Investigations of Amavadin.
The development of the understanding of the co-ordination chemistry and the properties of Amavadin, the chemical form in which vanadium is accumulated by the Amanita genus of mushrooms, is reviewed.
Amanita↗
Biomedical subjects
J J Cooney
Publications and source records attributed to J J Cooney.
Action of inorganic tin and organotins on a hydrocarbon-using yeast, Candida maltosa.
Two inorganic tin compounds, as well as mono- and tri-substituted methyl-, butyl-, and phenyltins were examined for their interactions with a hydrocarbon-using strain of Candida maltosa. Neither of the inorganic tins (SnII and SnIV) inhibited growth at concentrations up to 0.8 mM while binding to the yeast cells occurred to levels of 0.3 and 0.23 mM Sn/g cells, respectively. Neither inorganic tin caused leakage of potassium from the yeast cells. Among the organotins, tributyl- and triphenyltins caused total viability loss and near maximum potassium loss at initial concentrations of 0.08 mM. For these compounds binding to the cells increased with increasing initial concentrations to maximum values of 0.51 and 0.65 mM Sn/g cells respectively. The other organotin compounds were not inhibitory and did not cause potassium leakage from the cells. Tin from them became cell associated only in the cases of monobutyl- and monophenyl tin, which were bound at markedly lower levels (<0.1 mM Sn/g cells). These results are consistent with the conclusion that the inhibitory compounds can act on the yeast cell membrane but, although binding to the cells is a prerequisite for growth inhibition and cell leakage, no simple correlation was established between binding levels and toxicity effects.
Candida↗
Quantifying effects of antifouling paints on microbial biofilm formation.
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Biofilms↗
Organotin compounds and their interactions with microorganisms.
Organotin compounds are ubiquitous in the environment. The general order of toxicity to microorganisms increases with the number and chain length of organic groups bonded to the tin atom. Tetraorganotins and inorganic tin have little toxicity. Because of their lipophilicity, organotins are regarded as membrane active. There is evidence that the site of action of organotins may be both at the cytoplasmic membrane and intracellular level. Consequently, it is not known whether cell surface adsorption or accumulation within the cell, or both is a prerequisite for toxicity. Biosorption studies on a fungus, cyanobacteria, and microalgae indicates that cell surface binding alone occurred in these organisms, while studies on the effects of TBT (tributyltin) on certain microbial enzymes indicated that in some bacteria TBT can interact with cytosolic enzymes. Microorganism-organotin interactions are influenced by environmental conditions. In aquatic systems, both pH and salinity can determine organotin speciation and therefore reactivity. These environmental factors may also alter selectivity for resistant microorganisms in polluted systems. Tin-resistant microorganisms have been identified, and resistance can be either plasmid or chromosomally mediated. In one TBT-resistant organism, an Altermonas sp., an efflux system was suggested as the resistance mechanism. Biotransformation of organotin compounds by debutylation or methylation has been observed. These reactions may influence the toxicity, mobility, and environmental fate of organotin compounds.
Bacteria↗
Tracing the interaction of bacteriophage with bacterial biofilms using fluorescent and chromogenic probes.
Phages T4 and E79 were fluorescently-labeled with rhodamine isothiocyanate (RITC), fluoroscein isothiocyanate (FITC), and by the addition of 4'6-diamidino-2-phenylindole (DAPI) to phage-infected host cells of Escherichia coli and Pseudomonas aeruginosa. Comparisons of electron micrographs with scanning confocal laser microscope (SCLM) images indicated that single RITC-labeled phage particles could be visualized. Biofilms of each bacterium were infected by labeled phage. SCLM and epifluorescence microscopy were used to observe adsorption of phage to single-layer surface-attached bacteria and thicker biofilms. The spread of the recombinant T4 phage, YZA1 (containing an rII-LacZ fusion), within a lac E. coli biofilm could be detected in the presence of chromogenic and fluorogenic homologs of galactose. Infected cells exhibited blue pigmentation and fluorescence from the cleavage products produced by the phage-encoded beta-galactosidase activity. Fluorescent antibodies were used to detect non-labeled progeny phage. Phage T4 infected both surface-attached and surface-associated E. coli while phage E79 adsorbed to P. aeruginosa cells on the surface of the biofilm, but access to cells deep in biofilms was somewhat restricted. Temperature and nutrient concentration did not affect susceptibility to phage infection, but lower temperature and low nutrients extended the time-to-lysis and slowed the spread of infection within the biofilm.
