria, etc. The regulatory network comprising enzymatic and non-enzymatic antioxidant systems tends to keep the magnitude of ROS within plant cells to a non-damaging level. However, under stress conditions, the production rate of ROS increases exponentially, exceeding the potential of antioxidant scavengers instigating oxidative burst, which affects biomolecules and disturbs cellular redox homeostasis. ROS are similar to a double-edged sword; and, when present below the threshold level, mediate redox signaling pathways that actuate plant growth, development, and acclimatization against stresses. The production of ROS in plant cells displays both detrimental and beneficial effects. However, exact pathways of ROS mediated stress alleviation are yet to be fully elucidated. Therefore, the review deposits information about the status of known sites of production, signaling mechanisms/pathways, effects, and management of ROS within plant cells under stress. In addition, the role played by advancement in modern techniques such as molecular priming, systems biology, phenomics, and crop modeling in preventing oxidative stress, as well as diverting ROS into signaling pathways has been canvassed.


The eff ect of the non-opiate analog of leu-enkephalin (peptide NALE: Phe – D – Ala – Gly – Phe – Leu – Arg) on the reactive oxygen species generation in the heart of albino rats in the early postnatal period was studied. Peptide NALE was administered intraperitoneally in the dose of 100 μ/kg daily from 2 to 6 days of life. Reactive oxygen species generation was assessed by chemiluminescence in the heart homogenates of 7-day-old animals. Decreasing of reactive oxygen species generation nearly by 30 % and an increasing in antioxidant system activity by the 20-27 %, compared with the control parameters, were found. The antioxidant eff ect of peptide NALE is associated with the presence of the amino acid Arg in the structure of the peptide. An analogue of NALE peptide, devoid of Arg (peptide Phe – D – Ala – Gly – Phe – Leu – Gly), had a signifi cant lower antioxidant eff ect. The NO-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the dose 50 mg/kg, administered with NALE peptide, reduced the severity of the NALE antioxidant eff ect. The results of the study suggest that the pronounced antioxidant eff ect of NALE peptide in the heart of albino rats, at least in part, is due to the interaction with the nitric oxide system.


1993 ◽  
Vol 149 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Donald L. Weese ◽  
Michael L. Peaster ◽  
Kyle K. Himsl ◽  
Gary E. Leach ◽  
Pramod M. Lad ◽  
...  

2020 ◽  
Vol 21 (14) ◽  
pp. 4970
Author(s):  
Juan Perdomo ◽  
Carlos Quintana ◽  
Ignacio González ◽  
Inmaculada Hernández ◽  
Sara Rubio ◽  
...  

Melatonin is present in all living organisms where it displays a diversity of physiological functions. Attenuation of melanogenesis by melatonin has been reported in some mammals and also in rodent melanoma cells. However, melatonin may also stimulate melanogenesis in human melanoma cells through mechanisms that have not yet been revealed. Using the human melanoma cells SK-MEL-1 as a model, an increase in both tyrosinase activity and melanin was already observed at 24 h after melatonin treatment with maximal levels of both being detected at 72 h. This effect was associated with the induction in the expression of the enzymes involved in the synthesis of melanin. In this scenario, glycogen synthase kinase-3β seems to play a significant function since melatonin decreased its phosphorylation and preincubation with specific inhibitors of this protein kinase (lithium or BIO) reduced the expression and activity of tyrosinase. Blocking of PI3K/AKT pathway stimulated melanogenesis and the effect was suppressed by the inhibitors of glycogen synthase kinase-3β. Although melatonin is a recognized antioxidant, we found that it stimulates reactive oxygen species generation in SK-MEL-1 cells. These chemical species seem to be an important signal in activating the melanogenic process since the antioxidants N-acetyl-l-cysteine and glutathione decreased both the level and activity of tyrosinase stimulated by melatonin. Our results support the view that regulation of melanogenesis involves a cross-talk between several signaling pathways.


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