The effects of Glutathione S-transferase isoforms at the growth, morphology change and the response to carcinogens of hepatocyte

• Main Authors: Hwei-Mei Lin, 林惠美
• Other Authors: Chou, Fen-Pi
• Format: Others
• Language: zh-TW
• Published: 2002
• Online Access: http://ndltd.ncl.edu.tw/handle/43528507832009292648

碩士 === 中山醫學大學 === 生物化學研究所 === 90 === Glutathione S-transferase (GSTs) are a family of enzymes with several functions. Although they play a role in detoxification and protection in normal liver cell, some papers reported that over-expression or down-regulation of certain GSTs might be one of the causes that lead to the formation of hepatoma or the development of drug resistance. However, it is still not clear what the relationship is between the differential expression of GST isoforms and the causes and drug resistance of hepatoma. In this study, the effects of rat GST Yb1 at the growth, the morphology change and the response to carcinogens of hepatoma cells (Hep G2) and hepatocytes (Change liver) were investigated by the transient transfection system. Chang liver cells were transfected with rGSTYb1 plasmid, and then treated with AFB1. The results showed that the percentage of survival cells was higher, and the activities of GOT and GPT were lower in these cells than the vector control. There was no difference in the activities of GST alpha and GST pi between the GSTYb1-transfected cells and the vector control. The data indicated that the expression of rGSTYb1was able to protect normal hepatocytes (Chang liver cells) against the damage of AFB1. When Hep G2 cells were used for the same experiments, the results were opposite to that of Chang liver cells. The percentage of survival cells were lower and the activities of GOT and GPT were higher in the rGSTYb1-transfected and AFB1-treated cells than the vector control. The activities of GST alpha and GST pi were not affected by the expression of rGSTYb1. The data indicated that the expression of rGSTYb1 was not able to protect hepatoma cells against the damage of AFB1. In conclusion, the expression of rGSTYb1 showed differential effects in different cell lines by protecting normal hepatocytes and, on the other hand, promoting the cells death of cancerous liver cells. Therefore, in addition to its important role in the protection function of normal liver, GSTYb1 might be also involved in some pathway that leads to the death of cancer cells.