Molecular & Cellular Toxicology

The Korean Society of Toxicogenomics and Toxicoproteomics (대한독성유전 단백체학회)
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Gene Expression Profiling of Early Renal Toxicity Induced by Gentamicin in Mice

  • Oh, Jung-Hwa (Toxicogenomics Team, Korea Institute of Toxicology) ;
  • Park, Han-Jin (Toxicogenomics Team, Korea Institute of Toxicology) ;
  • Lim, Jung-Sun (Toxicogenomics Team, Korea Institute of Toxicology) ;
  • Jeong, Sun-Young (Toxicogenomics Team, Korea Institute of Toxicology) ;
  • Hwang, Ji-Yoon (Toxicogenomics Team, Korea Institute of Toxicology) ;
  • Kim, Yong-Bum (Clinical Pathology Team, Korea Institute of Toxicology) ;
  • Yoon, Seok-Joo (Toxicogenomics Team, Korea Institute of Toxicology)
  • Published : 2006.09.30
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Abstract

To elucidate the molecular mechanisms associated with early renal injury induced by gentamicin, the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. We have identified genes differentially expressed at different duration of gentamicin administration. C57BL/6 female mice were treated daily with gentamicin (20 mg/kg, 100 mg/kg, and 200mg/kg) for 7 days and then sacrificed at day 1, 3, and 7 after administration. Standard blood biochemistry and histopathological observation indicative of nephrotoxicity were made. Total RNA was extracted from the kidney for microarray analysis using Affymetrix $GeneChip^{\circledR}$. Five hundred and seventy eight genes were identified as being either up-or down-regulated over 2-fold changes during early renal injury (p<0.05) and were analyzed by hierarchical clustering. The results showed that the genes involved in early immune responses were differentially regulated during early renal injury. Principal component analysis (PCA) confirmed sample separation according to the degree of renal toxicity. In addition, we identified two potential biomarkers that may predict early renal toxicity. This data may contribute to elucidate of the genetic events during early renal injury and to discover the potential biomarkers for nephrotoxicity induced by gentamicin.

Keywords

References

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