PURPOSE: To study the interplay of drugs and energy metabolism of tumor cells, metabolic changes induced by chloroacetaldehyde and cytochalasin B were analyzed in colon carcinoma cells LS174T. METHODS: O(2)-consumption and extracellular acidification were recorded using a bioelectronic sensor-chip system, which monitors these parameters in a culture continuously for at least 24 h. In parallel cultures cell number, cellular ATP-content, mitochondrial transmembrane potential, and the content of reactive oxygen species (ROS) were determined. RESULTS: When cell death was induced by chloroacetaldehyde (50 muM), the rate of acidification declined gradually for the next 15 h, while O(2)-consumption decreased rapidly within 30 min. This correlated with a loss in mitochondrial potential. However, cellular ATP-level showed a transient increase at 2 h; also ROS levels increased up to 6 h. In cells treated with cytochalasin B (2 muM), which inhibits glucose uptake, the rate of O(2)-consumption increased and the acidification activity dropped, even upon glutamine depletion. Mitochondrial membrane potential transiently increased after 1 h, while ATP-content decreased; there was no change in the level of ROS. CONCLUSION: The pattern of changes in basic energy metabolism differs with the type of cell death and growth inhibition involved in the cytotoxic action of two different drugs.
PURPOSE: To study the interplay of drugs and energy metabolism of tumor cells, metabolic changes induced by chloroacetaldehyde and cytochalasin B were analyzed in colon carcinoma cells LS174T. METHODS:O(2)-consumption and extracellular acidification were recorded using a bioelectronic sensor-chip system, which monitors these parameters in a culture continuously for at least 24 h. In parallel cultures cell number, cellular ATP-content, mitochondrial transmembrane potential, and the content of reactive oxygen species (ROS) were determined. RESULTS: When cell death was induced by chloroacetaldehyde (50 muM), the rate of acidification declined gradually for the next 15 h, while O(2)-consumption decreased rapidly within 30 min. This correlated with a loss in mitochondrial potential. However, cellular ATP-level showed a transient increase at 2 h; also ROS levels increased up to 6 h. In cells treated with cytochalasin B (2 muM), which inhibits glucose uptake, the rate of O(2)-consumption increased and the acidification activity dropped, even upon glutamine depletion. Mitochondrial membrane potential transiently increased after 1 h, while ATP-content decreased; there was no change in the level of ROS. CONCLUSION: The pattern of changes in basic energy metabolism differs with the type of cell death and growth inhibition involved in the cytotoxic action of two different drugs.
Authors: R Ehret; W Baumann; M Brischwein; M Lehmann; T Henning; I Freund; S Drechsler; U Friedrich; M L Hubert; E Motrescu; A Kob; H Palzer; H Grothe; B Wolf Journal: Fresenius J Anal Chem Date: 2001-01-01
Authors: David G Pfister; John McCaffrey; Andrew J Zahalsky; Gary K Schwartz; Eric Lis; William Gerald; Andrew Huvos; Jatin Shah; Dennis Kraus; Ashok Shaha; Bhuvanesh Singh; Suzanne Wolden; Michael Zelefsky; Ilana Palgi Journal: Invest New Drugs Date: 2002-02 Impact factor: 3.850
Authors: A Serafino; P Sinibaldi-Vallebona; G Lazzarino; B Tavazzi; D Di Pierro; G Rasi; G Ravagnan Journal: Anticancer Res Date: 2000 Sep- Oct Impact factor: 2.480
Authors: N Zamzami; P Marchetti; M Castedo; D Decaudin; A Macho; T Hirsch; S A Susin; P X Petit; B Mignotte; G Kroemer Journal: J Exp Med Date: 1995-08-01 Impact factor: 14.307