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Plasmapheresis (PE) is an established form of therapeutic apheresis (TA). Purpose of this longitudinal prospective single center study was to investigate the effect of PE on albumin redox state (ARS), as infusion of commercial albumin during PE may alter albumin oxidation which has an impact on its functional properties and oxidative stress level. 43 subjects with autoimmune-mediated neurological disorders were included. 20 subjects in the experimental group received five treatments of PE. 13 subjects received five treatments of immunoadsorption and 10 subjects received no TA as controls. ARS was determined before and after TA and 12 days after the last TA by fractionating it into human mercaptalbumin (HMA), human non-mercaptalbumin 1 (HNA-1), and human non-mercaptalbumin 2 (HNA-2) by high-performance liquid chromatography. Irreversibly oxidised HNA-2 increased over the course of five PE treatments from 2.8% (IQR 1.3-3.7%) to 13.6% (IQR 10.9-15.9) (P < 0.01) and remained elevated 12 days after the last PE procedure (7.7% IQR 7.1-10.5, P < 0.05). The study showed for the first time that PE exerts a severe and long-lasting alteration on ARS indicating a new adverse effect of PE, that may influence oxidative stress level., (© 2022. The Author(s).)

Purpose: Numerous studies suggest that reactive oxygen species play a crucial role in the development of glaucoma. Since glaucoma patients exhibit posterior vitreous detachment earlier than controls, it has been suggested that reactive oxygen species-increased in glaucoma-also affect the vitreous. In the present study we evaluated the influence of open-angle glaucoma oxidative stress on the redox state of vitreous albumin., Methods: Albumin redox states of the vitreous and plasma were evaluated in 22 subjects-11 open-angle glaucoma patients and 11 controls-matched for age, gender, and vitreous state. According to the redox state of cysteine-34, albumin can be separated into: human mercaptalbumin (the thiol form), human nonmercaptalbumin1 (a reversible modification due to mild oxidation), and human nonmercaptalbumin2 (an irreversible modification due to severe oxidation)., Results: Albumin of both, the open-angle glaucoma group and the control group, was more oxidized in the vitreous compared to plasma. Furthermore, significantly higher human nonmercaptalbumin1 fractions were found in the vitreous of open-angle glaucoma patients compared to controls. No significant differences were found in the plasma albumin fractions between the groups., Conclusion: Our results support the hypothesis that oxidative stress plays a crucial role in open-angle glaucoma and that reactive oxygen species in glaucomatous eyes may also affect the vitreous.

Oxidative stress occurs when free radicals and other reactive species overwhelm the availability of antioxidants. Reactive oxygen species (ROS), reactive nitrogen species, and their counterpart antioxidant agents are essential for physiological signaling and host defense, as well as for the evolution and persistence of inflammation. When their normal steady state is disturbed, imbalances between oxidants and antioxidants may provoke pathological reactions causing a range of nonrespiratory and respiratory diseases, particularly chronic obstructive pulmonary disease (COPD). In the respiratory system, ROS may be either exogenous from more or less inhalative gaseous or particulate agents such as air pollutants, cigarette smoke, ambient high-altitude hypoxia, and some occupational dusts, or endogenously generated in the context of defense mechanisms against such infectious pathogens as bacteria, viruses, or fungi. ROS may also damage body tissues depending on the amount and duration of exposure and may further act as triggers for enzymatically generated ROS released from respiratory, immune, and inflammatory cells. This paper focuses on the general relevance of free radicals for the development and progression of both COPD and pulmonary emphysema as well as novel perspectives on therapeutic options. Unfortunately, current treatment options do not suffice to prevent chronic airway inflammation and are not yet able to substantially alter the course of COPD. Effective therapeutic antioxidant measures are urgently needed to control and mitigate local as well as systemic oxygen bursts in COPD and other respiratory diseases. In addition to current therapeutic prospects and aspects of genomic medicine, trending research topics in COPD are presented.

