Detail of "133681-84-2"

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Cytosolic calcium increase in coronary endothelial cells after hydrogen peroxide exposure and the inhibitory effect of U78517F

Cytosolic calcium increase in coronary endothelial cells after hydrogen peroxide exposure and the inhibitory effect of U78517F. Kimura, Masaaki; Maeda, Kaori; Hayashi, Shigehiro (Tsukuba Res. Lab., Upjohn Pharm. Ltd., Japan).In this experiment, several chemicals are used like 133681-84-2 Br. J. Pharmacol., 107(2), 488-93 (English) 1992. CODEN: BJPCBM. ISSN: 0007-1188. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Cytosolic calcium concns. ([Ca2+]i were detd. with fura-2 on both resting (unstimulated) and A23187-stimulated coronary endothelial cells following injury by hydrogen peroxide (H2O2). Treatment of cells with H2O2 (10-4 M) caused an increase in the resting [Ca2+]i, which reached a max. of five fold after 3 h. The increase in resting [Ca2+]i was significantly attenuated by treatment with U78517F, a potent inhibitor of lipid peroxidn., at a concn. of 10-6 M or greater. Catalase (50 u mL-1) also markedly inhibited the H2O2-induced rise in [Ca2+]i. Pretreatment with verapamil (10-5 M), nifedipine (10-6 M) or diltiazem (10-5 M) had no effect on the increase in [Ca2+]i following addn. of H2O2. A23187 produced a transient increase in [Ca2+]i followed by a sustained plateau. The initial peak and plateau phase responses to A23187 were augmented by H2O2. This augmentation of [Ca2+]i was suppressed by U78517F or catalase but not by Ca-entry blockers. Thus, it is likely that lipid peroxidn. plays a crit. role in the sustained increase in [Ca2+]i that occurs following treatment with H2O2 and that this continues in the presence of agonists which stimulate the endothelium. Voltage-gated Ca2+ channels do not seem to be involved in the genesis of cellular damage assocd. with sustained large increases in [Ca2+]i. .