scholarly journals Choline Chloride Mediates Salinity Tolerance in Cluster Bean (Cyamopsis tetragonoloba L.) by Improving Growth, Oxidative Defense, and Secondary Metabolism

Dose-Response ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 155932582110550
Author(s):  
Saima Riaz ◽  
Iqbal Hussain ◽  
Muhammad Ibrahim ◽  
Rizwan Rasheed ◽  
Muhammad Arslan Ashraf

Choline chloride (CC) application enhanced the tolerance of cluster bean ( Cyamopsis tetragonoloba L.) against salinity stress. The aim of the study was to determine the protective role of CC on plant growth, photosynthesis, and biochemical indicators of oxidative stress. The seeds of BR-99 (tolerant) and BR-2017 (sensitive) were surface sterilized and sown in plastic pots containing river sandy soil. The design of the experiments was completely randomized with 4 replicates per treatment. Three weeks after germination, salinity (150 mM) was imposed. Then plants were sprayed with different concentrations of CC (3, 5, and 10 mM), while normal plants were sprayed with distilled water. Salinity decreased growth attributes, relative water contents, photosynthetic attributes, total soluble proteins, total free amino acids, phenolic, flavonoids, ascorbic acid, proline, and glycine betaine and increased the levels of oxidative stress indicators. However, the application of CC (particularly 5 mM) improved growth attributes, photosynthetic pigments, and activities of antioxidant compounds by reducing the levels of H2O2, malondialdehyde in salt-stressed plants in both cluster bean varieties. BR-99 variety showed more tolerance to salinity stress than that of BR-2017 in the form of greater oxidative defense and osmotic adjustment and clear from greater plant dry masses. Thus, our results showed that the application of CC (5 mM) is an efficient strategy for field use in the areas, where salt stress soils limit agriculture production.

2014 ◽  
Vol 73 (2) ◽  
pp. 347-358 ◽  
Author(s):  
Valerija Vujčić ◽  
Sandra Radić Brkanac

Abstract Water deficit in the soil leads to osmotic stress in plants. The type of stress affects plant water relations, osmolyte accumulation and oxidative stress balance. The present study aimed to investigate the effects of osmotic stress on the Croatian perennial species Fibigia triquetra (DC.) Boiss, adapted to a hot and dry habitat. Plants grown in culture conditions were subjected to isoosmotic concentrations of mannitol and polyethylene glycol (PEG) and certain physiological and oxidative stress parameters were analyzed during a period of 14 days. Dry weight and proline content in Fibigia triquetra shoots increased in response to osmotic stress while the relative water content decreased. After an initial rise, chlorophyll and carotenoid levels in treated plants dropped to untreated plant levels. Oxidative damage to proteins and especially to lipids was evident upon PEG-induced osmotic stress. Superoxide dismutase and ascorbate peroxidase appear to play an essential protective role in stressed plants. Regardless of the osmotic agent, accumulation of heat-shock proteins of 70 kDa was noticed under osmotic stress. The tolerance of the plant species to osmotic stress seems to be associated with increased capacity of the antioxidative system and efficient photoprotective system.


Plants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 625
Author(s):  
Md Tariqul Islam ◽  
Wenzi Ckurshumova ◽  
Michael Fefer ◽  
Jun Liu ◽  
Wakar Uddin ◽  
...  

To date, managing salinity stress in agriculture relies heavily on development of salt tolerant plant varieties, a time-consuming process particularly challenging for many crops. Plant based biostimulants (PBs) that enhance plant defenses under stress can potentially address this drawback, as they are not crop specific and are easy to apply in the field. Unfortunately, limited knowledge about their modes of action makes it harder to utilize them on a broader scale. Understanding how PBs enhance plant defenses at cellular and molecular levels, is a prerequisite for the development of sustainable management practices utilizing biostimulants to improve crop health. In this study we elucidated the protective mechanism of copper chlorophyllin (Cu-chl), a PB, under salinity stress. Our results indicate that Cu-chl exerts protective effects primarily by decreasing oxidative stress through modulating cellular H2O2 levels. Cu-chl treated plants increased tolerance to oxidative stress imposed by an herbicide, methyl viologen dichloride hydrate as well, suggesting a protective role against various sources of reactive oxygen species (ROS). RNA-Seq analysis of Cu-chl treated Arabidopsis thaliana seedlings subjected to salt stress identified genes involved in ROS detoxification, and cellular growth.


