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Biomedical subjects

A Haug

Publications and source records attributed to A Haug.

At least 19 recordsLinked to original sources

Prenatal exposure to corticosterone impairs embryonic development and increases fluctuating asymmetry in chickens (Gallus gallus domesticus).

1. The level of corticosterone in fertilised eggs from hens (Gallus gallus domesticus) was manipulated experimentally to elucidate whether stress in laying hens is harmful to the chicks, as manifested by impaired survival and reduced growth, and whether bilateral asymmetry may represent an indicator of environmental stress in poultry. 2. Three hundred and fifty eggs were randomly divided into 4 groups; 1. untreated, 2. control, 3. 10 ng corticosterone/ml and 4. 20 ng corticosterone/ml. Each of the eggs in groups 2, 3 and 4 were injected with 100 microl ethanol-saline solution (25% ethanol in saline) containing 0, 0.6 and 1.2 microg corticosterone, respectively. After the injections, the final concentration of ethanol in the egg (albumen and yolk) was 0.03%, and the concentration of added corticosterone was 0, 10 and 20 ng/ml, respectively, in groups 2, 3 and 4. All the eggs were treated on developmental d 1. 3. Corticosterone injections resulted in greater embryonic mortality, earlier termination of foetal development and reduced growth. Moreover, chicks developing in eggs with an elevated concentration of corticosterone displayed reduced developmental stability as evidenced by increased fluctuating asymmetry (FA) in tarsus length. 4. In conclusion, an increased concentration of corticosterone in the egg was detrimental to survival and growth of the chicks. Prenatal stress also generated bilateral asymmetry, and illustrates the potential application of FA as an indicator of environmental stress in poultry.

Agriculture↗

Effects of soaking temperature and soaking time during preparation of water extract of tea on anticlastogenicity against environmental tobacco smoke in the sister-chromatid exchange assay.

Water extract of tea (WET) was prepared by soaking green tea at different temperatures for various periods of time and was used to test whether the soaking temperature and soaking time during the preparation of WET influence the content of polyphenols and the anticlastogenicity of WET against environmental tobacco smoke (ETS). Five major polyphenols in WET were measured. Extractable-respirable particulate (ERP) was obtained from ETS-contaminated indoor air (ERP-ETS). The sister-chromatid exchange assay (SCE) was utilized to evaluate the clastogenic effects of ERP-ETS and the anticlastogenic effects of WET. The results indicate that ERP-ETS is clastogenic and WET has significant anticlastogenic effects on ERP-ETS. The content of polyphenols and the anticlastogenic potential of WET depended on the soaking temperature and soaking time during WET preparation. At the soaking temperature of 80 degrees C, an increased soaking time was correlated with a higher percentage of polyphenols and a concomitantly enhanced anticlastogenic efficacy. By contrast, at the soaking temperature of 100 degrees C, a longer soaking time was associated with a higher percentage of polyphenols concomitant with a lower anticlastogenic efficacy. The data suggest that, besides polyphenols, and additional material(s), which may be partially inactivated at 100 degrees C, is contributing to the anticlastogenicity of WET.

Antimutagenic Agents↗

Effect of environmental tobacco smoke on intracellular free calcium of boar sperm incubated in seminal plasma.

The extractable-respirable particulate of environmental tobacco smoke (ERP-ETS) was collected and tested for its effect on the intracellular free Ca(2+) concentration, [Ca(2+)](i), in boar sperm incubated in seminal plasma in vitro. The intracellular free Ca(2+) level is reportedly closely related to in sperm capacitation and acrosome reaction, which must take place to confer upon sperm the full fertilizing potential. In the absence of ERP-ETS [Ca(2+)](i) in the boar sperm increased dramatically from initially 75 nM to about 248 nM after a 5-h incubation in seminal plasma. However, such an increase was virtually inhibited by ERP-ETS at a concentration of 10 microg/ml, without any significant reduction of the sperm motility and viability. We conclude that application of ERP-ETS negatively affected the [Ca(2+)](i) of boar sperm in vitro.

Acrosome Reaction↗

Comparison of environmental tobacco smoke concentrations and mutagenicity for several indoor environments.

