Effects of cadmium exposure on hepatic viability and bioenergy

• Main Authors: Li-Wei Kuo, 郭力瑋
• Other Authors: Rei-Chen Yang
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/45175359897355699961

碩士 === 高雄醫學大學 === 生理及分子醫學研究所 === 98 === Introduction：Cadmium is a highly toxic heavy metal in our environment. It is widely used in many industry such as：color pigment, batteries, plastic stabilizers. In human, cadmium causes organs dysfunction, especially in the liver. It has been reported that cadmium causes apoptosis, necrosis, which way be due to mitochondrial dysfunction in hepotocytes. However, the mechanisms are rare investigated. Several reports have revealed that mitochondrial respiratory enzyme activity decreases, leading to the decreased intracellular ATP content after cadmium exposure. Rare studies have been performed concerning about the hydrolysis effect of ATP after cadmium exposure. In this study, we focused on the in vitro effect of ATP hydrolysis after cadmium exposure, and the role of IF1, a regulator in ATP hydrolysis, is also investigated. Materials and methods：We used clone 9 hepatocytes to observe the cell viability, ATP content, mitochondrial membrane potential, IF1 protein, the activity of ATP hydrolysis and the IF1 mRNA expression after cadmium treatment, and the mechanism was discussed. Results：Our results showed that, after cadmium treatment, the cell viability, ATP content, IF1 protein level and the IF1 mRNA expression were significantly decreased simultaneously the mitochondrial membrane potential collapsed, and the activity of ATP hydrolysis was significantly increased in clone 9 hepatocytes. Conclusion：We concluded that cadmium induces the decrease in cell viability of clone 9 cells, and the suppressed IF1 protein and the following increased ATP hydrolysis may play a role in bioenergetic failure after cadmium exposure.