Exogenously Applied Spermidine Alleviates Hypoxia Stress in Phyllostachys Praecox Seedlings Via Changes in Endogenous Hormones and Gene Expression

Author(s):  
JS Gao ◽  
Shunyao Zhuang ◽  
YH Zhang ◽  
ZZ Qian

Abstract PurposeHypoxia stress is thought to be one of the major abiotic stresses that inhibits the growth and development of higher plants. Phyllostachys pracecox is sensitive to oxygen and suffers soil hypoxia during cultivation; however, the corresponding measures to mitigate this stress are still limited in practice. In this study, a simulated hypoxia stress with flooding was conducted to investigate the regulatory effect of Spermidine (Spd) on P. praecox seedlings. MethodsIndicators including growth, membrane lipid peroxidation, S-adenosylmethionine decarboxylase (SAMDC), ACC oxidase (ACO) and ACC synthetase (ACS) activities, indole-3-acetic acid (IAA) and abscisic acid (ABA) content, and expression of hormone-related genes in P. praecox were measured. ResultsApplication of 1 mM and 2 mM Spd could alleviate plant growth inhibition and reduce oxidative damage from hypoxia stress. Exogenous Spd significantly (P<0.05) increased SAMDC activity, enhanced ABA and IAA content, and reduced ACO and ACS activities to protect membranes from lipid peroxidation. Moreover, exogenous Spd up-regulated the expression of auxin-related genes auxin responsive factor1 (ARF1), auxin1 protein (AUX1), auxin2 protein (AUX2), auxin3 protein (AUX3) and auxin4 protein (AUX4), and down-regulated the expression of ethylene-related ACO and ACS genes during flooding. ConclusionThe results indicated that exogenous Spd altered hormone concentrations and the expression of hormone-related genes, thereby protecting the bamboo growth. Our data suggest that Spd can be used to reduce hypoxia-induced cell damage and improve the adaptability of P. praecox to flooding stress.

1999 ◽  
Vol 7 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Klara D Vichnevetskaia ◽  
D N Roy

Increased levels of active oxygen species or free radicals can create an oxidative stress. Concentration of free radicals in living cells increases as a result of exposure to environmental stresses that lead to aging, carcinogenesis, and immunodeficiencies in animals, and membrane leakage, senescence, chlorophyll destruction, and decreased photosynthesis in plants. The antioxidative system of higher plants consists of enzymes, low molecular weight compounds (among them peptides, vitamins, flavonoids, phenolic acids, alkaloids, etc.), and integrated detoxification chains. Enzymatic defense in plants include enzymes capable of removing, neutralizing, or scavenging oxy-intermediates. Catalases and superoxide dismutases are the most efficient antioxidant enzymes. Free radicals cause cell damage by a lipid peroxidation mechanism, which results in a blockade of natural antioxidant systems. Application of synthetic antioxidants can assist in coping with oxidative stress. There are very few publications on effects of synthetic antioxidants on plant growth and physiology. One of the examples of such synthetic antioxidant is 2-methyl-4-dimethylaminomethyl-5-hydroxybenzimidazole (Ambiol), which substantially promoted growth of agricultural and forestry plant species. Ambiol also demonstrated antitranspirant properties, increasing drought tolerance of conifers and agricultural species. The response of plants to Ambiol is under high genetic control. The identification of genes responsible for the reaction of plants to Ambiol may lead to attempts in genetic engineering of organisms with increased tolerance to oxidative stress. It seems impossible to find a universal scavenger trapping all free radicals active in the organism. However, analysis of the structure–activity relationships in antioxidants can contribute to the search for effective antioxidants.Key words: oxidative stress, lipid peroxidation, free radicals, natural and synthetic antioxidants, Ambiol.


2021 ◽  
Vol 11 ◽  
Author(s):  
Zafar Iqbal ◽  
Ali Sarkhosh ◽  
Rashad Mukhtar Balal ◽  
Celina Gómez ◽  
Muhammad Zubair ◽  
...  

Flooding induces low oxygen (hypoxia) stress to plants, and this scenario is mounting due to hurricanes followed by heavy rains, especially in subtropical regions. Hypoxia stress results in the reduction of green pigments, gas exchange (stomatal conductance and internal CO2 concentration), and photosynthetic activity in the plant leaves. In addition, hypoxia stress causes oxidative damage by accelerating lipid peroxidation due to the hyperproduction of reactive oxygen species (ROS) in leaf and root tissues. Furthermore, osmolyte accumulation and antioxidant activity increase, whereas micronutrient uptake decreases under hypoxia stress. Plant physiology and development get severely compromised by hypoxia stress. This investigation was, therefore, aimed at appraising the effects of regular silicon (Si) and Si nanoparticles (SiNPs) to mitigate hypoxia stress in muscadine (Muscadinia rotundifolia Michx.) plants. Our results demonstrated that hypoxia stress reduced muscadine plants’ growth by limiting the production of root and shoot dry biomass, whereas the root zone application of both Si and SiNP effectively mitigated oxidative and osmotic cell damage. Compared to Si, SiNP yielded better efficiency by improving the activity of enzymatic antioxidants [including superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT)], non-enzymatic antioxidants [ascorbic acid (AsA) and glutathione contents], and accumulation of organic osmolytes [proline and glycinebetaine (GB)]. SiNP also regulated the nutrient profile of the plants by increasing N, P, K, and Zn contents while limiting Mn and Fe concentration to a less toxic level. A negative correlation between antioxidant activities and lipid peroxidation rates was observed in SiNP-treated plants under hypoxia stress. Conclusively, SiNP-treated plants combat hypoxia more efficiently stress than conventional Si by boosting antioxidant activities, osmoprotectant accumulation, and micronutrient regulation.


Diabetes ◽  
1989 ◽  
Vol 38 (12) ◽  
pp. 1539-1543 ◽  
Author(s):  
S. K. Jain ◽  
R. McVie ◽  
J. Duett ◽  
J. J. Herbst

2020 ◽  
Vol 20 (7) ◽  
pp. 1010-1014 ◽  
Author(s):  
Dana Filatova ◽  
Christine Cherpak

Background: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. Objective: The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. Conclusion: Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.


1991 ◽  
Vol 19 (3) ◽  
pp. 206-213
Author(s):  
Bruce L. Homer ◽  
Kenneth R. Pierce ◽  
Charles H. Bridges ◽  
James E. Womack ◽  
Blair A. Sowa ◽  
...  

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