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Int. J. Mol. Sci. 2017, 18(1), 169; doi:10.3390/ijms18010169

Bacterial Responses to Glyoxal and Methylglyoxal: Reactive Electrophilic Species

Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Yuseong-gu, Daejeon 305-701, Korea
Current address: Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, 17177 Stockholm, Sweden.
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Author to whom correspondence should be addressed.
Academic Editor: Casper G. Schalkwijk
Received: 15 December 2016 / Revised: 10 January 2017 / Accepted: 11 January 2017 / Published: 17 January 2017
(This article belongs to the Special Issue Glyoxalase System)
View Full-Text   |   Download PDF [2205 KB, uploaded 17 January 2017]   |  

Abstract

Glyoxal (GO) and methylglyoxal (MG), belonging to α-oxoaldehydes, are produced by organisms from bacteria to humans by glucose oxidation, lipid peroxidation, and DNA oxidation. Since glyoxals contain two adjacent reactive carbonyl groups, they are referred to as reactive electrophilic species (RES), and are damaging to proteins and nucleotides. Therefore, glyoxals cause various diseases in humans, such as diabetes and neurodegenerative diseases, from which all living organisms need to be protected. Although the glyoxalase system has been known for some time, details on how glyoxals are sensed and detoxified in the cell have not been fully elucidated, and are only beginning to be uncovered. In this review, we will summarize the current knowledge on bacterial responses to glyoxal, and specifically focus on the glyoxal-associated regulators YqhC and NemR, as well as their detoxification mediated by glutathione (GSH)-dependent/independent glyoxalases and NAD(P)H-dependent reductases. Furthermore, we will address questions and future directions. View Full-Text
Keywords: glyoxal; reactive electrophilic species (RES); glyoxalase glyoxal; reactive electrophilic species (RES); glyoxalase
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Lee, C.; Park, C. Bacterial Responses to Glyoxal and Methylglyoxal: Reactive Electrophilic Species. Int. J. Mol. Sci. 2017, 18, 169.

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