Background & Aims: Impaired binding function of albumin has been demonstrated in end-stage liver disease. This and other functional disturbances of albumin may be related to oxidative stress which is believed to play an important role in the pathogenesis of liver failure as well as sepsis. The aim of the present study was to relate oxidative modification of albumin to loss of albumin binding function in advanced chronic liver failure and in sepsis., Methods: Patients with decompensated cirrhosis or sepsis and healthy controls were investigated. Three fractions of albumin were separated by chromatography according to the redox state of cysteine-34: non-oxidized human mercaptalbumin, reversibly oxidized human non-mercaptalbumin-1, and irreversibly oxidized human non-mercaptalbumin-2 (HNA2). Binding properties of albumin site II were measured using dansylsarcosine as a ligand., Results: Both in cirrhotic and septic patients, fractions of oxidized albumin were increased and binding capacity for dansylsarcosine was decreased. Mass spectroscopy confirmed specific oxidation of cysteine-34. In cirrhotic patients, dansylsarcosine binding correlated strongly with liver function parameters and moderately with HNA2. Baseline levels of HNA2 accurately predicted 30-day and 90-day survival in cirrhotic patients and this was confirmed in an external validation cohort., Conclusions: Our results suggest that oxidative damage impairs binding properties of albumin. In advanced liver disease, reduced binding capacity of albumin site II is mainly related to impaired liver function. The plasma level of HNA2 is closely related to survival and may represent a novel biomarker for liver failure., (Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)

Purpose: To investigate the redox state of human serum albumin concerning cysteine-34 as a possible systemic redox marker in patients with different eye diseases with and without complications and with consideration of possible effects of age., Methods: Cataract (CAT), glaucoma, age-related macular degeneration (AMD), diabetes mellitus (DM), diabetic retinopathy and hypertension were the pathologies investigated. Albumin redox state concerning cysteine-34 was measured by high-performance liquid chromatography with fluorescence detection. The separation gives three fractions: the fully reduced form containing a thiol group, the disulphide form and a higher oxidized form. Statistical analysis was done by Student's t-test, analysis of variance and stepwise regression analysis., Results: Albumin as a systemic marker for oxidative stress was shifted to a more oxidized state by DM. An even stronger shift to the oxidized form was observed in patients with proliferative diabetic retinopathy. Notably, these effects were independent from age. In contrast, CAT and AMD had no influence on serum albumin redox state., Conclusion: Serum albumin is not shifted to more oxidized forms by localized oxidative stress, but it is in systemic diseases like DM., (© 2010 The Authors. Journal compilation © 2010 Acta Ophthalmol.)

Oxidative stress is believed to play an important role in acute-on-chronic liver failure (AoCLF). Albumin, an important transport vehicle, was found to be severely oxidized in AoCLF patients. Extracorporeal liver support systems may exert beneficial effects in AoCLF via removal of albumin-bound toxins. At present, two systems are commercially available, the molecular adsorbents recirculating system (MARS) and fractionated plasma separation, adsorption and dialysis (FPAD, also known as Prometheus). The aim of this study was to compare the effect of MARS and Prometheus treatments on the redox state of human serum albumin. Eight patients with AoCLF underwent alternating treatments with either MARS or Prometheus in a randomized cross-over design. Sixteen treatments (eight MARS and eight Prometheus) were available for analysis. The fraction of human mercaptalbumin (HMA), human nonmercaptalbumin-1 (HNA1), and human nonmercaptalbumin-2 (HNA2) were measured before and after single MARS and Prometheus treatments and during follow-up. In AoCLF patients the oxidized fractions of albumin, HNA1, and HNA2 were markedly increased. Both MARS and Prometheus treatments resulted in a shift of HNA1 to HMA, while HNA2 was not significantly affected. This shift in albumin fractions was transient and disappeared within 24 h after treatment. There were no significant differences between MARS and Prometheus treatments with respect to the redox state of albumin. Both MARS and Prometheus treatments lead to transient improvements of the redox state of albumin, which could be beneficial in the treatment of AoCLF.

