Abstract
Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is an enzyme involved in the glycolytic pathway. From the substrates of GAPDH, toxic aldehydes, such as glyceraldehyde and methylglyoxal, can be generated. Inhibition of GAPDH in HCT116 cells by koningin acid increased glyceraldehyde. Animal experiments demonstrated that high fat diet-feeding significantly decreased mice liver GAPDH in protein level with increase of lipid peroxidation, liver damage, and shortage of liver cysteine. On the other hand, some food compounds, a water extract of chlorella and its constituent (phenethylamine), ameliorated high fat diet-induced decrease of GAPDH and following pathological events. Treatment with these compounds significantly decreased liver methylglyoxal. Cysteine can react with short chain glyceraldehydes including methylglyoxal and convert them to nontoxic metabolites. These facts indicate that decrease of GAPDH can increase toxic aldehydes in liver and induce liver damage and some food compounds can ameliorate liver damage via recovering GAPDH.
