Increased oxidized form of human serum albumin in patients with diabetes mellitus

Suzuki, Eiji; Yasuda, Keigo; Takeda, Noriyuki; Sakata, Shigeki; Era, Seiichi; Kuwata, Kazuo; Sogami, Masaru; Miura, Kiyoshi

doi:10.1016/0168-8227(92)90140-m

Cited by 88 publications

(63 citation statements)

References 17 publications

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“…Overall, this reaction should involve 20 to 25% of albumin that is the amount of nonmercapto plus dimeric albumin in plasma. Even if in vitro studies furnish a solid chemical background to a participation of albumin into the antioxidant response in plasma, evidence that albumin oxidation takes place in vivo has never been reported, with the exception of scattered reports of partial albumin oxidation in ESRF (30) and diabetes that had been obtained with indirect techniques (31,32). Studies in patients with ESRF are of particular interest because they show the increase of nonmercaptoalbumin that should represent the product of reaction of free plasma thiols such as GSH and/or homocysteine with the sulfenic derivative of albumin.…”

Section: Discussionmentioning

confidence: 99%

“…Overall, the process of oxidation of albumin in FSGS seems substantially different from oxidation that is reported in patients with ESRF because, as already discussed, it mainly involves only the formation of an instable intermediate in this condition. According to the literature on the topic (31,32), the amount of sulfonic end product in patients with ESRF is approximately 5% of total albumin and is under the limit of sensitivity of the maleimide assay. Lack of observation of this peculiar structural modification on the basis of a direct spectroscopic approach in other cohorts of patients with primary and secondary glomerulonephritis with and without nephrotic syndrome and in young adults with ESRF suggests, therefore, a good degree of specificity for FSGS.…”

Section: Discussionmentioning

confidence: 99%

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Active Focal Segmental Glomerulosclerosis Is Associated with Massive Oxidation of Plasma Albumin

Musante¹,

Candiano²,

Petretto

et al. 2007

Journal of the American Society of Nephrology

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The basic mechanism for idiopathic FSGS still is obscure. Indirect evidence in humans and generation of FSGS by oxidants in experimental models suggest a role of free radicals. In vitro studies demonstrate a main role of plasma albumin as antioxidant, its modification representing a chemical marker of oxidative stress. With the use of complementary liquid chromatography electron spray ionization tandem mass spectrometry (LC-ESI-MS/MS) and biochemical methods, plasma albumin was characterized in 34 patients with FSGS; 18 had received a renal transplant, and 17 had IgM mesangial deposition. Patients with FSGS that was in remission or without recurrence after transplantation had normal plasma albumin, and the same occurred in patients with primary and secondary nephrites and with chronic renal failure. In contrast, patients with active FSGS or with posttransplantation recurrence had oxidized plasma albumin. This finding was based on the characterization of albumin Cys 34 with an mass-to-charge ratio of 511.71 in triple charge that was consistent with the formation of a cysteic acid carrying a sulfonic group (alb-SO 3 ؊ ). The exact mass of albumin was increased accordingly (؉48 Da) for incorporation of three oxygen radicals. Direct titration of the free sulfhydryl group 34 of plasma albumin and electrophoretic titration curves confirmed loss of free sulfhydryl group and formation of a fast-moving isoform in all cases with disease activity. This is the first demonstration of in vivo plasma albumin oxidation that was obtained with an adequate structural approach. Albumin oxidation seems to be specific for FSGS, suggesting some pathogenetic implications. Free radical involvement in FSGS may lead to specific therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Active Focal Segmental Glomerulosclerosis Is Associated with Massive Oxidation of Plasma Albumin

Musante¹,

Candiano²,

Petretto

et al. 2007

Journal of the American Society of Nephrology

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“…Recently, a progressive oxidative modification of albumin with increasing severity of liver failure has been reported (52). The fraction of oxidized albumin is also increased in diabetes mellitus (53), disorders of the temporomandibular joint (54), senile cataract (55), and invasive surgery (56). Furthermore, it has been shown that the fraction of oxidized albumin also increases with aging (26,35) and intense exercise (57).…”

Section: Implications In Pathologymentioning

confidence: 99%

Oxidation of the albumin thiol to sulfenic acid and its implications in the intravascular compartment

Turell

Carballal

Botti

et al. 2009

Braz J Med Biol Res

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Human serum albumin (HSA) is the most abundant protein in the intravascular compartment. It possesses a single thiol, Cys34, which constitutes ~8 0% of the total thiols in plasma. This thiol is able to scavenge plasma oxidants. A central intermediate in this potential antioxidant activity of human serum albumin is sulfenic acid (HSA-SOH). Work from our laboratories has demonstrated the formation of a relatively stable sulfenic acid in albumin through complementary spectrophotometric and mass spectrometric approaches. Recently, we have been able to obtain quantitative data that allowed us to measure the rate constants of sulfenic acid reactions with molecules of analytical and biological interest. Kinetic considerations led us to conclude that the most likely fate for sulfenic acid formed in the plasma environment is the reaction with low molecular weight thiols to form mixed disulfides, a reversible modification that is actually observed in ~2 5% of circulating albumin. Another possible fate for sulfenic acid is further oxidation to sulfinic and sulfonic acids. These irreversible modifications are also detected in the circulation. Oxidized forms of albumin are increased in different pathophysiological conditions and sulfenic acid lies in a mechanistic junction, relating oxidizing species to final thiol oxidation products.

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“…effective as an antioxidant) can vary (Era et al 1995); for example, in healthy young adults 76% is present in the reduced form, whereas in healthy elderly subjects this percentage is decreased to 46 (Era et al 1995). The redox state is also altered by cardiac surgery, diabetes, renal dysfunction and haemodialysis (Suzuki et al 1992;Hayakawa et al 1997;Soejima et al 2004;Terawaki et al 2004); thus, although it is not known whether there is a change in redox state in critically-ill populations, it is likely to be altered compared with that of healthy young males. Albumin is given to many critically-ill patients as an oncotic support and, although this treatment repletes plasma thiols (Quinlan et al 1998(Quinlan et al , 2004, most commercial sources of albumin have a decreased proportion of the thiol groups in the reduced form compared with that in the plasma of healthy adult males (Bar-Or et al 2005).…”

Section: Other Water-soluble Compounds With Antioxidant Activitymentioning

confidence: 99%

The biochemical basis of antioxidant therapy in critical illness

Eaton

2006

Proc. Nutr. Soc.

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During critical illness free radical production may increase as a result of, for example, sepsis or tissue trauma. In addition, because of a potential for increased losses, and the possibility of inadequate nutrition, the antioxidant defences of the body may become compromised. Thus, the delicate balance between free radicals and antioxidants may be disturbed. Various nutritional and pharmacological strategies to enhance antioxidant defences have been proposed, which aim either to maintain or enhance endogenous antioxidant stores or to provide alternative antioxidant agents. Trace elements and amino acids are particularly important, and their synergistic role in the maintenance of the body's antioxidant defence network will be discussed.

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Increased oxidized form of human serum albumin in patients with diabetes mellitus

Cited by 88 publications

References 17 publications

Active Focal Segmental Glomerulosclerosis Is Associated with Massive Oxidation of Plasma Albumin

Active Focal Segmental Glomerulosclerosis Is Associated with Massive Oxidation of Plasma Albumin

Oxidation of the albumin thiol to sulfenic acid and its implications in the intravascular compartment

The biochemical basis of antioxidant therapy in critical illness

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