In diabetes mellitus, chronic hyperglycemia drives excessive formation of reactive oxygen species (ROS), establishing a sustained state of oxidative stress biomarker imbalance that contributes to erythrocyte dysfunction and progressive anemia. In advanced renal disease, the hemodialysis environment introduces additional biochemical stressors, amplifying systemic redox disruption and accelerating molecular injury within circulating blood components. Within this context, a clinical cohort consisting of patients with diabetes undergoing hemodialysis, patients with diabetes with preserved renal function, and healthy controls demonstrates distinct biochemical and hematological profiles reflecting graded oxidative injury. Assessment of hemoglobin oxidative modification reveals increased formation of methaemoglobin (Met-Hb), hemichrome accumulation, and measurable hemoglobin conformational changes, indicating structural instability of oxygen-carrying proteins. Concurrent evaluation of plasma demonstrates altered plasma oxidative biomarkers, including significant modulation of ferric reducing ability of plasma (FRAP) as a compensatory antioxidant response, alongside variations in protein carbonyl content (PCO) reflecting protein oxidation burden. Furthermore, biochemical profiling indicates dysregulated metabolic and renal parameters characterized by elevated blood urea nitrogen (BUN), creatinine, and uric acid, together with reduced albumin concentrations, highlighting systemic metabolic impairment. Correlation analyses strengthen mechanistic interpretation, demonstrating strong inverse relationships between protein carbonyl content (PCO) and oxy-hemoglobin stability (r = −0.88), as well as spectral hemoglobin signatures at 340 nm, 420 nm, and 577 nm, suggesting profound erythrocyte oxidative injury and disruption of hemoglobin structural integrity. In parallel, positive correlations between PCO and altered hemoglobin absorbance at 275 nm and 560 nm further confirm oxidative protein remodeling. Collectively, these findings establish a coherent mechanistic axis linking diabetes mellitus oxidative stress, chronic kidney disease oxidative stress, and hemodialysis-associated oxidative stress to progressive hemoglobin dysfunction. Importantly, FRAP antioxidant capacity emerges as a protective redox indicator, whereas protein carbonyl content (PCO) and hemoglobin derivatives function as sensitive negative biomarkers of oxidative injury, reinforcing their value in clinical biochemistry oxidative stress assessment and biomarker-based renal disease monitoring.
Reference:
Ansarihadipour H, Dorostkar. Comparison of plasma oxidative biomarkers and conformational modifications of hemoglobin in hemodialysis diabetics. Iran Red Crescent Medical Journal. 2014;16(11):e22045. i