Environmental tobacco smoke (ETS) is a major source for indoor air pollution. Although ETS-caused indoor air pollution has been well studied in the developed countries, few studies have examined ETS indoor air pollution in China, which currently has the largest population of tobacco smokers. In this study, respirable-particulate (RP) from ETS-contaminated (RP-ETS) indoor air was collected and measured in 5 different indoor environments during the winter in the northwestern Liaoning Province, China. The extractable portion of RP-ETS (ERP-ETS) was obtained by dichloromethane extraction and used in the Salmonella mutagenicity assay in the presence of S9 using strains TA98, TA100, and TA1538. The percentage of RP-ETS attributable to ETS (ETS-RP) and the percentage of ERP-ETS attributable to ETS (ETS-ERP) were estimated by measuring the concentration of solanesol, an ETS marker. Comparative results in 5 different indoor environments were: (1) the concentration of RP-ETS ranged from 197.3 to 1227.6 microg/m(3) and approximately 64.7 to 92. 0% of the RP-ETS originated from ETS; (2) the concentration of ERP-ETS ranged 88.8 to 601.5 microg/m(3) and approximately 83.1 to 95.4% of the ERP-ETS originated from ETS; (3) the mutagenic potency (revertants/m(3)) of ERP-ETS ranged from 60.4 to 595.5 for TA98, from 33.7 to 312.8 for TA100, and from 49.7 to 475.2 for TA1538. The data indicate that the extent of ETS pollution and the potential health hazards of ETS to humans in the five indoor environments are in the following increasing order: rural bedrooms, urban living rooms, office rooms, restaurants, and passenger cars in that area.

Air Pollution, Indoor↗

Aluminum interaction with phosphoinositide-associated signal transduction.

Concerning molecular and cellular mechanisms of aluminum toxicity, recent studies support the hypothesis that interactions of aluminum ions with elements of signal transduction pathways are apparently primary events in cells. In the case of the phosphoinositide-associated signalling pathway of neuroblastoma cells, guanine nucleotide-binding proteins (G proteins) and a phosphatidylinositol-4,5-diphosphate (PIP2)-specific phospholipase C are probable interaction sites for inhibitory actions of aluminum ions. Following interiorization of aluminum by the cell, metal interactions decrease the accumulation of inositol phosphates, especially that of inositol-1,4,5-triphosphate (IP3), concomitant with derangements of intracellular Ca2+ homeostasis. In the presence of high concentrations of Ca2+, formation of IP3 is also diminished in aluminum-pretreated cells, presumably involving a process not requiring Mg(2+)-dependent G proteins. At higher aluminum doses, metal-induced changes in the lipid milieu of the membrane-bound phospholipase may play a role. These types of primary interactions of aluminum ions with elements of cellular communication channels are probably crucial in the manifestation of the multifacetted aluminum toxicity syndrome. If present as a phosphate-like fluoro-aluminate, a stimulatory role of aluminum ions is displayed in G protein-coupled transmembrane signalling.

Aluminum↗

Aluminium impacts elements of the phosphoinositide signalling pathway in neuroblastoma cells.

Inositol phosphate formation was examined in aluminium-treated murine neuroblastoma cells labelled with [3H]-myoinositol. Employing fluoride-stimulated intact cells, aluminium (0.2 microM to 1 mM) reduced inositol phosphate formation in a dose-dependent manner. In digitonin-permeabilized cells, stimulated with nonhydrolyzable GTP[S], inositol phosphate formation was also inhibited by increasing aluminium doses; the IC50 value was about 20 microM aluminium, while the inositol phosphate level was reduced 2.5 to 3 fold by 50 microM aluminium. The inhibitory effect of aluminium (50 microM) could not be reversed by increasing GTP[S] concentrations up to 500 microM. Prechelation of aluminium to citrate or EGTA completely abolished the aluminium-triggered inhibition of fluoride-stimulated inositol phosphate formation in intact cells, but had little effect on the inhibition of permeabilized cells stimulated with GTP[S]. In neuroblastoma cells phosphoinositide hydrolysis could be evoked either through a pathway involving the Mg2+/guanine nucleotide binding (Gp) protein, or via a pathway operative in the presence of high intracellular Ca2+ concentrations. In the Mg2+/Gp protein-mediated pathway, formation of inositol triphosphate, IP3, inositol diphosphate, IP2, and inositol monophosphate, IP, was apparently inhibited by aluminium in an interdependent manner. As to the Ca(2+)-mediated pathway, aluminium application mainly diminished the release of IP3. Following interiorization, aluminium thus acts upon elements critical for phosphoinositide-associated signal transduction. An aluminium target apparently resides on the Gp protein. Phosphatidylinositol-4,5-diphosphate-specific phospholipase C probably harbours a second aluminium target.

