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Biomedical subjects

G A Burton

Publications and source records attributed to G A Burton.

At least 19 recordsLinked to original sources
PubMed2002

Biological responses of Lumbriculus variegatus exposed to fluoranthene-spiked sediment.

Lumbriculus variegatus was used as a bioassay organism to examine the impact of the sediment-associated polycyclic aromatic hydrocarbon (PAH) fluoranthene on behavior, reproduction, and toxicokinetics. The number of worms increased between the beginning and end of the experiment at 59 microg x g(-1) fluoranthene, but at the next higher treatment (108 microg x g(-1)) the number of worms found was lower and not different from the control. Worms exposed to 95 microg x g(-1) also exhibited increased reproduction when fed a yeast-cerophyl-trout chow mixture. On a total biomass basis, only the 95 microg x g(-1) exposure with food exhibited a statistically significant increase over the nonfed control. Evaluation of reproduction at the two highest treatments was compromised by a brief aeration failure 2 days before the end of the experiment. The behavioral responses were followed as changes in biological burial rate (sediment reworking rate) of a 137Cs-labeled marker layer. The biological burial rate increased toward a plateau as the concentration increased from the control (3.9 microg x g(-1) dry weight total PAH) to 355 microg x g(-1) dry weight fluoranthene in sediment. The aeration failure had minimal impact on the determination of reworking rate because all the data for the rate determination were collected prior to the aeration failure. Uptake and elimination rates declined with increasing treatment concentration across the range of fluoranthene concentrations, 59-355 microg x g(-1) dry weight sediment. The disconnect between the increasing biological burial rates and the decreasing toxicokinetics rates with increasing exposure concentration demonstrates that the toxicokinetic processes are dominated by uptake and elimination to interstitial water. The bioaccumulation factor (concentration in the organisms on a wet weight basis divided by the concentration in sediment on a dry weight basis) ranged from 0.92 to 1.88 on day 10 and declined to a range of 0.52 to 0.99 on day 28 with the lowest value at the highest dose.

Animals↗
PubMed1999

Physiologically based pharmacokinetic modeling of inhaled trichloroethylene and its oxidative metabolites in B6C3F1 mice.

A physiologically based pharmacokinetic (PBPK) model for inhaled trichloroethylene (TCE) was developed for B6C3F1 mice. Submodels described four P450-mediated metabolites of TCE, which included chloral hydrate (CH), free and glucuronide-bound trichloroethanol (TCOH-f and TCOH-b), trichloroacetic acid (TCA), and dichloroacetic acid (DCA). Inhalation time course studies were carried out for calibration of the model by exposing mice to TCE vapor concentrations of either 100 or 600 ppm for 4 h. At several time points, mice were euthanized and blood, liver, kidney, lung, and fat were collected and analyzed for TCE and its oxidative metabolites. Peak blood TCE concentrations were 0.86 and 7.32 microgram/mL, respectively, in mice exposed to 100 and 600 ppm TCE. The model overpredicted the mixed venous blood and tissue concentrations of TCE for mice of both exposure groups. Fractional absorption of inhaled TCE was proposed to explain the discrepancy between the model predictions and the TCE blood time course data. When fractional absorption (53%) of inhaled TCE was incorporated into the model, a comprehensive description of the uptake, distribution, and clearance of TCE in the blood was obtained. Fractional uptake of inhaled TCE was further verified by collecting TCE in exhaled breath following a 4-h constant concentration exposure to TCE and validation was provided by testing the model against TCE blood concentrations from an independent data set. The submodels adequately simulated the distribution and clearance kinetics of CH and TCOH-f in blood and the lungs, TCOH-b in the blood, and TCA and DCA, which were respectively detected for up to 43 and 14 h postexposure in blood and livers of mice exposed to 600 ppm TCE. This is the first extensive tissue time course study of the major metabolites of TCE following an inhalation exposure to TCE and the PBPK model predictions were in good general agreement with the observed kinetics of the oxidative metabolites formed in mice exposed to TCE concentrations of 100 and 600 ppm.

Adipose Tissue↗
PubMed1999

Sediment toxicity and stormwater runoff in a contaminated receiving system: consideration of different bioassays in the laboratory and field.

