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Dr Anne Colville

Image of Anne Colville
Research Assistant, School of Life Sciences
B.Sc (Hons) (Sydney U), M. Sc. (UTS), M.Sc. (Uni. Melb), PhD (UTS)
+61 2 9514 7841

Journal articles

Scott, P.D., Coleman, H.M., Colville, A., Lim, R., Matthews, B., McDonald, J.A., Miranda, A., Neale, P.A., Nugegoda, D., Tremblay, L.A. & Leusch, F.D.L. 2017, 'Assessing the potential for trace organic contaminants commonly found in Australian rivers to induce vitellogenin in the native rainbowfish (Melanotaenia fluviatilis) and the introduced mosquitofish (Gambusia holbrooki).', Aquat Toxicol, vol. 185, pp. 105-120.
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In Australia, trace organic contaminants (TrOCs) and endocrine active compounds (EACs) have been detected in rivers impacted by sewage effluent, urban stormwater, agricultural and industrial inputs. It is unclear whether these chemicals are at concentrations that can elicit endocrine disruption in Australian fish species. In this study, native rainbowfish (Melanotaenia fluviatilis) and introduced invasive (but prevalent) mosquitofish (Gambusia holbrooki) were exposed to the individual compounds atrazine, estrone, bisphenol A, propylparaben and pyrimethanil, and mixtures of compounds including hormones and personal care products, industrial compounds, and pesticides at environmentally relevant concentrations. Vitellogenin (Vtg) protein and liver Vtg mRNA induction were used to assess the estrogenic potential of these compounds. Vtg expression was significantly affected in both species exposed to estrone at concentrations that leave little margin for safety (p<0.001). Propylparaben caused a small but statistically significant 3 increase in Vtg protein levels (p=0.035) in rainbowfish but at a concentration 40 higher than that measured in the environment, therefore propylparaben poses a low risk of inducing endocrine disruption in fish. Mixtures of pesticides and a mixture of hormones, pharmaceuticals, industrial compounds and pesticides induced a small but statistically significant increase in plasma Vtg in rainbowfish, but did not affect mosquitofish Vtg protein or mRNA expression. These results suggest that estrogenic activity represents a low risk to fish in most Australian rivers monitored to-date except for some species of fish at the most polluted sites.
Mohammed Abdul, J., Colville, A.E., Lim, R.P., Vigneswaran, S. & Kandasamy, J.K. 2012, 'Use of duckweed (Lemna disperma) to assess the phytotoxicity of the products of Fenton oxidation of metsulfuron methyl', Ecotoxicology And Environmental Safety, vol. 83, pp. 89-95.
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Because of pressure on water supplies world-wide, there is increasing interest in methods of remediating contaminated ground waters. However, with some remediation processes, the breakdown products are more toxic than the original contaminant. Organic matter and salinity may also influence degradation efficiency. This study tested the efficiency of Fenton oxidation in degrading the sulfonylurea herbicide metsulfuron methyl (MeS), and tested the reaction products for phytotoxicity with the Lemna (duckweed) bioassay. The efficiency of degradation by Fenton&acirc;s reagent (Fe2&Atilde;&frac34; &Acirc;&frac14;0.09 mM; H2O2&Acirc;&frac14;1.76mM, 4 h) decreased with increasing initial MeS concentration, from 98% with 5 mg/L MeS, to 63% with 70 mg/L MeS. Addition of NaCl (10 mM) and organic matter (humic acid at 0.2 and 2.0 mg C/L as Total Organic Carbon) reduced the efficiency of degradation at low initial MeS concentrations (5 and 10mg/L), but had no effect at high concentrations. The residual Fenton&acirc;s reagent after Fenton&acirc;s oxidation was toxic to Lemna. After removal of residual iron and H2O2, the measured toxicity to Lemna in the treated samples could be explained by the concentrations of MeS as measured by HPLC/UV detection, so there was no evidence of additional toxicity or amelioration due to the by-products or formulation materials.