Aluminum↗

Elevation of intracellular free calcium levels in sperm in response to long-term feeding of fungicides to mice.

To assess the impact of long-term feeding of fungicides on sperm quality, mice were fed a daily diet containing a mixture of maneb and zineb, at concentrations of 30, 300, and 3000 ppm, respectively. Employing epididymal sperm suspended in a medium permitting in vitro capacitation, the intracellular free Ca2+ concentration, [Ca2+]i, was determined with a fluorescent Ca2+ indicator, Fura-2. Regardless of the fungicide dosages applied, [Ca2+]i was about 50 percent higher in treated animals relative to a value of 123 nM [Ca2+]i in the control group. Fungicide-treated mice were mated to mature, non-treated females; as in the control, the litter sizes were the same. In conclusion, the observed elevation in [Ca2+]i seems to reflect cellular adaptation responses to toxic stress at moderate fungicide doses.

Animals↗

Aluminium interferes with signal transduction in neuroblastoma cells.

The effects of aluminium on inositol phosphate formation were examined in murine neuroblastoma cells labelled with [3H]-myo-inositol. In aluminium-pretreated cells, the bradykinin-triggered inositol triphosphate, IP3, release and the change in intracellular [Ca2+] were appreciably less compared with the control group. Stimulating digitonin-permeabilized cells with non-hydrolyzable guanosine 5'-[gamma-thio]-triphosphate, GTP[S], inositol phosphate formation decreased in the presence of aluminium. A primary target of aluminium toxicity may reside on the guanine nucleotide-binding protein(Gp)/phospholipase C system, at a site different from that of the GTP[S] binding site.

Aluminum↗

Changes in intracellular calcium of porcine sperm during in vitro incubation with seminal plasma and a capacitating medium.

The intracellular free Ca2+ concentration in ejaculated, porcine sperm was determined with a fluorescent, Ca2(+)-specific probe, Fura 2. Following suspension of sperm in a medium capable of sustaining capacitation and the acrosome reaction, the intracellular [Ca2+] increased from an initial value of about 75 nM to a peak value of 130 nM, after about 4 to 5 h of incubation. Within this period of time, a peak value of 246 nM was attained when sperm was incubated in seminal plasma. Ca2+ uptake is presumably not associated with membrane potential-dependent channels. The results indicate that a pronounced increase in intracellular free Ca2+ occurs towards the end of the incubation period when rather synchronous acrosome reactions take place in the sperm population, either in capacitating medium or in seminal plasma.

Animals↗

Aluminum uptake by neuroblastoma cells.

Aluminum uptake studies in viable neuroblastoma cells were performed. Aluminum uptake was largely dependent on the pH of the suspension medium. At physiological pH values, cells were apparently unable to incorporate detectable amounts of aluminum in the absence of proper mediators. Aluminum uptake was enhanced as the pH decreased, attaining a plateau at about pH 6.0. In experiments with 2 x 10(6) cells/ml, pH 6.0, and 25 microM aluminum in the medium, aluminum incorporation reached saturation at 5 nmol of aluminum/mg of cellular protein, accounting for 60-70% of aluminum added. At pH 6.0, cells showed a large capacity for accumulating aluminum; about 70% of intracellular aluminum was associated with the postmitochondrial fraction. At neutral pH, application of apotransferrin seemed to facilitate aluminum translocation into cells via membrane receptors. Fatty acids were also capable of mediating aluminum uptake at neutral pH, probably by forming aluminum-fatty acid complexes. Low molecular weight aluminum chelators, e.g., citrate, inhibited aluminum uptake. Treatment of cells with energy metabolism blockers had virtually no influence on aluminum uptake, indicative of passive mechanisms. The results suggest that aluminum uptake occurs via different modes dependent on growth conditions, such as medium pH.

