Effect of mitochondrial inhibitors on metaphase-telophase progression and nuclear membrane formation in XXXX cells.

@entity3569 @entity49030 @entity8581 @entity4527 @entity3212 @entity3213 @entity141 @entity2755 @entity1098 @entity855
@entity3569 Don cells in log-phase were exposed to Colcemid during the G2 period with and without a combination of divalent cation chelators and mitochondrial inhibitors. Isolated metaphase cells were incubated as follows: (i) without Colcemid but with other agents and the progression was monitored from metaphase (M) to telophase (Tel) and to cell division; (ii) with @entity49030 and other agents and the rate of micronuclei formation in the absence of anaphase was studied. Both @entity1098 and @entity4527 accelerated the progression from M to Tel, but did not affect the overall rate of cell division. @entity2755 (CAP), an inhibitor of mitochondrial protein synthesis, blocked the effect of the chelators and also retarded the progression. An inhibitor of mitochondrial respiration, @entity8581 (AA), also retarded the progression in the absence of the chelators and prevented the promoting effect of the chelators. A stimulator of ATPase for @entity855 breakdown. @entity3212 ( @entity3213 ), accelerated the M to Tel progression. @entity2755 (CAP) and AA, as well as @entity3213 , appeared to have little effect on the formation of micronuclei in the presence of Colcemid. @entity4527 , which affects cell surface @entity141 , stimulated the formation of micronuclei. This study indicates that @entity141 ions and mitochondrial function are involved in the regulation of a certain segment of mitosis beyond metaphase, with @entity141 sequestration in the mitochondria and chelation of @entity141 by @entity4527 as dominant factors.
