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Updated: May 14, 2025

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Oxidative Stress, DNA Damage, Inflammation and Endothelial Dysfunction in Snakebite-Induced Acute Kidney Injury.

Lakshmi Aishwarya Pavuluri1, Aparna R Bitla2, Siva Kumar Vishnubotla1

  • 1Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, India.

Indian Journal of Nephrology
|May 12, 2025
PubMed
Summary

Snakebite-induced acute kidney injury (SAKI) involves significant oxidative stress, DNA damage, inflammation, and endothelial dysfunction. These findings highlight key mechanisms contributing to SAKI, paving the way for new diagnostic and therapeutic approaches.

Keywords:
8-OHdGDNA damageEndothelial dysfunctionInflammationOxidative stressSAKI

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Area of Science:

  • Nephrology
  • Toxicology
  • Molecular Biology

Background:

  • Snakebite-induced acute kidney injury (SAKI) is a critical health concern with poorly understood cellular and molecular underpinnings.
  • Limited research exists on the roles of oxidative stress, DNA damage, inflammation, and endothelial dysfunction in SAKI pathogenesis.
  • This study addresses this knowledge gap by investigating these specific mechanisms in SAKI patients.

Purpose of the Study:

  • To investigate the role of oxidative stress, oxidative DNA damage, inflammation, and endothelial dysfunction in snakebite-induced acute kidney injury (SAKI).
  • To identify key biomarkers associated with these pathophysiological processes in SAKI patients.

Main Methods:

  • Assessed biomarkers of oxidative stress, DNA damage, inflammation, and endothelial dysfunction in 30 SAKI patients and 30 healthy controls.
  • Measured malondialdehyde (MDA), protein carbonyl content (PCC), advanced glycation end products (AGEs), 8-hydroxy-2'-deoxyguanosine (8-OHdG), ferric reducing ability of plasma (FRAP), high-sensitivity C-reactive protein (hs-CRP), and nitric oxide (NO).

Main Results:

  • SAKI patients exhibited significantly elevated MDA, PCC, and 8-OHdG, indicating increased oxidative damage to lipids, proteins, and DNA.
  • Antioxidant capacity (FRAP) was significantly reduced in SAKI patients.
  • Inflammation (hs-CRP) and endothelial dysfunction (NO) were significantly elevated in SAKI patients compared to controls.

Conclusions:

  • The study confirms the presence of oxidative stress, oxidative DNA damage, inflammation, and endothelial dysfunction in snakebite-induced acute kidney injury (SAKI).
  • Understanding these mechanisms is crucial for developing novel diagnostic tools and therapeutic strategies for SAKI.