Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy

Yi Chieh Li, Shin Han Tsai, Shih Ming Chen, Ya Min Chang, Tzu Chuan Huang, Yu Ping Huang, Chen Tien Chang, Jen Ai Lee

Research output: Contribution to journalArticlepeer-review

37 Citations (Scopus)

Abstract

Aristolochic acid, found in the Aristolochia species, causes aristolochic acid nephropathy (AAN) and can develop into renal failure. Methylglyoxal (MGO) is a highly cytotoxic compound generated from the metabolic process of glucose or fatty acids. It binds to proteins and forms N ε-(carboxymethyl)lysine (CML), which contributes to aging and diabetes mellitus complications. However, no relevant literature explores the relationship of MGO and CML with AAN. By injecting AA (10mg/kg BW) into C3H/He mice for 5 consecutive days, we successfully developed an AAN model and observed tubular atrophy with decreased renal function. Creatinine clearance also decreased from 10.32±0.79ml/min/kg to 2.19±0.29ml/min/kg (p

Original languageEnglish
Pages (from-to)832-837
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume423
Issue number4
DOIs
Publication statusPublished - Jul 13 2012

Keywords

  • Advanced glycation end products
  • Aristolochic acid
  • Aristolochic acid nephropathy
  • Glutathione
  • Methylglyoxal
  • N -(carboxymethyl)lysine

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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