This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Smith, G. J. Articles by Fatteh, M. M. Search for Related Content PubMed PubMed Citation Articles by Smith, G. J. Articles by Fatteh, M. M.

American Journal of Pathology, Vol 122, 488-492, Copyright © 1986 by American Society for Investigative Pathology

REGULAR ARTICLES

Kinetics of cell death induced in 10T1/2 cells by methyl methanesulfonate and the effects of extracellular calcium on cell death

GJ Smith, JW Grisham and MM Fatteh

The cytotoxic effect of methyl methanesulfonate (MMS) on C3H 10T1/2 cells is characterized by a complex pattern of changes in the permeability of the cell membrane to trypan blue and, therefore, presumably to extracellular calcium. 10T1/2 cells are temporarily, and reversibly, permeable to trypan blue during the initial 30 minutes following exposure to MMS when incubated in the presence of extracellular calcium. By 90-120 minutes after the exposure, the MMS treated cells have restored control of the membrane permeability, and for the next 6-7 hours they exhibit a level of trypan blue uptake comparable to that observed in the untreated cohort population. Between 9 and 15 hours after exposure to MMS the fraction of the population permeable to trypan blue increases rapidly, ultimately approximating the level of cell killing measured concurrently in a colony formation assay. Transient culture in calcium-free medium immediately after exposure to MMS does not protect 10T1/2 cells from cytotoxicity, but incubation in the calcium-free medium does prevent the initial transient episode of permeability to trypan blue observed when the 10T1/2 cells are incubated in calcium-containing medium. These observations suggest that MMS-induced cytotoxicity results from a complex course of events, possibly from damage to an intracellular target rather than from damage to the plasma membrane.

This article has been cited by other articles:

				P. Pandey, S. Avraham, S. Kumar, A. Nakazawa, A. Place, L. Ghanem, A. Rana, V. Kumar, P. K. Majumder, H. Avraham, et al. Activation of p38 Mitogen-activated Protein Kinase by PYK2/Related Adhesion Focal Tyrosine Kinase-dependent Mechanism J. Biol. Chem., April 9, 1999; 274(15): 10140 - 10144. [Abstract] [Full Text] [PDF]

				P. Pandey, S. Avraham, A. Place, V. Kumar, P. K. Majumder, K. Cheng, A. Nakazawa, S. Saxena, and S. Kharbanda Bcl-xL Blocks Activation of Related Adhesion Focal Tyrosine Kinase/Proline-rich Tyrosine Kinase 2 and Stress-activated Protein Kinase/c-Jun N-terminal Protein Kinase in the Cellular Response to Methylmethane Sulfonate J. Biol. Chem., March 26, 1999; 274(13): 8618 - 8623. [Abstract] [Full Text] [PDF]

				P. Pandey, J. Raingeaud, M. Kaneki, R. Weichselbaum, R. J. Davis, D. Kufe, and S. Kharbanda Activation of p38 Mitogen-activated Protein Kinase by c-Abl-dependent and -independent Mechanisms J. Biol. Chem., September 27, 1996; 271(39): 23775 - 23779. [Abstract] [Full Text] [PDF]