@article{445fff03bc1743ff95b386ba0291f2b6,
title = "Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy",
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",
keywords = "Advanced glycation end products, Aristolochic acid, Aristolochic acid nephropathy, Glutathione, Methylglyoxal, N -(carboxymethyl)lysine",
author = "Li, \{Yi Chieh\} and Tsai, \{Shin Han\} and Chen, \{Shih Ming\} and Chang, \{Ya Min\} and Huang, \{Tzu Chuan\} and Huang, \{Yu Ping\} and Chang, \{Chen Tien\} and Lee, \{Jen Ai\}",
note = "Funding Information: The authors would like to thank Han, Chuan-Hsiao, and Chang, Chia-hao for their useful advice on experimental techniques. This study was financially supported by the Shuang-Ho Medical Center–Taipei Medical University Joint Research Program ( 99TMU-SHH-04-4 ).",
year = "2012",
month = jul,
day = "13",
doi = "10.1016/j.bbrc.2012.06.049",
language = "English",
volume = "423",
pages = "832--837",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier B.V.",
number = "4",
}
