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Application of flow cytometry to determine the cytotoxicity of urethane dimethacrylate in human cells
Author(s) -
Nassiri M. Reza,
Hanks Carl T.,
Cameron Mark J.,
Strawn Susan E.,
Craig Robert G.
Publication year - 1994
Publication title -
journal of biomedical materials research
Language(s) - English
Resource type - Journals
eISSN - 1097-4636
pISSN - 0021-9304
DOI - 10.1002/jbm.820280203
Subject(s) - flow cytometry , cytotoxicity , cell cycle , cell growth , incubation , cell culture , microbiology and biotechnology , cell , population , doubling time , propidium iodide , dna synthesis , biology , chemistry , andrology , biochemistry , apoptosis , dna , in vitro , programmed cell death , medicine , genetics , environmental health
The effects of an oligomer, urethane dimethacrylate (UDMA), on two human cell lines were studied using flow cytometry (FCM). Untreated and treated cultures of propidium iodine‐stained KB (epidermal oral carcinoma cells) and human foreskin fibroblas (HFF) cells were analyzed for cellular DNA content. Concentrations of 10 and 25 μM of UDMA slightly perturbed the KB cell cycle progression at 24 and 48 h of incubation. However, the effect of 50 μ M was more pronounced at the latter incubation time period. In cell growth experiments, the sublethal concentrations (10 and 25 μM) produced inhibition of KB cell growth rate at a moderate level, which resulted in the prolongation of cell population doubling time. Significant inhibition of cell growth occurred when 50 μM (lethal concentration) was used. Data obtained from the cell cycle perturbation analysis, evidenced by FCM, correlated with the extent of inhibition in KB cell growth rates. The effects of sublethal concentrations were reversible during a 24 h period of oligomer withdrawal from culture medium. In contrast, the effects of 50 μM were not reversible. In HFF cells the depletion of S phase in the cell cycle was the major effect of 50 μM of UDMA. It was concluded that FCM technology is an ideal and practical approach for studying the cytotoxicity of components of dental composites. © 1994 John Wiley & Sons, Inc.

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