Bacteriophage T4↗
Lytic infection of Escherichia coli biofilms by bacteriophage T4.
Escherichia coli 3000 XIII formed biofilms on the surface of polyvinylchloride coupons in a modified Robbins device. Bacteriophage T4D+ infected cells in the biofilm and replicated. It is commonly held that bacteriophage cannot infect surface-attached bacteria (biofilms) because such bacteria are protected by an exopolymeric matrix that binds macromolecules and prevents their diffusion into the biofilm. To our knowledge this is the first observation that a bacteriophage can infect and multiply within cells growing as a biofilm.
Bacteriolysis↗
Tributyltin-resistant bacteria from estuarine and freshwater sediments.
Resistance to tributyltin (TBT) was examined in populations from TBT-polluted sediments and nonpolluted sediments from an estuary and from fresh water as well as in pure cultures isolated from those sediments. The 50% effective concentrations (EC50s) for populations were higher at a TBT-polluted freshwater site than at a site without TBT, suggesting that TBT selected for a TBT-resistant population. In contrast, EC50s were significantly lower for populations from a TBT-contaminated estuarine site than for those from a site without TBT, suggesting that other factors in addition to TBT determine whether populations become resistant. EC50s for populations from TBT-contaminated freshwater sediments were nearly 30 times higher than those for populations from TBT-contaminated estuarine sediments. We defined a TBT-resistant bacterium as one which grows on trypticase soy agar containing 8.4 microM TBT, a concentration which prevented the growth of 90% of the culturable bacteria from these sediments. The toxicity of TBT in laboratory media was influenced markedly by the composition of the medium and whether it was liquid or solid. Ten TBT-resistant isolates from estuarine sediments and 19 from freshwater sediments were identified to the genus level. Two isolates, each a Bacillus sp., may be the first gram-positive bacteria isolated from fresh water in the presence of a high concentration of TBT. There was a high incidence of resistance to heavy metals: metal resistance indices were 0.76 for estuarine isolates and 0.68 for freshwater isolates.(ABSTRACT TRUNCATED AT 250 WORDS)
Copper↗
Effect of organotins on fecal pollution indicator organisms.
Pure cultures of Escherichia coli and Streptococcus faecalis and environmental water samples were examined for the possibility that pollution involving organotin compounds could decrease the values for indicator organisms when standard methods were applied to the analysis of water samples. (CH3)2SnCl2 and (CH3)3SnCl decreased viable counts at about 10 to 100 mg of Sn liter-1 (8.4 X 10(-5) to 8.4 X 10(-4) mol of Sn liter-1), and tributyltin chloride was effective at about 0.1 to 1.0 mg of Sn liter-1 (8.4 X 10(-7) to 8.4 X 10(-6) mol of Sn liter-1. These concentrations, particularly for the methyltin compounds, are greater than the concentrations reported to date for these compounds in aquatic ecosystems. Thus, organotin compounds alone would not be likely to cause reductions in counts of indicator organisms measured by standard methods. However, it is suggested that, when combined with other environmental stressors or upon long exposure, organotins such as butyltins may contribute to the injury of indicator organisms.
Enterococcus faecalis↗
Replica plating method for estimating phenanthrene-utilizing and phenanthrene-cometabolizing microorganisms.