Purpose: To assess the effects of different exercise intensities and antioxidant supplementation on plasma protein modification., Methods: Trained men (n = 41) from a homogenous population were randomly assigned to perform cycle ergometer exercise either at 70% or 80% of individual .VO2max. Each intensity group was randomly assigned to receive either juice powder concentrate (JPC 70%, n = 11; JPC 80%, n = 10) or placebo (Plac 70%, n = 10; Plac 80%, n = 10) capsules for 28 wk. Four controlled exercise bouts and blood collections were conducted at baseline and study weeks 4, 16, and 28. Blood samples were drawn before (BE), immediately after (IE), and 30 min (30M) and 30 h (30H) postexercise. These samples were analyzed to estimate concentrations of carbonyl groups on plasma proteins (CP) and the redox state of human serum albumin (HSA)., Results: In the Plac group, CP concentrations increased at 80% of .VO2max IE and 30M, returning to preexercise concentrations by 30H (P < 0.05). At both 16 and 28 wk, the Plac groups had significantly higher BE and 30H CP concentrations than the JPC groups (P < 0.05). The reduced fraction of HSA, human mercaptalbumin (HMA), decreased at all four exercise tests at both exercise intensities IE and 30M, returning to preexercise values by 30H (P < 0.05). Supplementation had no influence on HSA., Conclusions: These results indicate that CP concentrations increase with 80% .VO2max intensity. The JPC group had lower baseline CP levels after 16 and 28 wk and no exercise-induced CP increase. HSA is reversibly shifted to a more oxidized state by recent intense exercise.

The question arises as to whether oxidative stress has a primary role in neurodegeneration or is a secondary end-stage epiphenomenon. The aim of the present study was to determine oxidative stress parameters like malondialdehyde (MDA), carbonyl proteins (CP) and Albumin-disulphide (Alb-SSR) and relate these parameters to the immune parameter neopterin, folic acid and vitamin B12 as vitamins and homocysteine in patients with neuro-degenerative diseases (NDD), namely mild cognitive impairment (MCI) and Alzheimer's disease (AD) compared to an aged matched control group. MDA, CP and Alb-SSR were significantly increased in the NDD group compared to controls, but not vitamin B12, folic acid and neopterin. Significant correlations were found between CP and Alb-SSR, CP and MDA and between MDA and Alb-SSR including patients with NDD and the control group. These results support the hypothesis that oxidative damage to lipids and proteins is an important early event in the pathogenesis of neurodegenerative diseases.

The purpose of this study was to investigate the effect of single bouts of exercise at three different intensities on the redox state of human serum albumin (HSA) and on carbonyl groups on protein (CP) concentrations in plasma. Trained men [n = 44, maximal oxygen consumption (Vo(2max)): 55 +/- 5 ml.kg(-1).min(-1), nonsmokers, 34 +/- 5 years of age] from a homogenous population, volunteers from a police special forces unit, were randomly assigned to perform on a cycle ergometer either at 70% (n = 14), 75% (n = 14), or 80% (n = 16) of Vo(2max) for 40 min. Blood was collected before exercise, immediately after the exercise test (IE), and 30 min after each test (30M) and 30 h after each test (30H). The reduced fraction of HSA, human mercaptalbumin (HMA), decreased at all three exercise intensities IE and 30M, returning to preexercise values by 30H (P < 0.05). HMA was primarily oxidized to its reversible fraction human nonmercaptalbumin 1 (HNA1). CP concentrations increased at 75% of Vo(2max) IE and 30M with a tendency (P < 0.1) and at 80% Vo(2max) IE and 30M significantly, returning to preexercise concentrations by 30H (P < 0.01). These results indicate that the HSA redox system in plasma is activated after a single bout of cycle ergometer exercise at 70% Vo(2max) and 40 min duration. The extent of the HSA modification increased with exercise intensity. Oxidative protein damage, as indicated by CP, was only significantly increased at 80% Vo(2max) intensity in this homogenous cohort of trained men.

