Drugs online research references
Can J Physiol Pharmacol. 1980 Sep;58(9):1114-6.
Effects of histamine on rat isolated atria.
Laher I, McNeill JH.
The effects of histamine were studied in atria obtained from untreated and reserpine-pretreated rats. At high doses, histamine caused a positive chronotropic response that was not antagonized by either promethazine or cimetidine. In the presence of propranolol or in atria from reserpine-pretreated rats histamine caused an atropine-sensitive negative chronotropic response. Large doses of histamine also caused a positive inotropic response in left atria that were antagonized by the beta adrenoceptor antagonist propranolol. Reserpine pretreatment abolished the inotropic response of histamine in the rat heart. The results indicate that in large doses histamine causes an indirect stimulation of beta adrenoceptors (right and left atrium) by releasing endogenous noradrenaline and of muscarinic receptors (right atrium) by releasing acetylcholine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7459701&dopt=Abstract
Arch Biochem Biophys. 1987 Dec;259(2):372-81.
Delayed, ferrous iron-dependent peroxidation of rat liver microsomes.
Goddard JG, Sweeney GD.
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Measurement of both chemiluminescence (CL) and the formation of 2-thiobarbituric acid-reacting substances (TBAR) has been used to study the delayed, nonenzymatic lipid peroxidation (LP) initiated in rat liver microsomes by ferrous chloride. Following Fe2+ addition, the CL technique revealed a burst of light emission (peak, Phase II) which was preceded by a period of little or no detectable photon production (delay, Phase I) and succeeded by an increased emission (Phase III). Analysis of TBAR indicated a low rate of LP during the delay which increased more than fivefold during a 1-min period and which corresponded to the CL peak. The delay length depended on both the Fe2+ concentration and the microsome concentration; increased Fe2+ yielded longer delays while increased microsome concentration decreased the delay. As reported by others [J. R. Bucher, M. Tien, and S. D. Aust (1983) Biochem. Biophys. Res. Commun. 111, 777-784; J. M. Braughler, L. A. Duncan, and R. L. Chase (1986) J. Biol. Chem. 261, 10282-10289], Fe3+ also decreased the delay. The ferric-nitrilotriacetate (Fe3+-NTA) complex was found to be more efficient than "free" Fe3+ [Fe(NO3)3]; a 100 microM concentration of the 1:1 Fe3+-NTA complex eliminated the delay due to 100 microM Fe2+, whereas 400 microM Fe(NO3)3 reduced the delay from 17.5 to 2.5 min. Incubation under reduced O2 tension demonstrated a requirement for O2 during the delay. The use of antioxidants [butylated hydroxytoluene, (+)-catechin, promethazine, and uric acid] and inhibitors of the Haber-Weiss reaction (mannitol, Tris buffer, dimethyl sulfoxide, catalase, and superoxide dismutase) indicated that the initiating species has characteristics of a weak oxidizing radical capable of either hydrogen or electron abstraction from suitable target molecules. We hypothesize that the delay that is sensitive to the Fe2+:microsome ratio is due to reductive elimination of the initiating species by "free" Fe2+. The nature of the initiating species has yet to be determined; however, the argument is presented that the perferryl ion (Fe3+-O2-.) may possess the characteristics required for the initiator.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3426233&dopt=Abstract
Cell Biol Toxicol. 1991 Apr;7(2):129-43.
Biochemical changes in isolated hepatocytes exposed to tert-butyl hydroperoxide. Implications for its cytotoxicity.
Buc-Calderon P, Latour I, Roberfroid M.
Unite de Biochimie Toxicologique et Cancerologique Ecole de Pharmacie, Universite Catholique de Louvain, Bruxelles, Belgium.
When isolated hepatocytes were exposed to tert-butyl hydroperoxide (tBOOH) they lost their cellular membrane integrity. Decreased levels of GSH, increased phosphorylase a activity (an indirect index of the amount of free cytosolic Ca2+), and increase in the formation of malondialdehyde (MDA)-like products (an index of lipid peroxidation) preceded the release into the culture medium of the cytosolic enzyme lactate dehydrogenase (LDH), indicating that this later process was the consequence of the former intracellular events. While ATP levels were not modified during the incubation of cells with increasing concentrations of tBOOH, protein synthesis was decreased in a concentration-dependent manner. The glycogen content decreased at the same time as the increase in LDH leakage. The addition of promethazine (PMZ) an antioxidant molecule, prevented the lipid peroxidation, but did not protect cells against the oxidative effects of tBOOH, including loss of membrane integrity. Nevertheless, the addition of GSH to cell suspensions incubated with tBOOH, decreased the formation of MDA-like products, restored the protein synthesis rate, prevented partially the activation of phosphorylase a and preserved cell viability. On the basis of these results, we postulate that both GSH depletion and modification in phosphorylase a activity (Ca2+ levels) were the most relevant intracellular events to explain the cytotoxicity of tBOOH.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1889005&dopt=Abstract
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