Conference Dates

May 8-13, 2016


Methylglyoxal is a toxic by-product of glycolysis and amino acid metabolism in mammalian systems. The major route for methylglyoxal detoxification is the glyoxalase pathway, which consists of the enzymes glyoxalase I (GLO1) and glyoxalase II (GLO2). A required co-factor for the glyoxalase pathway is reduced glutathione. Evidence suggests that GLOI and methylglyoxal have important roles to play in the signal pathways associated with oxidative stress and necrotic cell death1. Previous work has demonstrated that growth conditions found in industrial cell culture have marked effects on endogenous methylglyoxal levels in Chinese hamster ovary (CHO)2. Furthermore, decreased levels of methylglyoxal were associated with increased cell viability. More recently, this compound has been found to modify recombinant antibodies expressed in CHO at specific arginine residues3. Here, the implications of methylglyoxal are discussed in the context of past and current works relevant to industrial cell culture