Reactive Oxygen Species, Ascorbic Acid and Glutathione to Ozone Stress in Soybean (Glycine max) Leave

Author(s):  
Wang Yana ◽  
Zhao Tianhong ◽  
Wang Junli ◽  
Zhao Yixin ◽  
Guo Wei ◽  
...  
2016 ◽  
Vol 52 (27) ◽  
pp. 4888-4890 ◽  
Author(s):  
V. N. Carroll ◽  
C. Truillet ◽  
B. Shen ◽  
R. R. Flavell ◽  
X. Shao ◽  
...  

We report the radiosynthesis of an endogenous redox pair, [11C]ascorbic acid and [11C]dehydroascorbic acid and their application to ROS sensing.


2015 ◽  
Vol 51 (89) ◽  
pp. 16139-16142 ◽  
Author(s):  
Yuyuan Yao ◽  
Bin Jiang ◽  
Yajun Mao ◽  
Juan Chen ◽  
Zhenfu Huang ◽  
...  

A positive role of PFRs in enhancing reactive oxygen species (ROS) generation for an extreme rate enhancement in environmental pollutant decomposition is reported.


2010 ◽  
Vol 26 (5) ◽  
pp. 265-272 ◽  
Author(s):  
Sohini Singh ◽  
Suresh Vir Singh Rana

Arsenic is an ubiquitous and well-documented carcinogenic metalloid. The most common source of arsenic is drinking water. The mechanism of arsenic toxicity in a cell has historically been centered around its inhibitory effects on cellular respiration and mitochondrial injury. Ascorbic acid, a low molecular weight, water-soluble antioxidant, improves the reduced glutathione (GSH) status by recycling oxidized glutathione. Ascorbic acid can improve mitochondrial function by improving the thiol status; thereby preventing reactive oxygen species— mediated damage to liver as well as kidney. Ascorbic acid has been shown to protect membrane and other cellular compartments by regenerating vitamin E. Therefore, ascorbic acid seems to be a suitable protective factor against arsenic toxicity. Present reports describe the effect of ascorbic acid on oxidative phosphorylation, adenosine triphosphatase (ATPase), succinic dehydrogenase, caspase-3 and apoptosis in the liver of rats treated with arsenic trioxide (AsIII). Ultrastructural changes in the mitochondria have also been reported. We show that cotreatments with ascorbic acid and AsIII improve mitochondrial structure and function. We attribute these improvements mainly to antioxidative role of ascorbic acid. Apoptosis was restricted due to caspase-3 inhibition. Ascorbic acid could protect DNA from the attack of reactive oxygen species generated by AsIII. Consequently its events led to improved ADP:O ratio, normalized ATPase activity and restored the activity of succinic dehydrogenase. Overall, results support the protective role of ascorbic acid against As III-induced liver injury.


2018 ◽  
Vol 19 (11) ◽  
pp. 3347 ◽  
Author(s):  
Yayun Wang ◽  
Hui Zhao ◽  
Hua Qin ◽  
Zixuan Li ◽  
Hai Liu ◽  
...  

The root plays an important role in the responses of plants to stresses, but the detailed mechanisms of roots in stress responses are still obscure. The GDP-mannose pyrophosphate synthetase (GMPase) OsVTC1-3 is a key factor of ascorbic acid (AsA) synthesis in rice roots. The present study showed that the transcript of OsVTC1-3 was induced by salt stress in roots, but not in leaves. Inhibiting the expression of OsVTC1-3 by RNA interfering (RI) technology significantly impaired the tolerance of rice to salt stress. The roots of OsVTC1-3 RI plants rapidly produced more O2−, and later accumulated amounts of H2O2 under salt stress, indicating the impaired tolerance of OsVTC1-3 RI plants to salt stress due to the decreasing ability of scavenging reactive oxygen species (ROS). Moreover, exogenous AsA restored the salt tolerance of OsVTC1-3 RI plants, indicating that the AsA synthesis in rice roots is an important factor for the response of rice to salt stress. Further studies showed that the salt-induced AsA synthesis was limited in the roots of OsVTC1-3 RI plants. The above results showed that specifically regulating AsA synthesis to scavenge ROS in rice roots was one of important factors in enhancing the tolerance of rice to salt stress.


2019 ◽  
Vol 26 (07) ◽  
pp. 1036-1041
Author(s):  
Muhammad Yaqoob Shahani ◽  
Umbreen Bano ◽  
Shazia Begum Shahani ◽  
Pashmina Shaikh ◽  
Sameena Gul Memon ◽  
...  

