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Biomarkers of selenium and copper status in patients with traumatic spinal cord injury
Published in Gary Bañuelos, Zhi-Qing Lin, Dongli Liang, Xue-bin Yin, Selenium Research for Environment and Human Health: Perspectives, Technologies and Advancements, 2019
J. Seelig, R.A. Heller, J. Hackler, L. Schomburg, A. Moghaddam, B. Biglari
Traumatic Spinal Cord Injury (TSCI) is damage of the spinal cord resulting in devastating loss of motor and sensory functions. This injury involves complex pathological mechanisms with massive oxidative stress and extensive inflammatory processes, which can bear the risk for permanent paraplegia (Alizadeh et al. 2019). Selenium (Se) is an essential factor for neuronal development, protects from neuron degeneration, and plays a key role in the antioxidative defense. Selenoprotein P (SELENOP) is the transport protein of Se and an essential survival factor for neurons (Pitts et al. 2014). Copper (Cu) serves as an important catalytic cofactor in redox chemistry, e.g., in superoxide dismutase or cytochrome C oxidase. Other copper-containing proteins are relevant for fundamental biological functions, such as lysyl oxidase for the maturation of the extracellular matrix or ceruloplasmin (CP) for the transport of Cu throughout the system. CP accounts for 95% of the Cu content in serum and protects tissue from iron-mediated oxidative damage (Guengerich 2018). Notably, serum Se via SELENOP and Cu via CP are inversely regulated in infection and acute phase response. As TSCI is associated with severe inflammation, we decided to study the potential alterations of the Se and Cu status as potential diagnostic and predictive parameters, as there is a clinical need for informative biomarkers particularly during the first 24 h after injury.
Understanding selenium metabolism in plants and its role as a beneficial element
Published in Critical Reviews in Environmental Science and Technology, 2019
Reshu Chauhan, Surabhi Awasthi, Sudhakar Srivastava, Sanjay Dwivedi, Elizabeth A. H. Pilon-Smits, Om P. Dhankher, Rudra D. Tripathi
Selenium plays an important role in the scavenging and regulation of free radicals (Kaur, Sharma, Kaur, & Nayyar, 2014). Selenoprotein P plays a major role in antioxidant defense system against harmful reactive oxygen species (ROS) and reactive nitrogen species (Steinbrenner, Alili, Bilgic, Sies, & Brenneisen, 2006; Steinbrenner, Steinbrenner, et al., 2006). Selenoprotein P is identified as a major selenoprotein that regulates plasma cholesterol level by protecting low density lipoproteins from oxidation by ROS (Traulsen, Steinbrenner, Buchczyk, Klotz, & Sies, 2004). Glutathione peroxidase also contributes to overall antioxidant capacity. The presence of SeCys in the active sites of antioxidant enzymes gives higher catalytic efficiency due to greater nucleophilic power of SeCys in comparison to cysteine (Eshdat, Holland, Faltin, & Ben-Hayyim, 1997; Campbell, 2001). Selenium is an excellent hydrogen ion donor at normal blood pH levels and is therefore much effective in the control of ROS as compared to sulfur (Longtin, 2004). The mutations causing defects in SeCys biosynthesis or correct incorporation into Se-requiring proteins has been found to lead to severe neurological disorders or milder systemic disorders, respectively (Schmidt & Simonović, 2012). Thus, adequate Se intake is important for optimal antioxidant function. The beneficial effects of Se have been demonstrated in prevention against cancer and other diseases (Sanmartín, Plano, Font, & Palop, 2011). External Se supply has also been found to be beneficial in several animal models in terms of toxicity reduction of a drug/chemical or cure of a disease (Collery, 2018). However, Se administration is a critical process, as therapeutic effects of Se can be lost if the dose becomes high, this is further influenced by on other factors like Se species and bioavailability/bioaccessibility.