Alterations in Red Blood Cells and Plasma Properties after Acute Single Bout of Exercise

The aim of this study was to investigate alterations in haemoglobin conformation and parameters related to oxidative stress in whole erythrocytes, membranes, and plasma after a single bout of exercise in a group of young untrained men. Venous blood samples from eleven healthy young untrained males (age = 22 ± 2 years, BMI = 23 ± 2.5 kg/m2) were taken from the antecubital vein before an incremental cycling exercise test, immediately after exercise, and 1 hour after exercise. Individual heart rate response to this exercise was 195 ± 12 beats/min and the maximum wattage was 292 ± 27 W. Immediately after exercise, significant increase in standard parameters (haemoglobin, haematocrit, lactate levels, and plasma volume) of blood was observed as well as plasma antioxidant capacity one hour after exercise. Reversible conformational changes in haemoglobin, measured using a maleimide spin label, were found immediately following exercise. The concentration of ascorbic acid inside erythrocytes significantly decreased after exercise. A significant decline in membrane thiols was observed one hour after exercise, but simultaneously an increase in plasma thiols immediately after and 1 h after exercise was also observed. This study shows that a single bout of exercise can lead to mobilization of defensive antioxidant systems in blood against oxidative stress in young untrained men

Multimarker approach in discriminating patients with symptomatic and asymptomatic atherosclerotic carotid artery stenosis

BACKGROUND AND PURPOSE: Several circulating biomarkers have been implicated in carotid atherosclerotic plaque rupture and thrombosis; however, their clinical utility remains unknown. The aim of this study was to determine the role of a large biomarker panel in the discrimination of symptomatic (S) vs. asymptomatic (A/S) subjects in a contemporary population with carotid artery stenosis (CS). METHODS: Prospective sampling of circulating cytokines and blood lipids was performed in 300 unselected, consecutive patients with ≥50% CS, as assessed by duplex ultrasound (age 47-83 years; 110 with A/S and 190 with S) who were referred for potential CS revascularization. RESULTS: CS severity and pharmacotherapy did not differ between the A/S and S patients. The median values of total cholesterol, low-density lipoprotein cholesterol, and lipoprotein(a) did not differ, but high-density lipoprotein (HDL) cholesterol was significantly higher (p<0.001) and triglycerides were lower (p=0.03) in the A/S-CS group than in the S-CS group. Interleukin-6 (IL-6) and high-sensitivity C-reactive protein were higher (p=0.04 and p=0.07, respectively) in the S-CS group. Circulating visfatin, soluble CD 40 receptor ligand, soluble vascular cell adhesion molecule, leptin, adiponectin, IL-1β, IL-8, IL-18, monocyte chemoattractant protein-1, myeloperoxidase, matrix metalloproteinases-8, -9, and -10, and fibrinogen were similar, but tissue inhibitor of matrix metalloproteinases-1 (TIMP) was reduced in S-CS compared to A/S-CS (p=0.02). Nevertheless, incorporation of TIMP and IL-6 did not improve the HDL-cholesterol receiver operating characteristics for S-CS status prediction. S-CS status was unrelated to angiographic stenosis severity or plaque burden, as assessed by intravascular ultrasound (p=0.16 and p=0.67, respectively). Multivariate logistic regression analysis revealed low HDL-cholesterol to be the only independent predictor of CS symptoms, with an odds ratio of 1.81 (95% confidence interval=1.15-2.84, p=0.01) for HDL <1.00 mmol/L (first quartile) vs. >1.37 (third quartile). In S-CS, osteoprotegerin and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) were elevated in those with recent vs. remote symptoms (p=0.01 and p=0.02, respectively). CONCLUSIONS: In an all-comer CS population on contemporary pharmacotherapy, low HDL-cholesterol (but not other previously implicated or several novel circulating biomarkers) is an independent predictor of S-CS status. In addition, an increase in circulating osteoprotegerin and Lp-PLA(2) may transiently indicate S transformation of the carotid atherosclerotic plaque

EL virus del HIV-1 de pacientes de May Harbor de diferentes subtipos filogenéticos: las implicancias para la evolución de la pandemia HIV/SIDA

