Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Nov 1;14:739526. doi: 10.3389/fnmol.2021.739526

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2021 Yin, Ma, Luo, Luo, He, Liang, Zuo, Xu, Chen, Xiong, Tan, Fu, Lv, Dai, Wen, Zhu, Ye, Lin, Lin, Li, Chen, Luo, Li and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

A schematic illustrating the hypothesized regulatory process of the rs1781735 G-T mutation in the etiology of schizophrenia. Dicarbonyl compounds, such as methylglyoxal (MG), as a toxic species could lead to neural dysfunction and symptomatology in schizophrenia. Dicarbonyl compounds can be effectively detoxified via the metabolic pathway of the glyoxalase system. MG reacts with glutathione (GSH) and is converted to S-D-lactoylglutathione (SLG) by Glo-1. SLG is catalyzed into D-lactate by glyoxalase-2 (Glo-2), and GSH is recycled. As a rate-limiting enzyme in the glyoxalase system, Glo-1 plays a critical role in the detoxification of carbonyl stress in schizophrenia.