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PubMed1974

Development of a selective enterococcus medium based on manganese ion deficiency, sodium azide, and alkaline pH.

Rogosa broth, without its salt supplement and dissolved in deionized water, was adapted for the selective isolation and enumeration of enterococci. This medium supported good growth of enterococci, but it suppressed growth of other lactic acid bacteria. The sensitivity and specificity of the medium were tested after addition of various increasing concentrations of NaN(3) against known strains of enterococci and other bacteria. Many strains of Streptococcus faecium showed low azide tolerance; optimal growth was obtained at a concentration of 0.01% NaN(3), which totally or partially inhibited unrelated species of lactic acid bacteria. The selectivity of the medium was further increased by pH adjustment to 9.6. Carbonate and Tween 80 were added to overcome partial inhibition of enterococcal growth by the new combination of selective conditions. The final medium was evaluated in agar form in isolations from human and animal feces, polluted water, meat, and dairy products. Counts were obtained after 16 to 17 h of incubation at 37 C. The isolates satisfactorily conformed to the group characteristics of enterococci.

Azides↗
PubMed1990

Novel effect of azide on sodium channel of Xenopus oocytes.

Bath application of a few mM of sodium azide to a voltage clamped oocyte activated a voltage dependent Na+ current. Characteristics of the azide-induced current were the same as those of already described Na+ current induced by prolonged depolarization. The Na+ current induced either by azide or depolarization was suppressed by the application of Ca2+ channel blockers (Diltiazem and La3+). Azide is known to affect some metabolic processes (ATP and cGMP production etc.), but the present effect could not be attributed to metabolic actions.

Animals↗
PubMedDate not supplied

Metabolic activation and deactivation of mutagens and carcinogens.

The activity of some mutagens has been investigated in the Salmonella test either in the absence or in the presence of fortified rat liver microsomal fractions, together with an NADPH-generating system. With respect to their metabolic reactivity, the compounds tested could be distinguished according to four reproducible trends: (a) conversion of inert compounds into mutagenic metabolites (e.g. 2-aminofluorene and benzo(a)pyrene); (b) further enhancement of mutagenicity (e.g. 1,2-epoxybutane); (c) no effect on mutagenicity (e.g. glycidol, folpet, nitrofurantoin and 2-nitronaphtalene); (d) slight decrease (e.g. 1,1,1-trichlor 2,3-propenoxide), marked decrease (e.g. sodium nitrite, 5-nitro-2-furoic acid and captan) or even complete reversal of mutagenicity (e.g. styrene oxide, sodium azide, sodium dichromate and other Cr6+ compounds). The Salmonella/microsome test was effective in discriminating not only the mutagenic activity but also the metabolic reactivity of structurally related chemicals (e.g. the fungicides captan and folpet). In some cases, mutagens were tested also in the presence of other biological preparations (e.g. rat muscle or lung microsomal preparations, human gastric juice, serum, plasma or erythrocyte lysates). The mutagenic and metabolic properties of largely used products (e.g. an antibacterial drug containing nitrofurantoin and laboratory reagents containing sodium azide) have been also checked. The mechanisms underlying the metabolic behaviour of some of the mutagens tested have been reported. The results obtained have been correlated with the literature data on their carcinogenicity. Although these in vitro findings are only indicative of the possible metabolic fate of mutagens in the whole organism, the observed effects may be useful in order to explain the epidemiological data and the results of animal tests, and to assess the possible health hazards of mutagens.

Animals↗