Several field and laboratory assays were employed below an urban storm sewer outfall to define the relationship between stormwater runoff and contaminant effects. Specifically, two bioassays that measure feeding rate as a toxicological endpoint were employed in the field and in the laboratory, along with bioassays measuring survival and growth of test organisms. In 7 to 10 d in situ exposures, amphipod leaf disc processing, growth and survival were monitored. Different exposure scenarios were investigated by varying the mesh size (74 microns or 250 microns mesh) and method of deployment (water column, sediment surface, or containing sediment) of in situ exposure chambers. Hyalella azteca, Daphnia magna, and Pimephales promelas survival were monitored in 48 h in situ exposures. Feeding inhibition was investigated via enzyme inhibition of H. azteca and D. magna and via leaf disc processing measurements of the detritivore H. azteca. Additionally, we investigated the extent of phototoxicity at this site via field exposures in sun and shade and laboratory exposures with and without UV light. The measurement of detritivore leaf disc processing, and thus its usefulness as an endpoint, was hindered by individual variability in the amount of leaf consumed and by leaf weight gain during the summer field exposures. For D. magna, enzyme inhibition measured in a laboratory exposure did not reveal the toxicity observed in field exposures. For H. azteca, enzyme inhibition measured in the laboratory indicated toxicity similar to that observed in short term chronic in situ exposures. Enzyme inhibition also did not detect differences in toxicity due to variations in flow conditions. There were no statistically significant effects of any exposure on P. promelas survival or H. azteca growth, and there were no statistically significant effects due to mesh size or sun exposure. Survival of H. azteca was the most sensitive and the least variable endpoint. Effects on survival were noted in the same treatments over short-term chronic exposures in the laboratory and in situ. Significant differences in survival were noted due to the method of deployment under low flow conditions. In situ chambers containing sediment resulted in greater mortality in the 10 d low flow in situ experiments. Under high flow conditions, significant reductions in survival and leaf disc processing were noted under all methods of deployment at the two impacted sites over a 7 d exposure. Also under high flow conditions, significantly greater mortality of H. azteca was reported at the downstream field site when sediment was included in the chamber at deployment. These results suggest that significant toxicity at this site is due to accumulation of contaminants in the sediment and the mobilization of these contaminants during a storm event. In situ exposures detected toxicity not observed in laboratory exposures. These results suggest that a combination of laboratory and field bioassays is most useful in defining field effects.

Animals↗
PubMed1999

Photo-induced toxicity of PAHs to Hyalella azteca and Chironomus tentans: effects of mixtures and behavior.

In the aquatic environment, polycyclic aromatic hydrocarbon (PAH) contamination can result from several anthropogenic sources such as petroleum runoff, industrial processes, and petroleum spills. When ultraviolet light (UV) is present at sufficient intensity, the acute toxicity of some PAHs to aquatic biota is greatly enhanced. This photo-induced toxicity of PAHs is directly influenced by the amount of PAH and by the level of UV intensity present in the aquatic environment. Thus, behavioral responses and habits that affect an aquatic organism's exposure to UV as well as exposure to PAHs can influence the extent to which damage due to photo-induced toxicity occurs. Experiments demonstrated the effects of photo-induced toxicity of anthracene and fluoranthene on the survival of two benthic macroinvertebrates, the midge Chironomus tentans and the freshwater amphipod Hyalella azteca. This study further investigated the survival and behavior of the test organisms in different substrates (no substrate, a sand monolayer, leaf discs, and sediment) with and without UV. The free-swimming, epibenthic H. azteca avoided the effects of photo-induced toxicity of PAHs to some extent by hiding in leaves when this substrate was available. Results emphasize the importance of organisms' behavior in affecting the photo-induced toxicity of PAHs in the aquatic environment.

Journal Article↗
PubMed1997

Carrier effects of dosing the H4IIE cells with 3,3',4,4'-tetrachlorobiphenyl (PCB77) in dimethyl sulfoxide or isooctane.