Las variantes virales aisladas de pacientes infectados con HIV a través del mundo comparten una diversidad notable, especialmente en la glicoproteína de envoltura gp120. Los estudios filogenéticos han agrupado a los aislamientos de HIV-1 en ocho subtipos (A-H). No obstante, aún dentro de una sola persona infectada, el HIV está presente como unas «cuasi-especies,» o un enjambre de variantes estrechamente conexas. Esta diversidad genética, que en el caso del HIV-1 se acumula a una tasa de aproximadamente una sustitución de nucleótido por genoma por ciclo de replicación, da al virus una flexibilidad enorme para responder a un amplio conjunto de presiones de selección in vivo. Como una consecuencia, la droga-resistencia y las mutantes inmunológica se generan rápidamente en personas infectadas mediante todas las etapas de infección. Sobre una escala global, la pandemia del HIV se reconoce como consistiendo de muchas epidemias separadas, cada una con una geografía característica, poblaciones afectadas, y tipo predominante de cepa viral. Con unos estimados 15 millones de personas infectadas, la distribución geográfica de los subtipos virales está llegando a ser más dispersa, y estas demarcaciones son además confundidas por la evidencia creciente de infecciones mixtas.Facultad de Ciencias Veterinaria

EL virus del HIV-1 de pacientes de May Harbor de diferentes subtipos filogenéticos: las implicancias para la evolución de la pandemia HIV/SIDA

Las variantes virales aisladas de pacientes infectados con HIV a través del mundo comparten una diversidad notable, especialmente en la glicoproteína de envoltura gp120. Los estudios filogenéticos han agrupado a los aislamientos de HIV-1 en ocho subtipos (A-H). No obstante, aún dentro de una sola persona infectada, el HIV está presente como unas «cuasi-especies,» o un enjambre de variantes estrechamente conexas. Esta diversidad genética, que en el caso del HIV-1 se acumula a una tasa de aproximadamente una sustitución de nucleótido por genoma por ciclo de replicación, da al virus una flexibilidad enorme para responder a un amplio conjunto de presiones de selección in vivo. Como una consecuencia, la droga-resistencia y las mutantes inmunológica se generan rápidamente en personas infectadas mediante todas las etapas de infección. Sobre una escala global, la pandemia del HIV se reconoce como consistiendo de muchas epidemias separadas, cada una con una geografía característica, poblaciones afectadas, y tipo predominante de cepa viral. Con unos estimados 15 millones de personas infectadas, la distribución geográfica de los subtipos virales está llegando a ser más dispersa, y estas demarcaciones son además confundidas por la evidencia creciente de infecciones mixtas.Facultad de Ciencias Veterinaria

EL virus del HIV-1 de pacientes de May Harbor de diferentes subtipos filogenéticos: las implicancias para la evolución de la pandemia HIV/SIDA

Las variantes virales aisladas de pacientes infectados con HIV a través del mundo comparten una diversidad notable, especialmente en la glicoproteína de envoltura gp120. Los estudios filogenéticos han agrupado a los aislamientos de HIV-1 en ocho subtipos (A-H). No obstante, aún dentro de una sola persona infectada, el HIV está presente como unas «cuasi-especies,» o un enjambre de variantes estrechamente conexas. Esta diversidad genética, que en el caso del HIV-1 se acumula a una tasa de aproximadamente una sustitución de nucleótido por genoma por ciclo de replicación, da al virus una flexibilidad enorme para responder a un amplio conjunto de presiones de selección in vivo. Como una consecuencia, la droga-resistencia y las mutantes inmunológica se generan rápidamente en personas infectadas mediante todas las etapas de infección. Sobre una escala global, la pandemia del HIV se reconoce como consistiendo de muchas epidemias separadas, cada una con una geografía característica, poblaciones afectadas, y tipo predominante de cepa viral. Con unos estimados 15 millones de personas infectadas, la distribución geográfica de los subtipos virales está llegando a ser más dispersa, y estas demarcaciones son además confundidas por la evidencia creciente de infecciones mixtas.Facultad de Ciencias Veterinaria

