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

doi:10.1016/j.bbrc.2012.06.049

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 journal › Article › peer-review

39 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 language	English
Pages (from-to)	832-837
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	423
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2012.06.049
Publication status	Published - Jul 13 2012

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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

Access to Document

10.1016/j.bbrc.2012.06.049

Cite this

Li, Y. C., Tsai, S. H., Chen, S. M., Chang, Y. M., Huang, T. C., Huang, Y. P., Chang, C. T., & Lee, J. A. (2012). Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. Biochemical and Biophysical Research Communications, 423(4), 832-837. https://doi.org/10.1016/j.bbrc.2012.06.049

Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. / Li, Yi Chieh; Tsai, Shin Han ; Chen, Shih Ming et al.
In: Biochemical and Biophysical Research Communications, Vol. 423, No. 4, 13.07.2012, p. 832-837.

Research output: Contribution to journal › Article › peer-review

Li, YC, Tsai, SH , Chen, SM, Chang, YM, Huang, TC, Huang, YP, Chang, CT & Lee, JA 2012, 'Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy', Biochemical and Biophysical Research Communications, vol. 423, no. 4, pp. 832-837. https://doi.org/10.1016/j.bbrc.2012.06.049

Li YC, Tsai SH , Chen SM, Chang YM, Huang TC, Huang YP et al. Aristolochic acid-induced accumulation of methylglyoxal and N ε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy. Biochemical and Biophysical Research Communications. 2012 Jul 13;423(4):832-837. doi: 10.1016/j.bbrc.2012.06.049

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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",

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AU - Chang, Chen Tien

AU - Lee, Jen Ai

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