A rat hepatoma cell line, H4IIE, serves as a bioassay tool to assess the potential toxicity of dioxin-like chemicals, including polychlorinated biphenyls (PCB) in environmental samples. PCB exposure to these cells induces cytochrome (CYP) P4501A1 activity in a dose-dependent fashion, thus allowing assessment of mixtures. The objective of this study was to determine the effect of different carriers, dimethyl sulfoxide (DMSO) and isooctane on the concentrations of PCBs in the H4IIE cells and induction of CYP1A1 activity as measured by ethoxyresorufin O-deethylase (EROD) activity. H4IIE cells were dosed with three micrograms of UL-14C-PCB77/plate dissolved in DMSO or isooctane, and were harvested at sequential time periods for 4 days. PCB77 concentration and EROD activity were measured in the cells. EROD activity was greater when using DMSO as compared to isooctane, while there was no difference in the distribution of PCB77-derived radioactivities within the cell culture system based upon the carrier solvent used to deliver PCB77.

Animals↗
PubMed1996

In vivo/in vitro comparison of the pharmacokinetics and pharmacodynamics of 3,3',4,4'-tetrachlorobiphenyl (PCB77).

The rat hepatoma cell line, H4IIE, serves as a useful tool to assess potential biological effects such as induction of cytochrome P4501A1 expression. The objectives of this study were twofold: to investigate the kinetic time course and dosimetry of PCB77 in rat hepatoma cells dosed with PCB77 and in liver of rats given i.p. doses of PCB77, and to compare in vitro and in vivo P4501A1 enzyme induction responses. For the 4-day time-course study, H4IIE cells were exposed with two doses of [14C]PCB77 (0.9 and 3 microg/plate) and harvested at 15 and 30 min, 1, 2, 4, 8, and 12 hr, and 1, 2, 3, and 4 days. PCB77-derived radioactivity was detected in the cells as early as 15 min postdosing. For the dose-response study, the cells were dosed with various concentrations of PCB77 (0.00316-5.37 microg/plate) and harvested on Day 3 since ethoxyresorufin O-deethylase (EROD) activity in vitro reached its maximum on the third day postdosing. Time-course and dose-response studies revealed that only 1-3% of the total delivered dose was found in the cells, with the remainder in the media and adhering to the culture plates. For the dose-response study in vivo, male Fischer rats were dosed with a single i.p. injection of various concentrations of PCB77 (0.1-50 mg/kg body wt) and euthanized on Day 3. PCB77-derived radioactivity and EROD induction in vivo were measured. When EROD activity and PCB77-derived radioactivity in the rat hepatoma cells and in the rat liver were compared on an equivalent weight basis, there was a significant correlation (r2 = 0.985) between them. Prior to this study, no information on quantitative dosimetry and EROD activities of PCB77 has been reported to validate the in vitro assay with in vivo data.

Animals↗
PubMed1992

Iloprost preserves endothelial function against cyclosporin A and sensitises microvessels towards endothelium-dependent and -independent vasodilatation.

The effects of iloprost have been investigated on the endothelial damage produced by cyclosporin-A (Cy-A) and on the microvascular reactivity to sodium nitroprusside (SNP), acetylcholine (ACh) and isoprenaline (ISO) following iloprost treatment i.e. in the absence of effective plasma levels, using the hamster cheek pouch. It has been shown that iloprost protects the microvascular arteriolar endothelium from functional damage by Cy-A and that iloprost infusion for 12-14 hr sensitizes the arterioles to ACh, SNP and ISO, an effect which is evident 5 hr but not 24 hr following treatment and in the case of ACh is abolished by indomethacin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Effects of atrial natriuretic factor, nitroprusside and acetylcholine on cGMP immunostaining in the isolated perfused rat kidney.

In the present study the localization of the cGMP production in response to the vasodilators acetylcholine (ACh) and sodium nitroprusside (SNP) and to atrial natriuretic factor (ANF) was studied in the isolated perfused rat kidney using cGMP immunocytochemistry. After ACh (0.3 microM) infusion increased cGMP immunoreactivity was found in kidney interlobar and segmental arteries and in glomeruli. SNP (1 microM) and ANF (0.01 microM) elevated cGMP staining in the same elements of the kidney as ACh. In the glomeruli ACh and SNP stimulated cGMP production in mesangial cells whereas ANF stimulated cGMP production in mesangial cells whereas ANF stimulated cGMP production in epithelial cells (podocytes). However, SNP at higher doses (10 microM) stimulated cGMP production not only in glomeruli, but also in interstitial cells throughout the cortex. In addition SNP and ANF increased cGMP production in the medulla.

Acetylcholine↗
PubMed1991

Renal sensitivity to endothelium-derived-relaxing-factor-mediated vasodilatation in the spontaneously hypertensive rat.

