Reactive oxygen species (ROS) and redox buffers as an interface between stress sensing, signalling and physiological responses in Daphnia magna

Author(s):  
D. Becker ◽  
B. Brinkmann ◽  
B. Budeus ◽  
U. Schnell ◽  
S. Zumbrägel ◽  
...  
2014 ◽  
Vol 26 (3) ◽  
pp. 268-277 ◽  
Author(s):  
Andresa Lana Thomé Bizzo ◽  
Aline Chaves Intorne ◽  
Pollyana Honório Gomes ◽  
Marina Satika Suzuki ◽  
Bruno dos Santos Esteves

AIM: To evaluate, in a short-time exposure, the physiological responses of Salvinia auriculata Aubl. under different concentrations of Cu. METHODS: The plants were exposed to treatments with 0.01, 0.1, 1 and 10 mM of Cu in a period of 2 days. Then development variables of S. auriculata (weight, photosynthetic pigments, and soluble carbohydrate), lipid peroxidation (malondialdehyde, aldehydes, and electrolyte leakage) and production of antioxidants (anthocyanins, carotenoids, flavonoids, and proline) were evaluated. RESULTS: It was observed fresh weight reductions in concentrations above 1 mM of Cu. Chlorophyll a decreased with the increase of Cu concentrations unlike chlorophyll b. The ratio chlorophyll a / chlorophyll b was changed due to the degradation of photosynthetic pigments. The reductions of carotenoids were more pronounced than that of total chlorophyll. The values of electrolyte leakage ranged from 14 to 82 % and lipid peroxidation from 7 to 46 nmol.g-1. Flavonoids and soluble carbohydrates showed reductions with the increase of Cu concentration. Anthocyanins, phenolic compounds, and proline when subjected to 0.1 mM of Cu had increased, suggesting adaptability of plant stress caused directly by metal and reactive oxygen species. In higher concentrations, degradation and/or direct modifications of these molecules possibly occurred. CONCLUSIONS: The data suggest that S. auriculata is provided with an efficient mechanism against stress caused by Cu in the concentration of 0.1 mM. As for higher concentrations (1 and 10 mM), despite its role as micronutrients, Cu was toxic to the plant due to the redox behavior of this metal, which leads to the exacerbated formation of reactive oxygen species, inducing to severe damage such as biological membrane degradation and protein denaturation.


2013 ◽  
Vol 40 (9) ◽  
pp. 832 ◽  
Author(s):  
Rengin Ozgur ◽  
Baris Uzilday ◽  
Askim Hediye Sekmen ◽  
Ismail Turkan

Production of reactive oxygen species (ROS), which are a by-product of normal cell metabolism in living organisms, is an inevitable consequence of aerobic life on Earth, and halophytes are no exception to this rule. The accumulation of ROS is elevated under different stress conditions, including salinity, due to a serious imbalance between their production and elimination. These ROS are highly toxic and, in the absence of protective mechanisms, can cause oxidative damage to lipids, proteins and DNA, leading to alterations in the redox state and further damage to the cell. Besides functioning as toxic by-products of stress metabolism, ROS are also important signal transduction molecules in controlling growth, development and responses to stress. Plants control the concentrations of ROS by an array of enzymatic and non-enzymatic antioxidants. Although a relation between enzymatic and non-enzymatic antioxidant defence mechanisms and tolerance to salt stress has been reported, little information is available on ROS-mediated signalling, perception and specificity in different halophytic species. Hence, in this review, we describe recent advances in ROS homeostasis and signalling in response to salt, and discuss current understanding of ROS involvement in stress sensing, stress signalling and regulation of acclimation responses in halophytes. We also highlight the role of genetic, proteomic and metabolic approaches for the successful study of the complex relationship among antioxidants and their functions in halophytes, which would be critical in increasing salt tolerance in crop plants.


2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.


2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  

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