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Selenium levels, selenoenzyme activities and oxidant/antioxidant parameters in H1N1-infected children
Pınar Erkekoğlu1, Ali Aşçı, Mehmet Ceyhan
1Department of Toxicology, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey. bgiray@hacettepe.edu.tr.
Insights
Selenium deficiency impairs antioxidant defenses in children with H1N1 influenza. This study highlights selenium
Area of Science:
- Biochemistry
- Nutrition
- Virology
Background:
- Selenium (Se) is vital for antioxidant defense, functioning through selenoproteins like glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs).
- H1N1 influenza caused significant mortality and morbidity, particularly in the context of potential selenium deficiency.
- Oxidative stress plays a role in viral pathogenesis and disease severity.
Purpose of the Study:
- To investigate selenium levels, selenoenzyme activities, and other redox parameters in children infected with H1N1 influenza.
- To determine the impact of H1N1 infection on the body's antioxidant status.
- To elucidate the role of selenium in H1N1 infection and its associated oxidative stress.
Main Methods:
- Measured plasma and erythrocyte selenium levels.
- Assessed activities of selenoenzymes (GPx1, GPx3, TrxR) and other antioxidant enzymes (CAT, SOD, GST).
- Quantified levels of glutathione (GSH) and markers of lipid peroxidation in H1N1-infected children and a control group.
Main Results:
- H1N1-infected children showed decreased plasma and erythrocyte selenium levels and reduced activities of GPx1, GPx3, and TrxR.
- Significant reductions in catalase, superoxide dismutase, and glutathione S-transferase activities were observed.
- Increased lipid peroxidation and decreased glutathione levels indicated heightened oxidative stress in infected children.
Conclusions:
- H1N1 influenza down-regulates both selenium-dependent and independent antioxidant systems.
- Selenium status is critical for managing oxidative stress during H1N1 infection.
- Adequate selenium levels may be important for mitigating H1N1-related morbidity and mortality.
Abstract:
Selenium (Se) is an essential trace element, and it shows its biological functions within low molecular Se compounds and Se-containing proteins, known as "selenoproteins". Glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs) are the most important selenoproteins functioning as antioxidant enzymes. These enzymes protect the body from the endogenous products of cellular metabolism that have been implicated in DNA damage, mutagenesis, and carcinogenesis. H1N1 virus is a subtype of the influenza A virus and was an endemic in humans in 2009 and 2010. Taking into account the high incidence of Se deficiency and the high mortality and morbidity rates in H1N1 infection, this study was designed to investigate the plasma and erythrocyte Se levels, selenoenzyme activities and other oxidant/antioxidant parameters in H1N1-infected children during the 2009-2010 pandemic. We observed a significant increase in C-reactive protein levels (245%) and marked decreases in both plasma and erythrocyte Se levels (11%, both) and in GPx1 (45%), GPx3 (16%) and TrxR (30%) activities in H1N1-infected children compared to the control group. In addition, significant decreases were observed in erythrocyte catalase (CAT) (38%), total superoxide dismutase (SOD) (42%) and glutathione S-transferase (GST) (19%) activities and in erythrocyte total glutathione (GSH) (18%) and plasma GSH (10%) concentrations, while marked increases were observed in plasma lipid peroxidation levels (27%). However, we did not find a significant difference in selenoprotein P (SePP) levels between the groups. Our findings show that Se-dependent and -independent blood redox systems are down-regulated in H1N1 influenza. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in infections, particularly in H1N1 influenza.
