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Kidney Ischemia-Reperfusion Decreases Hydrogen Sulfide and Increases Oxidative Stress in the Heart

Charith U B Wijerathne1,2, Susara Madduma Hewage1,3, Yaw L Siow1,3,4

  • 1St. Boniface Hospital Research Centre, Winnipeg, MB R2H 2A6, Canada.

Biomolecules
|November 20, 2020
PubMed

Insights

Acute kidney injury (AKI) impairs heart health by reducing protective hydrogen sulfide (H2S) production and increasing oxidative stress. This study reveals AKI disrupts the CSE enzyme, leading to cardiac damage and higher cardiovascular disease risk.

Area of Science:

  • Cardiovascular Science
  • Nephrology
  • Biochemistry

Background:

  • Acute kidney injury (AKI) is linked to increased cardiovascular disease risk.
  • The mechanisms of AKI-induced heart injury remain unclear.
  • Hydrogen sulfide (H2S) at physiological levels offers cardiovascular protection via redox balance and vasodilation.
  • Cystathionine gamma-lyase (CSE) is crucial for cardiac H2S generation.

Purpose of the Study:

  • To investigate the impact of AKI on cardiac H2S production.
  • To assess oxidative stress markers in the heart following AKI.
  • To explore the role of CSE and Nrf2 pathways in AKI-related cardiac dysfunction.

Main Methods:

  • AKI was induced using kidney ischemia-reperfusion in Sprague-Dawley rats.
  • Plasma creatinine and blood urea nitrogen were measured to confirm AKI.
  • Cardiac and plasma oxidative stress markers (lipid peroxidation, glutathione) were analyzed.
  • CSE expression, H2S levels, nuclear Nrf2, and inflammatory cytokines (IL-6, TNF-α) were quantified in heart tissue.

Main Results:

  • AKI induction led to elevated plasma creatinine and blood urea nitrogen.
  • Significant increases in lipid peroxidation and decreases in glutathione were observed systemically and cardially.
  • Kidney ischemia-reperfusion resulted in reduced cardiac CSE expression and H2S production.
  • Nuclear Nrf2 levels decreased, while cardiac IL-6 and TNF-α expression increased post-AKI.

Conclusions:

  • AKI significantly down-regulates CSE-mediated H2S production in the heart.
  • AKI exacerbates cardiac oxidative stress and inflammation.
  • Reduced H2S and increased oxidative stress in the heart following AKI may contribute to cardiovascular complications.

Keywords:
acute kidney injuryglutathionehearthydrogen sulfideoxidative stress

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