Aluminum↗

The membrane potential changes polarity during capacitation of murine epididymal sperm.

The membrane potential in murine epididymal sperm was determined with a voltage-sensitive, fluorescent probe. In freshly collected sperm, the potential was inside-negative, viz., -13 mV, and was associated with an intracellular K+ concentration of about 122 mM. Following incubation of sperm in a medium capable of sustaining capacitation and fertilization efficacy, the potential became gradually positive. An inside-positive potential, +24 mV, was obtained after 40 min of incubation, concomitant with an intracellular K+ concentration of approximately 30 mM. At this time, about 70 percent of sperm had capacitated. An inside-positive membrane potential may play a role in facilitating the acrosome reaction.

Animals↗

Aluminum-altered membrane dynamics in human red blood cell white ghosts.

Fluorescence polarization of the hydrophobic membrane probe 1,6-diphenyl hexatriene was used to investigate alterations in membrane dynamics caused by micromolar concentrations of aluminum. Metal titration onto resealed white ghost membranes showed a progressive increase in steady-state fluorescence anisotropy of the probe in the presence of aluminum which was twice the value obtained upon titration of calcium. As calculated from steady-state fluorescence data in the presence and absence of 20 microM aluminum, a temperature dependent lipid order parameter indicated increased lipid packing. Motional dynamics of the probe molecule on the nanosecond time scale showed severe constraints in the presence of 20 microM aluminum as indicated by decreased rotational rate, decreased cone angle, and increased values of time resolved limiting anisotropy. Physiological consequences of altered membrane dynamics are also discussed.

Aluminum↗

Plasma lipids, lipoproteins, and fecal excretion of neutral sterols and bile acids in rats fed various high fat diets or a low fat/high sucrose diet.

The effect of feeding various diets on plasma lipids and lipoproteins and on fecal excretion of neutral sterols and bile acids was studied in rats fed for 7 wk diets containing 42% of energy as either coconut oil (CO), sunflower seed oil (SO), fish body oil (FBO), cod liver oil (CLO), or a low fat/high sucrose diet (SU). Triacylglycerols (TG) in whole plasma and VLDL + LDL were lower in rats fed high amounts of polyunsaturated fatty acids (PUFA) than in those fed the CO diet. Plasma HDL2 components in FBO and CLO groups were generally lower than in the other groups. Percentages of liver and heart linoleic and arachidonic acid were higher in the SO group, but lower in groups fed marine oils, than in the CO group. There was a high relative amount of eicosapentaenoic and docosahexaenoic acid in liver and heart of rats fed marine oils. Fecal excretion of bile acids was lower in the PUFA groups than in the CO group, whereas the sum of neutral sterols was similar in all groups. Plasma HDL2 (and VLDL + LDL) correlated positively, but HDL3 negatively, with fecal bile acid excretion. Accordingly, increased bile acid excretion does not seem to account for hypolipemia following intake of PUFA diets.

Animals↗

Ligand-triggered conformational perturbations elicit changes at the single cysteinyl residue of spinach calmodulin.

Following application of stoichiometric amounts of Ca2+ or specific partner peptides to spinach calmodulin, dynamic changes in the nanosecond range could be monitored at a strategically anchored fluorescence or spin probe. For these studies the single cysteinyl residue 26 of spinach calmodulin was labelled with a thiol-specific proxyl (i.e. 2,2,5,5-tetramethyl-1-pyrrolidinyl-oxyl) spin probe or with a bimane fluorescence probe. With Ca2+ and a specific ligand (mastoparan) present, fluorescence studies (anisotropy, lifetime) indicated that the rotational motion of the protein complex becomes slower relative to the motion of calmodulin in the absence of the specific ligand. The probe's attachment site 26 appears to reside in a fairly polar microenvironment as reported by a series of proxyl spin probes varying in label length. The rotational correlation time of the shortest spin probe markedly changed upon binding of a specific peptide to a calmodulin region distant from that of the monitoring spin probe. We interpret these observations as indicating that ligand-triggered conformational perturbations are eliciting specific responses at the cysteinyl residue 26 of spinach calmodulin.

Bee Venoms↗