scholarly journals Reactive Oxygen Species at High Altitude (Hypobaric Hypoxia) on the Cardiovascular System

Author(s):  
Patricia Siques ◽  
Julio Brito ◽  
Eduardo Pena
2017 ◽  
Vol 174 (12) ◽  
pp. 1533-1554 ◽  
Author(s):  
Thomas Kietzmann ◽  
Andreas Petry ◽  
Antonina Shvetsova ◽  
Joachim M Gerhold ◽  
Agnes Görlach

Author(s):  
Arun Kumar ◽  
Shweta Guleria ◽  
Dipanshu Ghosh ◽  
Vivek Dogra ◽  
Sanjay Kumar

2016 ◽  
Vol 310 (1) ◽  
pp. R1-R14 ◽  
Author(s):  
Rita C. Tostes ◽  
Fernando S. Carneiro ◽  
Maria Helena C. Carvalho ◽  
Jane F. Reckelhoff

Androgens are essential for the development and maintenance of male reproductive tissues and sexual function and for overall health and well being. Testosterone, the predominant and most important androgen, not only affects the male reproductive system, but also influences the activity of many other organs. In the cardiovascular system, the actions of testosterone are still controversial, its effects ranging from protective to deleterious. While early studies showed that testosterone replacement therapy exerted beneficial effects on cardiovascular disease, some recent safety studies point to a positive association between endogenous and supraphysiological levels of androgens/testosterone and cardiovascular disease risk. Among the possible mechanisms involved in the actions of testosterone on the cardiovascular system, indirect actions (changes in the lipid profile, insulin sensitivity, and hemostatic mechanisms, modulation of the sympathetic nervous system and renin-angiotensin-aldosterone system), as well as direct actions (modulatory effects on proinflammatory enzymes, on the generation of reactive oxygen species, nitric oxide bioavailability, and on vasoconstrictor signaling pathways) have been reported. This mini-review focuses on evidence indicating that testosterone has prooxidative actions that may contribute to its deleterious actions in the cardiovascular system. The controversial effects of testosterone on ROS generation and oxidant status, both prooxidant and antioxidant, in the cardiovascular system and in cells and tissues of other systems are reviewed.


2019 ◽  
Vol 20 (3) ◽  
pp. 661 ◽  
Author(s):  
Afshin Beheshti ◽  
J. McDonald ◽  
Jack Miller ◽  
Peter Grabham ◽  
Sylvain Costes

Space radiation has recently been considered a risk factor for astronauts’ cardiac health. As an example, for the case of how to query and identify datasets within NASA’s GeneLab database and demonstrate the database utility, we used an unbiased systems biology method for identifying key genes/drivers for the contribution of space radiation on the cardiovascular system. This knowledge can contribute to designing appropriate experiments targeting these specific pathways. Microarray data from cardiomyocytes of male C57BL/6 mice followed-up for 28 days after exposure to 900 mGy of 1 GeV proton or 150 mGy of 1 GeV/n 56Fe were compared to human endothelial cells (HUVECs) cultured for 7 days on the International Space Station (ISS). We observed common molecular pathways between simulated space radiation and HUVECs flown on the ISS. The analysis suggests FYN is the central driver/hub for the cardiovascular response to space radiation: the known oxidative stress induced immediately following radiation would only be transient and would upregulate FYN, which in turn would reduce reactive oxygen species (ROS) levels, protecting the cardiovascular system. The transcriptomic signature of exposure to protons was also much closer to the spaceflight signature than 56Fe’s signature. To our knowledge, this is the first time GeneLab datasets were utilized to provide potential biological indications that the majority of ions on the ISS are protons, clearly illustrating the power of omics analysis. More generally, this work also demonstrates how to combine animal radiation studies done on the ground and spaceflight studies to evaluate human risk in space.


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