2020 ◽  
Vol 10 (5) ◽  
pp. 578-586
Author(s):  
Areeg M. Abdelrazek ◽  
Shimaa A. Haredy

Background: Busulfan (Bu) is an anticancer drug with a variety of adverse effects for cancer patients. Oxidative stress has been considered as a common pathological mechanism and it has a key role in the initiation and progression of liver injury by Bu. Aim: The study aimed to evaluate the antioxidant impact of L-Carnitine and Coenzyme Q10 and their protective role against oxidative stress damage in liver tissues. Methods and Material: Thirty-six albino rats were divided equally into six groups. G1 (con), received I.P. injection of DMSO plus 1 ml of distilled water daily by oral gavages; G2 (Bu), received I.P. injection of Bu plus 1 ml of the distilled water daily; G3 (L-Car), received 1 ml of L-Car orally; G4 (Bu + L-Car) received I.P. injection of Bu plus 1 ml of L-Car, G5 (CoQ10) 1 ml of CoQ10 daily; and G6 (Bu + CoQ10) received I.P. injection of Bu plus 1 ml of CoQ10 daily. Results: The recent data showed that Bu induced significant (P<0.05) elevation in serum ALT, AST, liver GSSG, NO, MDA and 8-OHDG, while showing significant (P<0.05) decrease in liver GSH and ATP. On the other hand, L-Carnitine and Coenzyme Q10 ameliorated the negative effects prompted by Bu. Immunohistochemical expression of caspase-3 in liver tissues reported pathological alterations in Bu group while also showed significant recovery in L-Car more than CoQ10. Conclusion: L-Car, as well as CoQ10, can enhance the hepatotoxic effects of Bu by promoting energy production in oxidative phosphorylation process and by scavenging the free radicals.


2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nesrine S. El Sayed ◽  
Mamdooh H. Ghoneum

Background. Many neurodegenerative diseases such as Alzheimer’s disease are associated with oxidative stress. Therefore, antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases. Objective. We investigated the ability of the antioxidant Antia to exert a protective effect against sporadic Alzheimer’s disease (SAD) induced in mice. Antia is a natural product that is extracted from the edible yamabushitake mushroom, the gotsukora and kothala himbutu plants, diosgenin (an extract from wild yam tubers), and amla (Indian gooseberry) after treatment with MRN-100. Methods. Single intracerebroventricular (ICV) injection of streptozotocin (STZ) (3 mg/kg) was used for induction of SAD in mice. Antia was injected intraperitoneally (i.p.) in 3 doses (25, 50, and 100 mg/kg/day) for 21 days. Neurobehavioral tests were conducted within 24 h after the last day of injection. Afterwards, mice were sacrificed and their hippocampi were rapidly excised, weighed, and homogenized to be used for measuring biochemical parameters. Results. Treatment with Antia significantly improved mice performance in the Morris water maze. In addition, biochemical analysis showed that Antia exerted a protective effect for several compounds, including GSH, MDA, NF-κB, IL-6, TNF-α, and amyloid β. Further studies with western blot showed the protective effect of Antia for the JAK2/STAT3 pathway. Conclusions. Antia exerts a significant protection against cognitive dysfunction induced by ICV-STZ injection. This effect is achieved through targeting of the amyloidogenic, inflammatory, and oxidative stress pathways. The JAK2/STAT3 pathway plays a protective role for neuroinflammatory and neurodegenerative diseases such as SAD.


2021 ◽  
Vol 10 (5) ◽  
pp. 1148
Author(s):  
Makedonka Atanasovska Velkovska ◽  
Katja Goričar ◽  
Tanja Blagus ◽  
Vita Dolžan ◽  
Barbara Cvenkel

Oxidative stress and neuroinflammation are involved in the pathogenesis and progression of glaucoma. Our aim was to evaluate the impact of selected single-nucleotide polymorphisms in inflammation and oxidative stress genes on the risk of glaucoma, the patients’ clinical characteristics and the glaucoma phenotype. In total, 307 patients with primary open-angle glaucoma or ocular hypertension were enrolled. The control group included 339 healthy Slovenian blood donors. DNA was isolated from peripheral blood. Genotyping was performed for SOD2 rs4880, CAT rs1001179, GPX1 rs1050450, GSTP1 rs1695, GSTM1 gene deletion, GSTT1 gene deletion, IL1B rs1143623, IL1B rs16944, IL6 rs1800795 and TNF rs1800629. We found a nominally significant association of GSTM1 gene deletion with decreased risk of ocular hypertension and a protective role of IL1B rs16944 and IL6 rs1800629 in the risk of glaucoma. The CT and TT genotypes of GPX1 rs1050450 were significantly associated with advanced disease, lower intraocular pressure and a larger vertical cup–disc ratio. In conclusion, genetic variability in IL1B and IL6 may be associated with glaucoma risk, while GPX and TNF may be associated with the glaucoma phenotype. In the future, improved knowledge of these pathways has the potential for new strategies and personalised treatment of glaucoma.


2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.


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