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Abstract: FR-PO1081

Uremic Toxin Indoxyl Sulfate Impairs Hydrogen Sulfide Formation in Nephrectomy Rats

Session Information

Category: CKD (Non-Dialysis)

  • 2303 CKD (Non-Dialysis): Mechanisms


  • Lu, Chien-Lin, Fu Jen Catholic University, New Taipei, Taiwan

Hydrogen sulfide (H2S) has antioxidant properties but is reduced in CKD, making the cells more vulnerable to oxidative damage. The interaction between Indoxyl Sulfate (IS) and H2S in CKD needs further exploration.


Male Wistar rats had nephrectomy and received CH-223191, an AhR antagonist. Blood and urine samples were collected post-treatment for H2S level measurement. Kidney tissue was evaluated for H2S-producing enzyme and Sp1 protein activity, and reduced GSH and oxidized GSSG levels.


Administering CH-223191 to rats after nephrectomy prevented the harmful effects of IS on the kidneys. CH-223191 restored H2S levels, reduced IS accumulation, and reversed the changes in H2S-producing enzymes and the transcription factor Sp1 (Fig1). It also decreased oxidative stress and lipid peroxidation in the nephrectomy rats(Fig2). These findings indicate that CH-223191 protects against kidney damage by mitigating IS-induced effects, preserving H2S generation, and reducing oxidative stress.


Impaired H2S generation caused by IS renders the kidney susceptible to oxidative stress damage, representing one of the mechanisms underlying IS-mediated kidney function loss.