No abstract

The metabolism of chlorogenic acid (CGA) through the intestinal tract was studied. As cadmium is a well-known toxic heavy metal, this study was carried out to investigate the comparative protective effect of CGA and its representative intestinal metabolite (3-(3-hydroxyphenyl) propionic acid, HPPA) against Cd-induced erythrocyte cytotoxicity in vitro and in vivo. We found that CGA and its intestinal metabolite appreciably prevented erythrocyte hemolysis, osmotic fragility, and oxidative stress induced by Cd. Also, we found that HPPA had a stronger protective ability than CGA against Cd-induced erythrocyte injury in vivo, such as increasing the ratio of protein kinase C from 7.7% (CGA) to 12.0% (HPPA). Therefore, we hypothesized that CGA and its microbial metabolite had protective effects against Cd-induced erythrocyte damage via multiple actions including antioxidation and chelation. For humans, CGA supplementation may be favorable for avoiding Cd-induced biotoxicity.

Cadmium (Cd) can invade gastrointestinal tract and induce the occurrence of gastrointestinal diseases. Rice hull insoluble dietary fiber (RHF) could be used as a novel dietary supplement strategy against Cd exacerbated colitis.

Aluminum (Al) is an important environmental neurotoxicity, and the speciation of Al largely determines the absorption and toxic effects in human body. The brain-type creatine kinase (CK-BB), which is an important kinase that regulates energy supply in brain tissue, has been found high affinity to Al. The research was carried to explore the potential neurotoxicity mechanism induced by different speciation of Al. In the current work, the C57BL/6 mice and C6 cells were used to explore the role of Al speciation in Al-induced neurotoxicity. The results showed that the expression levels of F-actin and Cyt C/Caspase 9/Caspase 3 signaling pathways were different in mice treated with AlCl3 and Al(mal)3. In C6 cells, the CK-BB activity decreased by 23.92% after 3.5 mM AlCl3 treatment. AlCl3 treatment resulted in insufficient local ATP supply of cells, thereby affecting the formation of F-actin and cell morphology. After Al(mal)3 treatment, the fluorescence intensity of membrane potential was increased by 141.37%, followed by activating apoptosis pathway of Cyt C/Caspase 9/Caspase 3. In addition, molecular docking showed that the binding site of AlCl3 on CK-BB subunit was closer to the active site. Al(mal)3 enhanced the hydrophobicity of CK-BB. The aim of this study is to demonstrate that CK-BB is an important factor in Al-induced energy metabolism disorder process, in which the speciation of Al compound has revealed particular toxicity mechanisms.