1. The sensitivity of the kidney to endothelium-derived-relaxing-factor-mediated vasodilatation has been investigated in the spontaneously hypertensive rat and the Wistar-Kyoto normotensive rat using an isolated perfused rat kidney model. 2. No difference in the slope, ED50 or maximum of the concentration-response curves for the endothelial-dependent vasodilators A23187, a calcium ionophore, and acetylcholine could be demonstrated between kidneys obtained from the spontaneously hypertensive and the Wistar-Kyoto normotensive rats. 3. No difference in the slope or the ED50 of the concentration-response curve for the endothelial-independent vasodilators, atrial natriuretic factor and sodium nitroprusside, could be demonstrated between kidneys obtained from the spontaneously hypertensive and the Wistar-Kyoto normotensive rats. However, in the spontaneously hypertensive rats, the maximum vasodilator response to atrial natriuretic factor, but not to sodium nitroprusside, was increased. 4. The perfused kidney from the spontaneously hypertensive rat also showed an increase in the maximum but not in the slope or ED50 of the concentration-response curve for vasoconstriction induced by the alpha 1-adrenoceptor agonist methoxamine. 5. The involvement of endothelium-derived relaxing factor in mediating the renal vasodilator response to A23187 and acetylcholine was confirmed in experiments performed in perfused kidneys obtained from normotensive Wistar rats. 6. It is concluded that the sensitivity of the kidney to endothelium-derived-relaxing-factor-mediated vasodilatation is not modified in the spontaneously hypertensive rat. This does not, however, exclude a role for the synthesis of endothelium-derived relaxing factor in the maintenance of blood pressure in the spontaneously hypertensive rat.

Acetylcholine↗
PubMed1990

Cyclic GMP release and vasodilatation induced by EDRF and atrial natriuretic factor in the isolated perfused kidney of the rat.

1. Guanosine 3':5'-cyclic monophosphate (cyclic GMP) release and vascular tone was measured in the isolated kidney of the rat perfused at constant flow with Krebs-Henseleit solution. The effects of 3 vasodilators, acetylcholine (ACh), atrial natriuretic factor (ANF) and sodium nitroprusside (SNP) on the renal release of cyclic GMP and vascular tone were examined. The ability of the endothelial-derived relaxing factor (EDRF) inhibitors, haemoglobin and gossypol, to modify vasodilatation and vasodilator-induced changes in cyclic GMP releases from the kidney was also investigated. 2. Renal cyclic GMP release was elevated 8 fold by ANF (0.01 microM), 5 fold by SNP (1 microM) and 3 fold by ACh (0.3 microM). 3. For ACh, both the increase in renal cyclic GMP release and the vasodilatation were reduced by the EDRF inhibitors, haemoglobin (1 microM) and gossypol (15 microM). For SNP, neither the increase in renal cyclic GMP release nor vasodilatation were inhibited by gossypol (15 microM). 4. For ANF, neither the increase in cyclic GMP release from the kidney nor its vasodilator activity were affected by haemoglobin (1 microM). 5. EDRF inhibitors reduced the basal release of cyclic GMP from 0.32 +/- 0.06 pmol min-1 to 0.18 +/- 0.03 pmol min-1, gossypol being more effective than haemoglobin. 6. The results are consistent with the ability of ACh to induce EDRF-mediated vasodilatation in the isolated perfused kidney of the rat. Basal EDRF release appears to contribute approximately 50% to the basal release of cyclic GMP from this preparation. The renal vasodilator action of ANF however, is independent of EDRF, although the renal vascular endothelium cannot be discounted as a site at which ANF stimulates cyclic GMP production.

Acetylcholine↗
PubMed1989

EDRF-mediated dilatation in the rat isolated perfused kidney: a microangiographic study.