A replica plating method was developed for detecting and enumerating phenanthrene-degrading microorganisms. The method is designed to discriminate between aquatic organisms that utilize phenanthrene as the sole carbon and energy source and organisms that cometabolize phenanthrene. The method was used to demonstrate that phenanthrene utilizers and phenanthrene cometabolizers coexist in estuarine sediments.
Journal Article↗
Factors affecting the toxic effect of tin on estuarine microorganisms.
Inorganic tin (SnCl(4).H(2)O) is toxic to microbial populations obtained from estuarine sediments plated on nutrient medium solidified with either agar or purified agar. The use of gelatin as a gelling agent decreased the apparent toxicity of tin, and toxicity was markedly reduced in medium solidified with silica gel. There was no evidence that toxic agar-tin complexes were involved. Cd, Cu, Pb, Ni, and Zn exhibited similar toxicity patterns; therefore, toxicity levels determined in the laboratory should be extrapolated to the environment with caution. The addition of cysteine to the medium had no effect on tin toxicity. Serine or 3-hydroxyflavone enhanced toxicity, while humic acids or gelatin inhibited toxicity. Replacement of SO(4) with NO(3) did not alter tin toxicity, but replacement of Cl with NO(3) decreased tin toxicity. Thus, the toxic effect(s) of tin depend as much on the chemical speciation of the metal as on the total concentration of the metal in the medium.
Journal Article↗
Tin and tin-resistant microorganisms in chesapeake bay.
Sediment and water samples from nine stations in Chesapeake Bay were examined for tin content and for microbial populations resistant to inorganic tin (75 mg of Sn liter as SnCl(4).5H(2)O) or to the organotin compound dimethyltin chloride [15 mg of Sn liter as (CH(3))(2)SnCl(2)]. Tin concentrations in sediments were higher (3.0 to 7.9 mg kg) at sites impacted by human activity than at open water sites (0.8 to 0.9 mg kg), and they were very high (239.6 mg kg) in Baltimore Harbor, which is impacted by both shipping and heavy industry. Inorganic tin (75 mg Sn liter) in agar medium significantly decreased viable counts, but its toxicity was markedly reduced in liquid medium; it was not toxic in medium solidified with silica gel. Addition of SnCl(4).5H(2)O to these media produced a tin precipitate which was not involved in the metal's toxicity. The data suggest that a soluble tin-agar complex which is toxic to cells is formed in agar medium. Thus, the toxicity of tin depends more on the chemical species than on the metal concentration in the medium. All sites in Chesapeake Bay contained organisms resistant to tin. The microbial flora was more sensitive to (CH(3))(2)SnCl(2) than to SnCl(4).5H(2)O. The elevated level of tin-resistant microorganisms in some aeas not containing unusually high tin concentrations suggests that factors other than tin may participate in the selection for a tin-tolerant microbial flora.
Journal Article↗
Inhibition of carotenoid synthesis in Micrococcus roseus.
Micrococcus roseus forms bicyclic keto-carotenoids. The effects of nicotine, piperonyl butoxide, and 2-(4-chlorophenylthio)-triethylamine hydrochloride (CPTA) were studied with regard to their ability to selectively inhibit carotenogenesis in the organism. Nicotine caused accumulation of beta-zeacarotene; piperonyl butoxide caused accumulation of phytoene and traces of phytofluene, zeta-carotene, and beta-zeacarotene. In both cases canthaxanthin biosynthesis was inhibited. CPTA inhibited canthaxanthin synthesis and caused accumulation of beta-zeacarotene and gamma-carotene and their mono- and di-hydroxy derivatives. Regardless of the inhibitor used, canthaxanthin was the major colored carotenoid biosynthesized. The expected precursors of carotenoid cyclization, neurosporene and (or) lycopene, were not detected in CPTA- or nicotine-inhibited cultures. Therefore, carotenoid cyclization in M. roseus does not involve neurosporene or lycopene and must occur early in carotene biosynthesis, prior to the formation of beta-zeacarotene, zeta-Carotene is proposed as the cyclization substrate and beta-zeacarotene as the substrate for oxygen insertion.
