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Biomedical subjects

I G Robertson

Publications and source records attributed to I G Robertson.

42 records · Page 3Linked to original sources
PubMed1982

A comparison of the requirements for antitumour activity and antibacteriophage lambda activity for a series of non-intercalative DNA-binding agents.

A series of non-intercalative DNA-binding agents, comprising mainly bisquaternary ammonium heterocyclic compounds, has been found to inhibit strongly the production of bacteriophage lambda following its induction in Escherichia coli. The inhibition is much greater than that found with a number of DNA intercalating agents, including 9-aminoacridine, ethidium and Daunorubicin. The inhibition correlated significantly with antitumour effect, as measured in a life extension assay with L1210 leukaemia. Activity in both biological systems demanded the presence of strongly charged groups and a rigid co-planar aromatic skeleton, these requirements being almost identical to those needed to displace ethidium efficiently from DNA in a simple assay system. It is suggested that biological activity is associated with the ability of these agents to bind in the minor groove of the DNA double helix. Data on the antibacteriophage action of one of these agents suggests possible models for antitumour activity.

Animals↗
PubMed1982

Selective activation of some dihydrodiols of several polycyclic aromatic hydrocarbons to mutagenic products by prostaglandin synthetase.

The ability of prostaglandin synthetase (PGS) to cooxidize benzo(a)pyrene, benzo(a)anthracene, chrysene, and several of their dihydrodiol derivatives to mutagenic products was tested with Salmonella typhimurium strains TA98 and TA100. The microsomal fraction of ram seminal vesicles, a known source of PGS, in the presence of the PGS substrate arachidonic acid, metabolized benzo(a)pyrene-7,8-dihydrodiol, benzo(a)anthracene-3,4-dihydrodiol, and chrysene-1,2-dihydrodiol to mutagenic products. This activity was inhibited by the PGS inhibitor indomethacin. Unlike the PGS system, however, a cytochrome P-450-reduced nicotinamide adenine dinucleotide phosphate-dependent system, present in an Aroclor 1254-induced rat liver 9000 x g supernatant fraction, also activated the parent compounds [benzo(a)pyrene, benzo(a)anthracene, chrysene] and several other benzo(a)anthracene dihydrodiols (the 1,2-dihydrodiol, the 8,9-dihydrodiol, and the 10,11-dihydrodiol). The chrysene trans-3,4, trans-5,6, and cis-5,6 diols were not activated to mutagens by either system. Thus, the PGS system appears to be more selective than does the cytochrome P-450 system in the activation of polycyclic aromatic hydrocarbons to mutagenic products, activating only those dihydrodiols with adjacent double bonds in the bay region from which the bay-region diol-epoxides are formed.

Animals↗
PubMed1981

A rapid and simple scheme for confirmation of Salmonella tester strain phenotype.

A simple scheme has been developed for confirming the phenotype of the standard set of Salmonella typhimurium tester strains. This scheme employs a series of filter paper discs impregnated with diagnostic mutagens or bacterial toxins. Up to 6 diagnostic discs can be placed on a petri dish to test a single Salmonella strain. The Salmonellae are distinguished by their responses to ampicillin, crystal violet, nitrofuratoin, 9-aminoacridine, 4-nitro-o-phenylenediamine and sodium azide.

Bacteriological Techniques↗
PubMed1979

Giant cell arteritis of the female genital tract.

In a patient who had a hysterectomy and bilateral salpingo-oophorectomy for endometrial adenocarcinoma, a giant cell arteritis was found in many of the myometrial and tubal vessels and in a few of the small arteries of the cervix and ovaries. On subsequent questioning, a history of treatment for polymyalgia rheumatica during the preceding 12 months was elicited. Of the three previously reported patients with giant cell arteritis of the uterus, two were suffering from polymyalgia rheumatica whilst one possibly had disseminated visceral giant cell arteritis.

Female↗
PubMedDate not supplied

Metabolism of the experimental antitumor agent acridine carboxamide in the mouse.

The metabolism of the experimental antitumor agent acridine carboxamide (AC) has been examined in the male BDF1 mouse. [3H]AC was administered at the optimal single intraperitoneal dose for antitumor activity (410 mumol/kg body weight) and the metabolites in urine, bile, and feces characterized using reversed-phase HPLC. In urine (0-24 hr) the main product appears to be a glucuronide, also present in bile, with lesser amounts of AC, AC-N-oxide, and at least 10 minor products. Biliary excretion of AC metabolites (examined after removal of the gallbladder at the appropriate times) is greatest at 1-2 hr after treatment when at least 14 products are detected, including AC, AC-N-oxide, and other products with UV/visible spectra characteristic of ring hydroxylated and/or acridone derivatives. In feces (0-24 hr) no AC-N-oxide is detected, the major metabolites being two polar species and AC. These polar species are both present in urine and bile where they are increased on incubation with crude beta-glucuronidase. These aglycones have been identified as the 7-hydroxy-9(10H)acridone derivatives of AC and N-monomethyl-AC by [1H]NMR and mass spectrometry. Thus the main pathways of elimination of AC appear to be 1) N-oxidation and 2) 9(10H)acridone formation plus 7-hydroxylation of both AC and its N-demethylated product followed by glucuronidation. Reduction of AC-N-oxide in the gut may allow reabsorption of AC. Both the back-reduction and reabsorption of AC, and enterohepatic circulation of the 7-hydroxyacridone derivatives may contribute to the slow elimination of AC metabolites.

Acridines↗