Phytonutrients from plant foods provide numerous antioxidants. We hypothesized that supplementation for 28 wk with a commercially available encapsulated juice powder concentrate (JPC) could influence indicators of oxidative stress, immunity, and illness. Trained men (n = 41; 34 +/- 5 y; maximum oxygen uptake = 55 +/- 7 mL x kg(-1) x min(-1)) from a homogenous police Special Forces unit were randomly assigned in a double blind manner to either JPC (n = 21) or placebo (n = 20). We used multiple 7-d food records to assess dietary intake and found inadequate mean daily fruit and vegetable consumption (3.2 +/- 1.2 servings). The group physician documented all duty days lost due to illness. We collected plasma at baseline and study wk 4, 8, 16, and 28 for analysis of carbonyl groups on protein (CP) and TNFalpha. Over the 28-wk investigation, CP was lower in the JPC group, with both a treatment and a time x treatment interaction (P < 0.05). Concentrations of both CP and TNFalpha at 16 and 28 wk were lower in the JPC than in the placebo group (P < 0.001). TNFalpha increased during the first 8 wk followed by a decrease in both groups for the following 20 wk (P < 0.001). Over the final 20 wk of the study, the placebo group tended to have more days of illness than the JPC group (P = 0.068). These data suggest beneficial JPC effects with regard to reduction of duty days lost due to illness and reduction of CP and TNFalpha concentrations in this group of trained men over 28 wk.

Despite the health-promoting effects of physical activity, exercise enhances the formation of free radicals and other reactive species in animals and humans. Numerous techniques have been established to investigate the diverse modifications of biomolecules by oxidative stress. These analytical procedures include different methods, ranging from simple photometric assays to a combination of chromatographic methods with mass spectrometry. We summarize briefly those analytical techniques of oxidative damage to biomolecules that have been applied to the investigation of oxidative stress during exercise.

Pteridine derivatives which have a widespread occurrence in nature have been investigated upon their interactions with free radicals and free radical mediated reactions utilizing a number of different experimental systems. Searching for biological functions, which are still unknown for the majority of pteridine compounds, the effect of pteridines in systems like luminol-induced chemiluminescence, enzyme activity, DNA photodamage, EPR experiments or radical induced injury--just to name a few--have been investigated. The general view during the initial phase of investigations on this special field was, that reduced pterins, i. e., tetra- as well as dihydropterins, generally act as radical scavengers, while aromatic pterins, if not inactive, exert radical promoting activity. Meanwhile the data available provide a more complex view: pteridines of all oxidation states have been shown to act anti- or prooxidatively, depending on the special conditions of the experiment. The reason is that reduced pterins, besides of being scavengers of free radicals, also are strongly reducing agents and therefore, in the presence of transition metal ions promote Fenton chemistry. Aromatic pterins have been described as inhibitors or substrates of enzymes involved--in vitro and in vivo--in free radical generation. Together with the unknown local concentrations of, e.g., neopterin and dihydroneopterin occurring in vivo, these reasons make it impossible to unequivocally predict a physiological net effect of pterins of different oxidation states concerning free radical mediated reactions in real biological systems.

Binding and transport of a number of endogenous and exogenous compounds is an important function of the main plasma protein, albumin. In vivo and in vitro, albumin may be oxidatively modified in different ways with different agents at different sites. These modifications have various consequences on the physiological functions of albumin. Diabetes mellitus, liver diseases and nephropathy are just a few examples of disorders in which oxidative stress is involved and altered albumin functions have been described. This review is focussed on the consequences of oxidative modification on the binding properties of albumin. These range from no effect to decreased or increased binding affinities depending on the ligand under investigation and the type of modification. Indicators for modification include glycosylation, disulphide formation or the content of carbonyl groups. The redox state of albumin can affect the binding properties in several ways, including altered conformation and consequently altered affinities at binding sites and altered binding when the binding reaction itself is redox sensitive. The physiological or pathophysiological concentrations of different oxidatively modified albumin molecules vary over a wide range and are crucial in assessing the clinical relevance of altered ligand binding properties of a particularly modified albumin species in various disease conditions.British Journal of Pharmacology (2007) 151, 580–590; doi:10.1038/sj.bjp.0707251; published online 30 April 2007 [ABSTRACT FROM AUTHOR]