Carotenoids↗
Photokilling of Micrococcus roseus.
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Light↗
Inhibition of glucose metabolism by n-hexadecane in Cladosporium (Amorphotheca) resinae.
When Cladosporium resinae is provided with n-hexadecane and glucose, n-hexadecane is used preferentially. Studies using [14C]glucose indicated that n-hexadecane did not inhibit glucose uptake but did retard oxidation of glucose to CO2 and assimilation of glucose carbon into trichloroacetic acid-insoluble material. Glucose could be recovered quantitatively from hydrocarbon-grown cells that had been transferred to glucose. Four enzymes that may be involved in glucose metabolism, hexokinase, glucose-6-phosphate dehydrogenase, glucose-phosphate isomerase, and succinate dehydrogenase, were not detected in cells grown on hexadecane but were present in cells grown on glucose. Addition of hexadecane to extracts of glucose-grown cells resulted in immediate loss of activity for each of the four enzymes, but two other enzymes did not directly involved in glucose metabolism, adenosine triphosphatase and alanine-ketoacid aminotransferase, were not inhibited by hexadecane in vitro. Cells grown on hexadecane and transferred to glucose metabolize intracellular hexadecane; after 1 day, activity of hexokinase, glucose-6-phosphate dehydrogenase, glucosephosphate isomerase, and succinate dehydrogenase could be detected and 22% of the intracellular hydrocarbon had been metabolized. Hexadecane-grown cells transferred to glucose plus cycloheximide showed the same level of activity of all the four enzymes as cells transferred to glucose alone. Thus, intracellular n-hexadecane or a metabolite of hexadecane can inthesis of those enzymes is not inhibited.
Adenosine Triphosphatases↗
Effects of poorly metabolized hydrocarbons on substrate oxidation by Cladosporium resinae.
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Alkanes↗
Action of visible light on enzymes in cell envelopes of Micrococcus roseus.
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Carotenoids↗
Extracellular lipids of Cladosporium (Amorphotheca) resinae grown on glucose or on n-alkanes.
Cladosporium (Amorphotheca) resinae was grown in shake culture on glucose, n-dodecane, or n-hexadecane. Growth was most rapid on glucose, and more acid accumulated in the medium than in n-alkane-grown cultures. Neutral lipid was the major lipid fraction and triglycerides were the only extracellular neutral lipids detected. Dodecanoic (lauir) acid was the predominant fatty acid (greater than 60%) in neutral lipids from all three media, with lesser amounts of tetradecanoic, hexadecanoic, and octadecanoic acids. Extracellular phospholipids identified were phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine, and cardiolipin or a cardiolipin-like compound. Phospholipids from all three media contained dodecanoic acid as their principle fatty acid. Dodecanoic acid was the only extracellular free fatty acid detected. Glucose medium contained acetic, glyoxylic, and glycolic acids and an unidentified organic acid which may contribute to the lower pH in cultures after growth on glucose. In all classes of extracellular lipids the fatty acids do not correspond to the fatty acids previously determined to be associated with cellular lipids. Moreover, the fatty acids of extracellular lipids do not reflect the chain length of the n-alkane growth substrate.
Acetates↗
Phospholipids of Cladosporium resinae cultured on glucose and on n-alkanes.
Cladosporium resinae was grown on glucose, on n-dodecane, and on n-hexadecane. Total lipid was greatest in dodecane-grown cells and least in hexadecane-grown cells, while glucose-grown cells contained the most phospholipid and hexadecane-grown cells contained the least. Cells from all three media contained phosphatidylethanolamine and phosphatidylcholine as their major phospholipids, with lesser amounts of phosphatidylserine and traces of a cardiolipin-like compound. The major fatty acids associated with each phospholipid were palmitic acid and one or more 18-carbon unsaturated fatty acids. There was no correlation between n-alkane growth substrate and fatty acyl components of cellular phospholipids.
Alkanes↗