The effect of microhydration on ionization energies of thymine

A combined theoretical and experimental study of the effect of microhydration on ionization energies (IEs) of thymine is presented. The experimental IEs are derived from photoionization efficiency curves recorded using tunable synchrotron VUV radiation. The onsets of the PIE curves are 8.85+-0.05, 8.60+-0.05, 8.55+-0.05, and 8.40+-0.05 eV for thymine, thymine mono-, di-, and tri-hydrates, respectively. The computed (EOM-IP-CCSD/cc-pVTZ) AIEs are 8.90, 8.51, 8.52, and 8.35 eV for thymine and the lowest isomers of thymine mono-, di-, and tri-hydrates. Due to large structural relaxation, the Franck-Condon factors for the 0&lt;-- 0 transitions are very small shifting the apparent PIE onsets to higher energies. Microsolvation strongly affects IEs of thymine -- addition of each water molecule reduces the first vertical IE by 0.10-0.15 eV. The adiabatic IE decreases even more (up to 0.4 eV). The magnitude of the effect varies for different ionized states and for different isomers. For the ionized states that are localized on thymine the dominant contribution to the IE reduction is the electrostatic interaction between the delocalized positive charge on thymine and the dipole moment of the water molecule

Reactive Oxygen Species and Their Involvement in Red Blood Cell Damage in Chronic Kidney Disease

Reactive oxygen species (ROS) released in cells are signaling molecules but can also modify signaling proteins. Red blood cells perform a major role in maintaining the balance of the redox in the blood. The main cytosolic protein of RBC is hemoglobin (Hb), which accounts for 95-97%. Most other proteins are involved in protecting the blood cell from oxidative stress. Hemoglobin is a major factor in initiating oxidative stress within the erythrocyte. RBCs can also be damaged by exogenous oxidants. Hb autoxidation leads to the generation of a superoxide radical, of which the catalyzed or spontaneous dismutation produces hydrogen peroxide. Both oxidants induce hemichrome formation, heme degradation, and release of free iron which is a catalyst for free radical reactions. To maintain the redox balance, appropriate antioxidants are present in the cytosol, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and peroxiredoxin 2 (PRDX2), as well as low molecular weight antioxidants: glutathione, ascorbic acid, lipoic acid, α-tocopherol, β-carotene, and others. Redox imbalance leads to oxidative stress and may be associated with overproduction of ROS and/or insufficient capacity of the antioxidant system. Oxidative stress performs a key role in CKD as evidenced by the high level of markers associated with oxidative damage to proteins, lipids, and DNA in vivo. In addition to the overproduction of ROS, a reduced antioxidant capacity is observed, associated with a decrease in the activity of SOD, GPx, PRDX2, and low molecular weight antioxidants. In addition, hemodialysis is accompanied by oxidative stress in which low-biocompatibility dialysis membranes activate phagocytic cells, especially neutrophils and monocytes, leading to a respiratory burst. This review shows the production of ROS under normal conditions and CKD and its impact on disease progression. Oxidative damage to red blood cells (RBCs) in CKD and their contribution to cardiovascular disease are also discussed

Acrolein Induces Changes in Cell Membrane and Cytosol Proteins of Erythrocytes

High concentrations of acrolein (2-propenal) are found in polluted air and cigarette smoke, and may also be generated endogenously. Acrolein is also associated with the induction and progression of many diseases. The high reactivity of acrolein towards the thiol and amino groups of amino acids may cause damage to cell proteins. Acrolein may be responsible for the induction of oxidative stress in cells. We hypothesized that acrolein may contribute to the protein damage in erythrocytes, leading to the disruption of the structure of cell membranes. The lipid membrane fluidity, membrane cytoskeleton, and osmotic fragility were measured for erythrocytes incubated with acrolein for 24 h. The levels of thiol, amino, and carbonyl groups were determined in cell membrane and cytosol proteins. The level of non-enzymatic antioxidant potential (NEAC) and TBARS was also measured. The obtained research results showed that the exposure of erythrocytes to acrolein causes changes in the cell membrane and cytosol proteins. Acrolein stiffens the cell membrane of erythrocytes and increases their osmotic sensitivity. Moreover, it has been shown that erythrocytes treated with acrolein significantly reduce the non-enzymatic antioxidant potential of the cytosol compared to the control