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Effect of Mitochondrial Inhibitors On Metaphase‐Telophase Progression and Nuclear Membrane Formation In Chinese Hamster Cells
Author(s) -
Chai Lee S.,
Schumer Joan M.,
Sandberg Avery A.
Publication year - 1985
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1985.tb00629.x
Subject(s) - colcemid , egta , antimycin a , biology , metaphase , mitochondrion , mitosis , chinese hamster , microbiology and biotechnology , biochemistry , chemistry , calcium , dna , organic chemistry , gene , chromosome
Chinese hamster Don cells in log‐phase were exposed to Colcemid during the G 2 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 Colcemid and other agents and the rate of micronuclei formation in the absence of anaphase was studied. Both EDTA and EGTA accelerated the progression from M to Tel, but did not affect the overall rate of cell division. Chloramphenicol (CAP), an inhibitor of mitochondrial protein synthesis, blocked the effect of the chelators and also retarded the progression. an inhibitor of mitochondrial respiration, Antimycin A (AA), also retarded the progression in the absence of the chelators and prevented the promoting effect of the chelators. A stimulator of ATPase for ATP breakdown. 2,4‐dinitrophenol (DNP), accelerated the M to Tel progression. Chloramphenicol (CAP) and AA, as well as DNP, appeared to have little effect on the formation of micronuclei in the presence of Colcemid. EGTA, which affects cell surface Ca 2+ , stimulated the formation of micronuclei. This study indicates that Ca 2+ ions and mitochondrial function are involved in the regulation of a certain segment of mitosis beyond metaphase, with Ca 2+ sequestration in the mitochondria and chelation of Ca 2+ by EGTA as dominant factors.

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