Alternative detoxification of methylglyoxal in GLO1(-/-) is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and methylglyoxal ) which is most likely caused by S-nitrosylation of aldose reductase.
Transgenic mice overexpressing Glo1 on both FVB/NJ (FVB) or C57BL/6J (B6) backgrounds showed increased voluntary EtOH consumption compared to their wild-type littermates. Transgenic Glo1 knockdown mice on a B6 background showed decreased voluntary EtOH consumption. Genetic manipulations of Glo1 had no effect on sucrose saccharin or water consumption.
Local overexpression in the mouse brain resulted in increased anxiety-like behaviour; Glo1 is involved in oxidative stress metabolism linking this pathway with anxiety-related behaviour
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