Objectives: To analyze the antioxidant activity of Resveratrol and Ascorbic Acid against hydrogen peroxide (an oxidant) mediated cell injury of human trabecular meshwork cells. Study Design: Experimental study. Setting: Molecular Biology Laboratory at Medical Research Centre, Liaquat University of Medical & Health Sciences, Jamshoro. Period: Six months. Materials and Methods: Human Trabecular Meshwork cells were purchased from ScienCell Research Laboratories, USA. TM cell metabolism, TM cell viability and Reactive oxygen species were detected by standard methods in co- and pre- treated TM cells. Results: A significant reduction in TM cell metabolism was observed approximating 61% at 1.0 mM H2O2 compared to Ascorbate – 99% and Resveratrol 99% (p=0.0001). Resveratrol was more effective than Ascorbate even at 4.0 mM H2O2, the TM cell activity was noted 76%. Compared to H2O2- treated TM cells, resveratrol improved mitochondrial function upto 4.0 mM H2O2 (76%). Compared to co-treatment, the pretreatment shows similar results except at 4.0 mM H2O2. At 4.0 mM H2O2 the pre-treat TM cell metabolic activity was found as 11%, 31% and 47% compared to co-treat as 9%, 31% and 76% in controls, ascorbate and resveratrol groups respectively (p<0.05). Resveratrol shows significant decrease in viability was seen in controls compared to Ascorbate and Resveratrol groups. Cell viability showed statistically significant differences at 2.0 and 4.0 mM H2O2 compared to controls (P=0.0001). For reactive oxygen species (ROS), cells were incubated and with Ascorbate and Resveratrol for 24 hours and TM cells were treated with 0.0mM, 0.5 mM, 1.0 mM, 2.0mM and 4.0mM H2O2. Significant decrease in ROS was noted by Resveratrol compared to Ascorbate. Conclusions: Resveratrol and Ascorbate may prove useful in preventing and delaying the glaucoma, and timely institution of these anti – oxidants may help maintain trabecular meshwork functions and prevent visual loss.


2019 ◽  
Vol 6 (2) ◽  
pp. 26-37
Author(s):  
Syukri ◽  
Risky Ridha

Wilayah pesisir mempunyai potensi cukup besar untuk dikembangkan menjadi lahan pertanian, namun peningkatan muka air laut akan menyebabkan terjadinya salinitas. Salah satu penyebab kerusakan tanaman pada kondisi salinitas adalah terjadinya cekaman oksidatif yang disebabkan oleh terakumulasinya senyawa Reactive Oxygen Species (ROS). Radikal ini dapat menyebabkan degradasi membran sel yang dapat menyebabkan hilangnya energi untuk biosintesis, cadangan makanan di embrio menjadi habis dan menurunnya viabilitas dan vigoritas benih. Penelitian ini bertujuan untuk mengkaji seberapa besar pengaruh dari ekstrak telur keong mas sebagai antioksidan alami dalam meningkatkan vigoritas benih kedelai (Glycine max (L.) Merril) pada kondisi cekaman salinitas. Penelitian disusun menggunakan Rancangan Acak Lengkap (RAL) faktorial dengan tiga ulangan. Sebagai faktor pertama yaitu kosentrasi ekstrak telur keong mas yang terdiri dari : E1 (45 %) dan E2 (0 %). faktor kedua yaitu kosentrasi larutan NaCl yang terdiri dari : N0 (NaCl 0,0 %), N1 (NaCl 0,5 %), N2 (NaCl 1,0 %) dan N3 (NaCl 1,5 %). Hasil penelitian menunjukkan bahwa pemberian ekstrak telur keong mas kosentrasi 45 % hanya dapat meningkatkan daya berkecambah sebesar 51,59 %, kecepatan tumbuh sebesar 24,18 %/etmal dan vigor kecambah sebesar 33,55 % pada kondisi cekaman salinitas hingga 0,5 %, namun pada cekaman salinitas 1,0 % dan 1,5 % benih sudah tidak mampu untuk berkecambah normal. Peningkatan cekaman salinitas     0 % - 1,0 % menyebabkan pengurangan panjang hipokotil dan panjang akar primer benih kedelai. Pemberian ekstrak telur keong mas kosentrasi 45 % menghasilkan hipokotil dan akar primer benih kedelai yang lebih panjang dibandingkan dengan tanpa pemberian ekstrak. Hasil penelitian membuktikan adanya perbaikan viabilitas dan vigoritas benih yang ditunjukkan oleh indikasi fisiologi yaitu perbaikan performansi panjang hipokotil dan akar primer, meningkatkan nilai kecepatan tumbuh dan vigor kecambah benih kedelai dengan perendaman ekstrak telur keong mas pada kondisi salinitas walaupun pada level yang rendah.


Sign in / Sign up

Export Citation Format

Share Document