Pablo, F., Krassoi, R., Jones, P.R., Colville, A.E., Hose, G.C. & Lim, R.P. 2008, 'Comparison of the fate and toxicity of chlorpyrifos - Laboratory versus a coastal mesocosm system', Ecotoxicology And Environmental Safety, vol. 71, no. 1, pp. 219-229.
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The widespread use of chlorpyrifos for pest control in urban and rural environments poses a risk of contamination to aquatic environments via runoff, spray drift or spillage. The aim of this study was to assess the fate of chlorpyrifos and its toxicity t
Colville, A.E., Jones, P.M., Pablo, F., Krassoi, R., Hose, G.C. & Lim, R.P. 2008, 'Effects of chlorpyrifos on macroinvertebrate communities in coastal stream mesocosms', Ecotoxicology, vol. 17, no. 3, pp. 173-180.
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This study measured the effects of a single pulse of chlorpyrifos at nominal concentrations of 1 and 10 mu g/l on the macroinvertebrate community structure of a coastal stream mesocosm system. Analysis of data using Principal Response Curves (PRC) and Monte Carlo tests showed significant changes in the treated stream mesocosms relative to that of the controls. These changes in the macroinvertebrate assemblages occurred within 6 h, and persisted for at least 124 days after dosing. Significant community-level effects were detected at the lowest concentration on days 2 and 16 post-dosing, giving a no-observed effect concentration (NOECcommunity) of 1.2 mu g/l (measured). The mayflies Atalophlebia sp. and Koorrnonga sp., Chironomidae and Acarina were all sensitive to chlorpyrifos and decreased in abundance in treated mesocosms after dosing. The fauna of these coastal stream mesocosms showed similar sensitivity to chlorpyrifos with that of other reported studies, but there was no evidence of recovery after 124 days.
Colville, A.E. & Lim, R.P. 2003, 'Microscopic structure of the mantle and palps in the freshwater mussels Velesunio ambigus and Hyridella depressa (Bivalvia : Hyriidae)', Mulluscan Research, vol. 23, pp. 1-20.
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Burnstock, G., Campbell, G., Satchell, D. & Smythe, A. 1997, 'Evidence that adenosine triphosphate or a related nucleotide is the transmitter substance released by non-adrenergic inhibitory nerves in the gut. 1970.', British journal of pharmacology, vol. 120, no. 4 Suppl, pp. 337-357.
Sneddon, J.D., Smythe, A., Satchell, D. & Burnstock, G. 1973, 'An investigation of the identity of the transmitter substance released by non-adrenergic, non-cholinergic excitatory nerves supplying the small intestine of some lower vertebrates', Comparative and General Pharmacology, vol. 4, no. 13, pp. 53-60.
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1. 1. Non-adrenergic, non-cholinergic excitatory postganglionic fibres in the splanchnic nerves supply the small intestine of the toad (Bufo marinus) and the lizard (Tiliqua rugosa). 2. 2. 5-Hydroxytryptamine, histamine, bradykinin, and prostaglandin E1 have been rejected as the putative neurotransmitters in these nerves on the grounds that they do not have actions which parallel those of nerve stimulation or that drugs which antagonize their effects do not similarly antagonize the effects of nerve stimulation. 3. 3. ATP produces excitatory responses, which closely mimic those of non-adrenergic, non-cholinergic nerve stimulation. Quinidine causes parallel block of the responses to nerve stimulation and exogenously applied ATP, but this action may be non-specific. 4. 4. While the results do not provide direct evidence for purinergic excitatory nerves to the small intestine of lower vertebrates, they are consistent with the hypothesis. &copy; 1973.
Burnstock, G., Satchell, D.G. & Smythe, A. 1972, 'A comparison of the excitatory and inhibitory effects of non-adrenergic, non-cholinergic nerve stimulation and exogenously applied ATP on a variety of smooth muscle preparations from different vertebrate species.', British journal of pharmacology, vol. 46, no. 2, pp. 234-242.
