Accumulation of methylglyoxal and d‐lactate in Pb‐induced nephrotoxicity in rats. (16th November 2016)

• Record Type: Journal Article
• Authors: Huang, Yu‐Shen; Li, Yi‐Chieh; Tsai, Pei‐Yun; Lin, Chia‐En; Chen, Chien‐Ming; Chen, Shih‐Ming; Lee, Jen‐Ai
• Is Part Of: Biomedical chromatography. Volume 31:Number 5(2017:May)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2016-11-16
• Subjects: d‐lactate -- heavy metal -- methylglyoxal -- nephrotoxicity -- Pb; Chromatographic analysis -- Periodicals; Biology -- Periodicals; Medicine -- Periodicals; Biology -- Periodicals; Chromatography -- methods -- Periodicals; Medicine -- Periodicals; 543.089
• DOI: 10.1002/bmc.3869
• Languages: English
• ISSNs: 0269-3879

Abstract

Abstract: Lead (Pb) is an environmental pollutant associated with several diseases, such as nephrotoxicity. Methylglyoxal (MG) is a reactive dicarbonyl compound formed during glycolysis and reported to increase in kidney damage. Metformin is used as an MG scavenger in the clinic. In this study, we investigated the mechanism of Pb‐induced renal injury and the effect of metformin on Pb‐induced nephrotoxicity. Eighteen Wistar rats were randomly divided into three groups: control, Pb, and Pb + metformin groups. Pb (250 ppm) was administered in drinking water, and 50 mg/kg of metformin was co‐administered orally. After 28 days, the levels of MG and its metabolited ‐lactate in urine, serum and renal tissues were examined. The elevation of renal MG (56.86 ± 17.47 vs 36.40 ± 5.69, p < 0.01) and urinaryd ‐lactate (0.68 ± 0.28 vs 0.32 ± 0.13, p < 0.01) was observed in Pb‐exposed rats compared with those in control rats. After co‐treatment with metformin, these phenomena were attenuated. In the present study, it was demonstrated for the first time that urinaryd ‐lactate might serve as the candidate marker for Pb‐induced nephrotoxicity in the clinic, and metformin might be a new therapeutic candidate for Pb poisoning.