The effects of hydrogen peroxide treatments on Escherichia coli KS400 and AB1157 cells were assessed by monitoring the accumulation of oxidative damage products, carbonyl proteins and thiobarbituric acid-reactive substances (TBARS), as well as the activities of selected antioxidant enzymes. H2O 2 treatment stimulated increases in both TBARS and carbonyl protein levels in dose- and time-dependent manners in KS400 cells. The accumulation of TBARS was much more variable with H2O2 treatment; TBARS content was significantly increased in response to 5 μM H2O 2, whereas a significant increase in carbonyl protein content occurred at 100 μM H2O2. Similarly, treatment with 20 μM hydrogen peroxide for different lengths of time resulted in peak TBARS accumulation by 20 min, whereas carbonyl protein levels were significantly elevated only after 60 min. In AB1157 cells, treatment with 20 μM hydrogen peroxide for 20 min led to strong increases in both carbonyl protein and TBARS levels. This treatment also triggered increased activities of enzymes of the oxyR regulon (catalase, peroxidase, and glutathione reductase) in both strains. In the AB1157 strain, H2O2 exposure also increased the activities of two enzymes of the soxRS regulon (superoxide dismutase and glucose-6-phosphate dehydrogenase) by 50-60%. The data show differential variability of lipids versus proteins to oxidative damage induced by H 2O2, as well as strain-specific differences in the accumulation of damage products and the responses by antioxidant enzymes to H2O2 stress.

Additional Metadata
Keywords Antioxidant enzymes, Carbonyl proteins, Escherichia coli, Hydrogen peroxide, Thiobarbituric acid-reactive substances
Persistent URL dx.doi.org/10.1016/j.cellbi.2005.08.002
Journal Cell Biology International
Citation
Semchyshyn, H. (Halyna), Bagnyukova, T. (Tetyana), Storey, K, & Lushchak, V. (Volodymyr). (2005). Hydrogen peroxide increases the activities of soxRS regulon enzymes and the levels of oxidized proteins and lipids in Escherichia coli. Cell Biology International, 29(11), 898–902. doi:10.1016/j.cellbi.2005.08.002