1. The responses to non-adrenergic, non-cholinergic nerve stimulation have been compared with those to exogenously applied ATP on seventeen different tissues from a number of vertebrate classes.2. Stimulation of all the mammalian gut preparations studied (with the exception of the guinea-pig ileum) after blockade of the effects of adrenergic and cholinergic nerve stimulation by guanethidine (3.5 muM) and hyoscine (1.3 muM) caused inhibition; exogenously applied ATP mimicked this inhibitory response.3. Stimulation of the guinea-pig ileum in the presence of hyoscine and guanethidine, usually caused a diphasic response, relaxation followed by contraction; exogenously applied ATP mimicked this response, in contrast to acetylcholine and noradrenaline which caused excitation and relaxation respectively.4. Stimulation of preparations of lower vertebrate gut and guinea-pig bladder in the presence of hyoscine and guanethidine caused contraction; exogenously applied ATP mimicked this contractile response.5. In each preparation the time course of the response to ATP was similar or identical to the response to non-adrenergic, non-cholinergic nerve stimulation.6. The results are consistent with the hypothesis that a purine nucleotide may be the transmitter substance released from non-adrenergic, non-cholinergic nerves supplying smooth muscle preparations from a number of vertebrate classes.
Burnstock, G., Dumsday, B. & Smythe, A. 1972, 'Atropine resistant excitation of the urinary bladder: the possibility of transmission via nerves releasing a purine nucleotide.', British journal of pharmacology, vol. 44, no. 3, pp. 451-461.
1. The possibility that a purine nucleotide is involved in excitatory transmission to the urinary bladder has been tested. All the purine compounds tested which contained a pyrophosphate bond produced contraction, adenosine triphosphate (ATP) being the most potent. Adenosine and adenosine monophosphate caused relaxation.2. The response to ATP closely mimicked the nerve-mediated contraction, both being characterized by a rapid contraction which was not maintained. A lack of sensitivity to ATP was noted in some preparations of the rat urinary bladder.3. Both nerve-mediated contractions and contractions caused by ATP were blocked by quinidine, while the response to acetylcholine persisted.4. Nerve-mediated responses were depressed during tachyphylaxis produced by high concentrations of ATP. Tachyphylaxis did not occur when low concentrations were used. Possible explanations for these results are discussed.5. The results are consistent with the hypothesis that non-cholinergic excitatory nerves to the guinea-pig bladder release a purine nucleotide, but do not provide critical evidence for it.
Burnstock, G., Campbell, G., Satchell, D. & Smythe, A. 1970, 'Evidence that adenosine triphosphate or a related nucleotide is the transmitter substance released by non-adrenergic inhibitory nerves in the gut.', British journal of pharmacology, vol. 40, no. 4, pp. 668-688.
1. Stimulation of the vagal non-adrenergic inhibitory innervation caused the release of adenosine and inosine into vascular perfusates from the stomachs of guinea-pigs and toads.2. Stimulation of portions of Auerbach's plexus isolated from turkey gizzard caused the release of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP).3. ATP, added to solutions perfused through the toad stomach vasculature, was broken down to adenosine, inosine and adenine.4. Of a series of purine and pyrimidine derivatives tested for inhibitory activity on the guinea-pig isolated taenia coli, ATP and ADP were the most potent.5. ATP caused inhibition of twelve other gut preparations previously shown to contain non-adrenergic inhibitory nerves. The inhibitory action of ATP was not prevented by tetrodotoxin.6. Quinidine antagonized relaxations of the guinea-pig taenia coli caused by catecholamines or adrenergic nerve stimulation. Higher concentrations of quinidine antagonized relaxations caused by ATP or non-adrenergic inhibitory nerve stimulation.7. When tachyphylaxis to ATP had been produced in the rabbit ileum, there was a consistent depression of the responses to non-adrenergic inhibitory nerve stimulation but not of responses to adrenergic nerve stimulation.8. It is suggested that ATP or a related nucleotide is the transmitter substance released by the non-adrenergic inhibitory innervation of the gut.