Ischemia-modified albumin and advanced oxidation protein products as potential biomarkers of protein oxidation in Alzheimer's disease.

BACKGROUND: The aim of the present study was to determine the systemic levels of oxidative stress markers, such as ischemia-modified albumin (IMA), advanced oxidation protein products (AOPP), ferric reducing antioxidant power (FRAP) and the prooxidant-antioxidant balance (PAB), to clarify protein redox homeostasis in patients with Alzheimer's disease, and to compare them with mentally healthy persons of the same age. METHODS: A total of 38 patients with Alzheimer's disease (AD) and 34 sex- and age-matched mentally healthy control subjects were included in this study. RESULTS: The patients had significantly higher AOPP, IMA and PAB in the patient group than in the control group (P = 0.004, P = 0.001, P = 0.007, respectively). The FRAP was significantly lower in the patients with AD than in the control subjects (P = 0.002), and according to the receiver operating characteristic curves, the IMA and AOPP areas are below the 0.700 receiver operating characteristic curve line (area under the curve 0.817 and 0.730, respectively; 95% CI 0.709-0.898 and 0.612-0.828, respectively). CONCLUSIONS: Increased IMA, AOPP and PAB, and decreased FRAP are likely to be results of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive oxygen species in AD. The IMA could be used for the better evaluation of clinical status, as well as the independent characteristic symptoms of AD, for the purposes of routine clinical laboratory analysis.

Total antioxidant status and markers of oxidative stress in subjects with normal or impaired glucose regulation (IFG, IGT) in diabetic patients.

BACKGROUND: We investigated the ischemia-modified albumin (IMA), advanced oxidation protein products (AOPPs), prooxidants-antioxidants balance (PAB), and ferric reducing antioxidant power (FRAP) concentrations in patients with impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and diabetes mellitus (DM) and compared the results to those of normoglycemic individuals at baseline and 2 hours after glucose loading. METHODS: An oral glucose tolerance test was performed on age-matched subjects (n = 110) with a body mass index (BMI) < 27 kg/m(2). Subjects were categorized as normoglycemic (n = 35), IFG (n = 25), IGT (n = 30) and DM (n = 20) according to the WHO criteria. The IMA, AOPP, PAB, FRAP concentrations were determined by colorimetric methods. RESULTS: At baseline, the AOPP concentrations were significantly higher in subjects with IFG and DM compared to normoglycemic subjects (p < 0.01 for all cases). The IFG, IGT and DM patients had a significantly higher IMA at baseline when compared with the normoglycemic individuals (p < 0.001 for all cases). The IMA in IFG subjects was significantly elevated (p < 0.05), while in DM patients, the IMA was significantly decreased (p < 0.001) after glucose loading with respect to baseline concentrations. Following glucose loading, the PAB was significantly decreased from baseline concentrations in normoglycemic individuals (p < 0.001) and in the IFG (p < 0.001) and IGT (p < 0.001) patients. CONCLUSION: In subjects with impaired glucose metabolism, the hyperglycemia is associated with increased IMA, AOPP and PAB concentrations. Increased IMA in subjects with IFG and decreased FRAP concentrations in subjects with IGT after glucose loading suggests that an increase in glucose concentrations can lead to tissue damage by increasing oxidative stress.