TDI致小鼠肝细胞损伤的机制分析

Analysis on mechanism of hepatic cells damnification induced by TDI

探讨甲苯二异氰酸酯(toluenediisocyanate,简称TDI)导致肝细胞损伤的机制以及雌雄差异．从氧化损伤的角度观察了TDI对肝组织中的超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)含量的影响,并应用激光共聚焦技术分析了TDI对肝细胞内DNA、RNA的影响,此外,还进行了毒性效应的雌雄差异比较．肝组织中的MDA含量有显著性增加(P＜0．01),同时SOD(P＜0．01)、GSH(P＜0．05)的含量均有不同程度的降低；染毒组肝细胞的RNA/DNA荧光像素之比明显升高(P＜0．01)；TDI通过氧化损伤的机制导致了肝组织的毒性；TDI对DNA合成有一定的抑制作用；TDI的毒性具有雌雄差异,雌性对TDI的耐受剂量高于雄性．

To explore the mechanism and male and female differences of hepatic cell＇s damnification induced by TDI. The effect of TDI on contents of superoxide dismutase （ SOD）, malondialdehyde （MDA）, and glutathione （GSH） in hepatic tissue was observed as a measurement for damage due to oxidation. Laser scanning confocal microscopy was used to analyze the effect of TDI on the RNA and DNA in hepatic cells. And sex differences of toxicity were compared. MDA contents in hepatic tissues has increased significantly （P 〈 0. 01 ）, while the contents of SOD （P 〈0. 01 ） and GSH （P 〈0.05） have declined to different degrees. The RNA/DNA ratio in hepatic cells has increased significantly after exposed to TDI. TDI exerts its toxic effect on the target organs through mechanism of oxidative damage; TDI can inhibit DNA synthesis. Furthermore, there is a difference between the dosage needed for causing damage in male and female. The endurable dosage of TDI on female is larger than that on male.