Effect of Cysteine on Methylglyoxal-Induced Renal Damage in Mesangial Cells
- Authors
- Lee, Jae Hyuk; Subedi, Lalita; Kim, Sun Yeou
- Issue Date
- Jan-2020
- Publisher
- MDPI
- Keywords
- methylglyoxal; advanced glycation end products; l-cysteine; glyoxalase-I; diabetic nephropathy
- Citation
- CELLS, v.9, no.1
- Journal Title
- CELLS
- Volume
- 9
- Number
- 1
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/26178
- DOI
- 10.3390/cells9010234
- ISSN
- 2073-4409
- Abstract
- Methylglyoxal (MGO), a highly reactive dicarbonyl compound, is a key precursor of the formation of advanced glycation end products (AGEs). MGO and MGO-AGEs were reportedly increased in patients with diabetic dysfunction, including diabetic nephropathy. The activation of glyoxalase-I (GLO-I) increases MGO and MGO-AGE detoxification. MGO-mediated glucotoxicity can also be ameliorated by MGO scavengers such as N-acetylcysteine (NAC), aminoguanidine (AG), and metformin. In this study, we noted that l-cysteine demonstrated protective effects against MGO-induced glucotoxicity in renal mesangial cells. l-cysteine prevented MGO-induced apoptosis and necrosis, together with a reduction of reactive oxygen species (ROS) production in MES13 cells. Interestingly, l-cysteine significantly reduced MGO-AGE formation and also acted as an MGO-AGE crosslink breaker. Furthermore, l-cysteine treatment accelerated MGO catabolism to D-lactate via the upregulation of GLO-I. The reduction of AGE formation and induction of AGE breakdown, following l-cysteine treatment, further supports the potential use of l-cysteine as an alternative for the therapeutic control of MGO-induced renal complications in diabetes, especially against diabetic nephropathy.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 약학대학 > 약학과 > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/26178)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.