Drugs online research references
Pharm Weekbl Sci. 1985 Jun 21;7(3):121-4.
Degradation products of the promethazine radical cation.
De Mol NJ, Koenen J.
The degradation products of the promethazine radical cation, generated from promethazine with horseradish peroxidase/H2O2, have been investigated. Several products have been identified which resulted from fission of the bond between the two ethanamine carbon atoms of the N10 side chain. The main product (approx. 90%) was identified as 10-formyl-5-oxophenothiazine. The likely structure of three minor products was also elucidated. The degradation of the promethazine radical cation is different from that of radical cations derived from the propanamine side chain containing phenothiazine drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4022763&dopt=Abstract
Res Commun Chem Pathol Pharmacol. 1983 Jan;39(1):127-37.
(3H)-imipramine binding and plasmid replication sites in Escherichia coli.
Molnar J, Csiszar K, Toth G.
Binding of (3H)-imipramine to F'lac plasmid-carrying E.coli was studied. The binding was saturated at 500 mM imipramine in the case of F'lac cells, and the imipramine binding of plasmid-carrying bacteria was inhibited by several tricyclic compounds, such as acridine orange, desimpramine and promethazine. Methylene blue enhanced the (3H)-imipramine binding of bacteria. Binding of radioactively labelled pBR322 plasmid DNA to the internal membrane was more efficient in the presence of plasmid-eliminating drugs than in that of their ineffective derivatives. It is concluded that a structural association exists between imipramine binding and plasmid replication sites in bacteria. The plasmid DNA is assumed to bind irreversibly to its replication site in the presence of the drug and this process can lead to plasmid elimination.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6342080&dopt=Abstract
Res Commun Chem Pathol Pharmacol. 1985 Aug;49(2):215-28.
The effectiveness of antioxidants in reducing paracetamol-induced damage subsequent to paracetamol activation.
Harman AW.
Paracetamol toxicity was studied in isolated mouse hepatocytes. This drug produced a concentration- and time-dependent loss of cell viability. Exposure to 5 mM paracetamol produced a rapid fall in intracellular reduced glutathione (GSH) followed by a decrease in plasma membrane integrity. The antioxidant, diphenyl-p-phenylenediamine (DPPD) had no effect on either the loss of GSH, the binding of 14C-paracetamol metabolites to protein or the loss of plasma membrane integrity when hepatocytes were incubated in 5 mM paracetamol. When hepatocytes were exposed to paracetamol for 1 hr they showed a loss of plasma membrane integrity during the subsequent 7 hr incubation. DPPD, alpha-tocopherol and promethazine reduced this effect when added after the paracetamol exposure. It appears that paracetamol exposure initiates toxic events subsequent to the generation of the reactive metabolite but prior to cell death and that the progression of these events can be interrupted by compounds with antioxidant properties.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4059651&dopt=Abstract
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