Studies on mechanism of free Nε-(carboxymethyl)lysine-induced toxic injury in mice.
Yi-Xin WangHao XuXin LiuLiang LiuYong-Ning WuZhi-Yong GongPublished in: Journal of biochemical and molecular toxicology (2019)
Nε-(carboxymethyl)lysine (CML), which is a compound produced when food is processed, has aroused concern in recent years because of its potentially dangerous effects. This study aimed to investigate the mechanism of free CML-induced toxic injury in mice. The inflammatory cytokine tumor necrosis factor-α, transforming growth factor-β, vascular cell adhesion molecule-1 mRNA expression levels of CML-infected mice liver and kidney tissues significantly increased. While CML receptor-receptor for advanced glycation end products (RAGE) protein expression in male mice liver tissue had a more significant change than the control group, there was no significant difference in other dose groups compared with the control group. In conclusion, the foodborne free CML can be induced by oxidative stress and immune response to liver and kidney tissue injury in mice. Additionally, the free CML may also bind to RAGE, which activates the downstream inflammatory pathway.
Keyphrases
- oxidative stress
- transforming growth factor
- high fat diet induced
- chronic myeloid leukemia
- diabetic rats
- high glucose
- cell adhesion
- gene expression
- rheumatoid arthritis
- dna damage
- type diabetes
- epithelial mesenchymal transition
- wild type
- drug induced
- endothelial cells
- heat stress
- human health
- heat shock protein
- endoplasmic reticulum stress