Aging is a multifactorial process that involves changes at the cellular, tissue, organ and the whole body levels resulting in decreased functioning, development of diseases, and ultimately death. Oxidative stress is believed to be a very important factor in causing aging and age-related diseases. Oxidative stress is caused by an imbalance between oxidants such as reactive oxygen species (ROS) and antioxidants. ROS are produced from the mitochondrial electron transport chain and many oxidative reactions. Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite formed during glucose, protein and fatty acid metabolism. MG levels are elevated in hyperglycemia and other conditions. An excess of MG formation can increase ROS production and cause oxidative stress. MG reacts with proteins, DNA and other biomolecules, and is a major precursor of advanced glycation end products (AGEs). AGEs are also associated with the aging process and age-related diseases such as cardiovascular complications of diabetes, neurodegenerative diseases and connective tissue disorders. AGEs also increase oxidative stress. In this review we discuss the potential role of MG in the aging process through increasing oxidative stress besides causing AGEs formation. Specific and effective scavengers and crosslink breakers of MG and AGEs are being developed and can become potential treatments to slow the aging process and prevent many diseases.

A bacterial ghost (BG)-based vaccine was developed against enterohemorrhagic Escherichia coli O157:H7 infection. The aim of this study was to evaluate the protective effect of E. coli O157:H7 BGs in a mouse model and to reveal the mechanism of the immune response. Booster immunization provided a higher protection rate (84%) than single-dose immunization (56%). Intragastric immunization of E. coli O157:H7 BGs induced both humoral and cellular immune responses. The proliferative response of CD4+ T cells was mediated by the antigen-presenting cells. The humoral immune response dominated the immune response, while the cellular immune response developed later. Inflammatory reaction was balanced by the mixed Th1/Th2 immune response. The immune sera anti-adhesion effect was confirmed by the inhibition effect, which could inhibit >90% of the adhesion of E. coli O157:H7 to Hep-2 target cells in vitro. Antibody titer specific for intimin, a molecule important for adhesion of E. coli O157:H7 to target cells, correlated with specific immunoglobulin A or G antibody titer. Therefore, it might be feasible to clinically test BG vaccines in the future.

Shiga toxins produced by Escherichia coli O157:H7 cause a wide spectrum of enteric diseases, such as lethal hemorrhagic colitis and hemolytic uremic syndrome. In this study, the B subunit protein of Shiga toxin type 1 (Stx1) was produced in the E. coli system, was further purified by Ni-column Affinity Chromatography method, and was then used as an immunogen to immunize laying hens for yolk immunoglobulin (IgY) production. Titers of IgY increased gradually with boosting vaccination and, finally, reached a level of 105, remaining steady over 1 year. Then the protective efficacy of IgY against Stx1 was evaluated by in vitro and in vivo experiments. It was shown that the anti-Stx1 IgY could effectively block the binding of Stx1 to the Hela cells and could protect BALB/c mice from toxin challenges. The data indicates the facility of using egg yolk IgY as a therapeutic intervention in cases of Shiga toxin intoxication.