scholarly journals Ethephon-Mediated Bloom Delay in Peach Is Associated With Alterations in Reactive Oxygen Species, Antioxidants, and Carbohydrate Metabolism During Dormancy

2021 ◽  
Vol 12 ◽  
Author(s):  
Md Tabibul Islam ◽  
Jianyang Liu ◽  
Sherif M. Sherif

Ethephon (ET) is an ethylene-based plant growth regulator (PGR) that has demonstrated greater efficacy in delaying bloom in deciduous fruit species. However, the underlying mechanisms by which ET modulates dormancy and flowering time remain obscure. This study aimed to delineate the ET-mediated modulations of reactive oxygen species (ROS), antioxidants, and carbohydrate metabolism in relation to chilling and heat requirements of “Redhaven” peach trees during dormancy. Peach trees were treated with ethephon (500ppm) in the fall (at 50% leaf fall), and floral buds were collected at regular intervals of chilling hours (CH) and growing degree hours (GDH). In the control trees, hydrogen peroxide (H2O2) levels peaked at the endodormancy release and declined thereafter; a pattern that has been ascertained in other deciduous fruit trees. However, H2O2 levels were higher and sustained for a more extended period than control in the ET-treated trees. ET also increased the activity of ROS generating (e.g., NADPH-oxidase; superoxide dismutase) and scavenging (e.g., catalase, CAT; glutathione peroxidase) enzymes during endodormancy. However, CAT activity dropped significantly just before the bud burst in the ET-treated trees. In addition, ET affected the accumulation profiles of starch and soluble sugars (hexose and sucrose); significantly reducing the sucrose and glucose levels and increasing starch levels during endodormancy. However, our study concluded that variations in ROS levels and antioxidation pathways, rather than carbohydrate metabolism, could explain the differences in bloom time between ET-treated and -untreated trees. The present study also revealed several important bud dormancy controlling factors that are subject to modulation by ethephon. These factors can serve as potential targets for developing PGRs to manipulate bloom dates in stone fruits to avoid the ever-increasing threat of spring frosts.

2006 ◽  
Vol 57 (3) ◽  
pp. 449-459 ◽  
Author(s):  
Ivan Couée ◽  
Cécile Sulmon ◽  
Gwenola Gouesbet ◽  
Abdelhak El Amrani

2015 ◽  
Vol 116 (4) ◽  
pp. 703-711 ◽  
Author(s):  
Karlia Meitha ◽  
Dennis Konnerup ◽  
Timothy D. Colmer ◽  
John A. Considine ◽  
Christine H. Foyer ◽  
...  

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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