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Effects of trifluoroacetic acid, a halothane metabolite, on C6 glioma cells.
Ma-TG; Ling-YH; McClure-GD; Tseng-MT
J Toxicol Environ Health 1990 Oct; 31(2):147-158
An investigation was conducted to determine the impact of trifluoroacetic-acid (76051) (TFA) on the growth, protein synthesis, and glycosylation of a murine glioma cell, C6, in-vitro. One day exposure to TFA caused a slight concentration dependent enhancement of cell growth. At 8.38 millimolar (mM) a 28% increase was noted. Exposure for 1 to 5 days caused an increase in leucine incorporation into C6 cells. The high dose of TFA (10mM) suppressed the intracellular ATP, GTP, and CTP pool. At lower concentrations, TFA elevated ATP levels 11 to 15% while it exerted no influence on UTP or CTP. Intracellular GTP concentration declined in a dose dependent fashion. One day exposure at 5mM reduced the rate of mannose incorporation into glycoproteins and dolichol linked oligosaccharide to 71 and 39% of control levels, respectively. Five days exposure caused further decline in mannose incorporation and caused an additional effect on the dolichol linked oligosaccharides. No significant decline in glucosamine incorporation in glycoprotein and dolichol linked oligosaccharide was observed. Treatment for 24 hours with 5 and 15mM TFA accelerated lectin induced agglutination. The observed loss of terminal sialyl residues in TFA treated cells could cause an increase in the amount of terminally exposed galactose residues. Such surfaces bind more readily to RCA, and the cells thus become more sensitive to the treatment of this particular lectin.
NIOSH-Publication; NIOSH-Grant; Protein-synthesis; Protein-chemistry; Cell-cultures; Fluorinated-hydrocarbons; Anesthetics; Metabolites
Anatomy University of Louisville Anatomy and Neurobiology Louisville, KY 40292
Issue of Publication
Journal of Toxicology and Environmental Health
University of Louisville, Louisville, Kentucky
Page last reviewed: September 2, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division