H2O2-induced oxidative injury in rat cardiac myocytes is not potentiated by 1,1,1-trichloroethane, carbon tetrachloride, or halothane.
Toraason-M; Heinroth-Hoffmann-I; Richards-D; Woolery-M; Hoffmann-P
J Toxicol Environ Health 1994 Apr; 41(4):489-507
The ability of the halocarbons 1,1,1-trichloroethane (71556), carbon- tetrachloride (56235) and halothane (151677) to enhance hydrogen- peroxide (7722841) (H2O2) induced oxidative injury in isolated rat neonatal cardiac myocytes was investigated. Myocytes were separated from cardiac ventricular cells isolated from 2 to 4 day old Sprague- Dawley-rats. Cells were exposed in culture to 20 to 200 micromolar H2O2 with or without 1 millimolar halocarbons for 1 hour. Lipid peroxidation was assayed by measuring thiobarbituric-acid reactive substances (TBARS) released in culture dishes. Cytotoxicity was assayed by lactate-dehydrogenase (LDH) determination in cell treatment buffer and in cells. Deferoxamine pretreatment was used to determine oxygen radical formation through the Fenton reaction. Intracellular calcium and amplitude of calcium transients were measured using the calcium sensitive fluorophore fura-2, and electrical stimulation, followed by dual excitation spectrofluorometric measurement at 340 and 380 nanometer. The results indicated that H2O2 increased the release of TBARS and LDH in a concentration dependent manner. H2O2 initially altered the configuration of intracellular calcium transients, after which it eliminated them, and finally caused calcium overload. Deferoxamine inhibited all of the effects of H2O2, while the halocarbons reversibly reduced intracellular calcium transients, but not TBARS release or LDH leakage. Exposure of the myocytes to H2O2 and halocarbons together did not effect responses to H2O2. The authors conclude that the halocarbons tested in neonatal rat cardiac myocytes do not enhance oxidative injury by H2O2.
NIOSH-Author; Muscle-cells; Cell-cultures; In-vitro-studies; Laboratory-animals; Peroxides; Oxidation; Halogen-compounds; Cytotoxic-effects; Lipids; Enzyme-activity; Calcium-compounds
71-55-6; 56-23-5; 151-67-7; 7722-84-1
Journal of Toxicology and Environmental Health