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Indoxyl Sulfate Induces Oxidative Changes in Plasma and Hemolysate
Anna Pieniazek1, Michal Kopera1, Lukasz Gwozdzinski2
1Department of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland.
Molecules (Basel, Switzerland)
|June 24, 2022
Summary
High levels of indoxyl sulfate (IS), a uremic toxin, cause oxidative damage to red blood cells and plasma components. This damage may accelerate chronic kidney disease (CKD) progression and reduce erythrocyte lifespan.
Area of Science:
- Nephrology
- Biochemistry
- Oxidative Stress Research
Background:
- Chronic kidney disease (CKD) is characterized by the accumulation of toxic metabolic products.
- Indoxyl sulfate (IS) is a protein-bound uremic toxin implicated in CKD pathogenesis.
- IS is known to induce oxidative stress.
Purpose of the Study:
- To investigate the impact of indoxyl sulfate (IS) on oxidative stress markers in plasma and erythrocytes.
- To determine if IS contributes to oxidative damage in components relevant to CKD progression.
Main Methods:
- In vitro evaluation of IS effects on plasma and hemolysate.
- Measurement of oxidative stress parameters, including total antioxidant capacity, catalase, and superoxide dismutase activity.
Main Results:
- Indoxyl sulfate (IS) induced significant oxidative damage to both plasma and hemolysate components.
- A decrease in total antioxidant capacity and altered enzyme activity (catalase, superoxide dismutase) were observed.
- Oxidative stress parameters showed greater changes in hemolysate compared to plasma following IS treatment.
Conclusions:
- Indoxyl sulfate (IS) directly causes oxidative damage to erythrocytes and plasma.
- Increased IS concentrations in CKD patients may impair erythrocyte function and survival.
- These findings suggest IS contributes to CKD progression through oxidative mechanisms affecting red blood cells.