1. X-ray microangiographic techniques were used to study the influence of endothelium-derived relaxing factor (EDRF) on vasomotion in the isolated, intact, buffer-perfused kidney of the rat. The main renal (R0), segmental (R1) and interlobar (R2) arteries (control diameters ca. 600, 400 and 300 microns respectively) were studied quantitatively. 2. Inhibition of basal EDRF activity by haemoglobin (1 microM) did not elevate perfusion pressure or constrict R0, R1 and R2 in control preparations, implying a low level of spontaneous myogenic tone. In preparations preconstricted by 0.3 microM methoxamine, haemoglobin caused a further rise in perfusion pressure and amplified constrictor responses in R1 and R2 while also inducing 'paradoxical' dilatation of R0. 3. A spatially heterogeneous pattern of diameter responses (constriction of R2 and R1 with minimal dilatation of R0) was observed with two concentrations of methoxamine (0.3 microM and 3 microM). The magnitude of these responses was, however, smaller with 3 microM than 0.3 microM methoxamine, even though it increased perfusion pressure to a greater extent (88 mmHg cf. 24 mmHg). This 'paradoxical' behaviour indicates more pronounced constriction of distal arteries (which could not be resolved quantitatively) with 3 microM methoxamine. 4. In contrast to the heterogeneity of constrictor responses induced by methoxamine, the dilator action of acetylcholine was spatially homogeneous: log IC50 values calculated from the diameter changes induced in R0, R1 and R2 were similar and, moreover, equivalent to that calculated from the corresponding alterations in perfusion pressure. The fall in perfusion pressure induced by an approximately median effective concentration of acetylcholine (0.3 microM) was completely reversed by haemoglobin, consistent with the involvement of EDRF, although, reversal of the acetylcholine-induced dilatation of R0, R1 and R2 was not observed. 5. The results are consistent with the idea that constriction of distal vessels can attenuate and even directionally reverse intrinsic constrictor responses in the proximal R0, RI and R2 'feed' arteries by producing an overriding increase in 'upstream' pressure. This effect explains the paradoxical dilatation of Ro induced by haemoglobin in the presence of 0.3 microM methoxamine, the smaller magnitude of the diameter changes induced in R0, RI and R2 by 3 microM as compared to 0.3 microM methoxamine, and the failure of haemoglobin to reverse the acetylcholine-induced dilatation of R0, R1 and R2.

Acetylcholine↗
PubMed1987

High incidence of selenite-resistant bacteria from a site polluted with selenium.

The level of selenium-resistant bacteria in water, algal mats, and sediment from Kesterson reservoir, Calif., a site with known selenium pollution, was compared with that in nearby Volta reservoir, a site with low selenium levels. A high percentage (greater than 50%) of all isolates from the Kesterson samples were resistant to 10 mM selenite. In contrast, only a small percentage of the Volta isolates were resistant to this level of selenite. The identity of some selenite-resistant isolates and MICs of selenite, selenate, arsenate, tellurite, and tellurate were determined.

Bacteria↗
PubMed1987

Survival of pathogenic bacteria in various freshwater sediments.

Four human-associated bacteria, Pseudomonas aeruginosa, Salmonella newport, Escherichia coli, and Klebsiella pneumoniae, were tested for survival in five freshwater sediments. Bacterial survival in continuous-flow chambers was monitored over 14-day periods on sediments ranging from organically rich high-clay fractions to organically poor sandy fractions. Bacterial die-off ranged from 1 to 5 orders of magnitude in sediments. E. coli survived as long as or longer than S. newport. P. aeruginosa and K. pneumoniae tended to survive longer than E. coli. Survival of E. coli and S. newport was greater in sediments containing at least 25% clay. Good reproducibility allowed the development of linear models to describe die-off rates.

Bacterial Physiological Phenomena↗
PubMed1987

Widespread occurrence of bacterial thiol methyltransferases and the biogenic emission of methylated sulfur gases.

A majority of heterotrophic bacteria isolated from soil, water, sediment, vegetation, and marine algae cultures methylated sulfide, producing methanethiol. This was demonstrated with intact cells by measuring the emission of methanethiol with a sulfur-selective chemiluminescence detector, and in cell extracts by detection of sulfide-dependent thiol methyltransferase activity. Extracts of two Pseudomonas isolates were fractionated by gel-filtration and ion-exchange chromatography, and with sulfide as the substrate a single peak of thiol methyltransferase activity was seen in each case. Extracts of several bacterial strains also contained thiol methyltransferase activity with organic thiols as substrates. Thus, S-adenosylmethionine-dependent thiol methyltransferase activities are widespread in bacteria and may contribute to biogenic emissions of methylated sulfur gases and to the production of methyl thioethers.

Bacteria, Aerobic↗