Drugs online research references
Acta Med Okayama. 1985 Aug;39(4):289-95.
Effect of tricyclic drugs on mitochondrial membrane.
Eto K, Fukuda T, Araki Y, Inoue B, Ogata M.
The effects of tricyclic drugs (clomipramine, imipramine, chlorpromazine and promethazine) on isolated liver mitochondria of rats were examined. All the drugs tested accelerated state 4 respiration. Their stimulative potency at concentrations below 100 microM was in the order of chlorpromazine greater than clomipramine greater than imipramine, promethazine. On state 3 respiration, the chlorine containing drugs had an inhibitive effect at high concentrations, while the other drugs seemed to have a slightly stimulative effect. These drugs stimulated latent ATPase activity of mitochondria. Clomipramine and chlorpromazine inhibited 2, 4-dinitrophenol-stimulated ATPase activity in a dose-dependent fashion. Imipramine also inhibited 2, 4-dinitrophenol-stimulated ATPase activity at high concentrations. Promethazine, however, had almost no effect. All the drugs induced potassium release from mitochondrial vesicles, and their potency was in the order of clomipramine greater than chlorpromazine greater than imipramine greater than promethazine. These results suggest that clomipramine, imipramine, chlorpromazine and promethazine cause impediments in both mitochondrial respiration and ion compartmentation, and that the chlorine containing drugs are more toxic than others on the functions of the mitochondrial membrane.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2931948&dopt=Abstract
J Pharmacol Exp Ther. 1988 May;245(2):493-500.
Effect of extracellular Ca++ omission on isolated hepatocytes. I. Induction of oxidative stress and cell injury.
Thomas CE, Reed DJ.
Department of Biochemistry and Biophysics and Environmental Health Sciences Center, Oregon State University, Corvallis.
The effect of varying extracellular Ca++ concentration and various antioxidants and metal ion chelators on the viability of isolated rat hepatocytes incubated under 95% O2-5% CO2 was evaluated. Decreasing the extracellular Ca++ concentration from 2 mM to 50 microM or less resulted in a progressive increase in cell injury as determined by lactate dehydrogenase (LDH) leakage. The generation of an oxidative stress, indicated by malondialdehyde formation, occurred before and concomitant with LDH leakage. The antioxidants vitamin E, N,N'-diphenyl-p-phenyl-enediamine, chlorpromazine and promethazine, as well as the iron chelators desferrioxamine and EDTA, all prevented both malondialdehyde production and LDH leakage induced by the absence of extracellular Ca++. A marked loss of cytosolic and mitochondrial glutathione was observed in cells incubated without Ca++, which could be significantly prevented by antioxidants and iron chelators. Similar effects on hepatocyte vitamin E levels also were noted. Addition of the Ca++ chelator ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid to the incubation medium totally prevented LDH leakage and malondialdehyde production and partially ameliorated glutathione and vitamin E loss. Conversely, cell injury resulting from disrupted cellular Ca++ homeostasis after treatment with the Ca++ ionophore A23187 plus 2 mM Ca++ was only slightly inhibited by antioxidants and iron chelators. However, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid also prevented A23187-induced cell injury. These results indicate that a decrease in extracellular Ca++ generates an oxidative stress in hepatocytes which leads ultimately to severe cell injury. This oxidative stress appears to be a Ca++-dependent phenomenon, precipitating all toxicity by a mechanism distinct from that induced by A23187 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3130475&dopt=Abstract
Immunopharmacology. 1988 Mar-Apr;15(2):117-22.
Influence of promethazine on immune reactions. I. Characterization of promethazine effects on natural killer cell-mediated cytotoxicity.
Rychlik G, Rychlik E, Wasik M.
Department of Experimental Immunosuppression, Warsaw School of Medicine, Poland.
Promethazine has been shown to possess definite immunosuppressive activity in clinical and experimental organ transplantation. However, there are few data concerning the mechanism of its influence on immune reactions. In the present studies promethazine was shown to inhibit natural killer cell-mediated cytotoxicity in vitro. Combined analysis of 51Cr-release and single-cell assays revealed that this agent affects some processes involved in delivering the 'lethal hit' but not the binding of target cells nor the recycling capacity of effector cells. The possible mechanism of promethazine action at the cellular level is discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3372227&dopt=Abstract
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