Prozialeck W C, Wellington D R, Mosher T L, Lamar P C, Laddaga R A
Department of Pharmacology, Midwestern University, Downers Grove, IL 60515, USA.
Life Sci. 1995;57(15):PL199-204. doi: 10.1016/0024-3205(95)02109-v.
Exposure of LLC-PK1 cells to low micromolar concentrations of Cd2+ for 1-4 hours causes the disruption of the adhering and occluding junctions between the cells, whereas exposure to higher concentrations of Cd2+ for longer periods of time causes more severe toxic effects and cell death. The objective of the present studies was to determine whether or not the junctional effects of Cd2+ might be a consequence of apoptotic injury. LLC-PK1 cells on cell culture inserts were exposed to either Cd2+ or tumor necrosis factor (TNF-alpha) plus cycloheximide, a treatment that has recently been shown to cause apoptosis in LLC-PK1 cells. The results showed that at the time the Cd2(+)-induced junctional changes were occurring, there was no increase in the number of apoptotic cells or evidence of DNA fragmentation. By contrast, TNF-alpha plus cycloheximide induced changes that were characteristic of apoptosis. These results indicate that the disruption of intercellular junctions by Cd2+ in the LLC-PK1 cell line occurs independently of apoptosis.
将LLC - PK1细胞暴露于低微摩尔浓度的Cd2 + 1 - 4小时会导致细胞间粘附连接和紧密连接的破坏，而长时间暴露于更高浓度的Cd2 +会导致更严重的毒性作用和细胞死亡。本研究的目的是确定Cd2 +对连接的影响是否可能是凋亡损伤的结果。将细胞培养插入物上的LLC - PK1细胞暴露于Cd2 +或肿瘤坏死因子（TNF - α）加环己酰亚胺中，最近的研究表明这种处理会导致LLC - PK1细胞凋亡。结果表明，在Cd2 +诱导连接变化发生时，凋亡细胞数量没有增加，也没有DNA片段化的证据。相比之下，TNF - α加环己酰亚胺诱导的变化具有凋亡特征。这些结果表明，LLC - PK1细胞系中Cd2 +引起的细胞间连接破坏独立于凋亡发生。
