Effects of acute CS2 intoxication on liver protein and drug metabolism

Rats pretreated with phenobarbitone and their controls were exposed to 0.15% atmospheric CS₂ for 2 h. Liver protein metabolism and microsomal drug metabolizing enzyme activities were analyzed 1, 4 and 46 h later. In the pretreated rats the [¹⁴C]leucine uptake was at first inhibited, then liver RNA tended to increase. This increase was followed by a decline in the [¹⁴C]leucine uptake, while RNA content diminished to the control level. In the control rats (not pretreated with phenobarbital) the effects of CS₂ on liver protein metabolism were less; only at 4 h after the exposure was liver RNA increased and [¹⁴C]leucine uptake slightly stimulated. In the pretreated rats CS₂ had decreased microsomal P-450 by about 50% at 1 and 4 h, and the activity of 7-O-dealkylase of ethoxycoumarin had decreased even more. The measurable UDPglucuronosyltransferase of the liver microsomes of the pretreated rats had increased by 26% at 1 h and by 80% at 4 h after the CS₂ exposure. The in vivo activation of microsomal UDPglucuronosyltransferase may result from a stimulated lipid peroxidation of reticuloendothelial membranes by CS₂ metabolites in vivo, as suggested by the diene conjugation spectra. In control rats CS₂ depressed only the ethoxycoumarin deethylase activity. All the microsomal changes caused by CS₂ exposure were restored within 46 h.It is suggested that the different action of CS₂ on the liver protein metabolism of rats pretreated with phenobarbitone and controls results from the different stage of protein turnover in the two groups, i.e. in the barbituratetreated animals there is a phase of increased protein synthesis and accordingly the protein turnover is more sensitive to the action of CS₂.     

Oxidative metabolism of carbon disulphide by the rat. Effect of treatments which modify the liver toxicity of carbon disulphide

The liver toxicity of a standard dose of CS₂ was increased by phenobarbitone pre-treatment and by fasting and decreased by prior administration of a small dose of CS₂; it was less marked in female than in male rats.Rats were given an intraperitoneal dose of ¹⁴CS₂ to study its in vivo conversion to ¹⁴CO₂ under conditions which modify the liver toxicity of CS₂. The radioactive CO₂ exhaled was found to be linearly related to the amount of cytochrome P-450 present in the liver at the time of administering ¹⁴CS₂; it was also found to be related to the severity of the toxic changes caused in the liver, but here the relationship was not linear and was more complex.When liver microsomes were incubated with CS₂, a marked loss of cytochrome P-450 was observed only when NADPH was present. In contrast with the loss of the cytochrome observed with NADPH alone, which is associated with the formation of malonaldehyde, that due to CS₂ still occurred in the presence of EDTA, even though the formation of malonaldehyde was largely prevented.These results are compatible with the hypothesis that CS₂ requires metabolism for its liver toxicity.     

Effect of acute sodium nitrite intoxication on some essential biometals in mouse spleen

Background and aimSodium nitrite (NaNO₂) is an inorganic salt with numerous applications in a variety of industries, as well as in medicine. Nevertheless, exposure to high levels of NaNO₂ is toxic for animals and humans. Sodium nitrite intoxication is shown to decrease the activity of major antioxidant defence enzymes which is dependent on the maintenance of specific ion equilibrium. The aim of the present study was to investigate the effect of acute NaNO₂ intoxication on the content of the essential metals iron (Fe), calcium (Ca) and zinc (Zn) in mouse spleen.MethodsMature male ICR mice were divided into four groups and subjected to acute NaNO₂ exposure by a single intraperitoneal injection of 120 mg/kg body weight. Animals in each group were sacrificed at certain time interval after treatment (1 h, 5 h, 1 day and 2 days). Spleens were excised and processed for atomic absorption spectrometry analysis of Fe, Ca and Zn content.ResultsAt the first hour after treatment, a decrease in Fe and Ca levels was observed. One day following NaNO₂ administration, Zn concentration reached its lowest value and Ca levels remained lower, compared to the untreated controls. In contrast, Fe concentration increased on the first and second day after treatment.ConclusionThe results of the present study demonstrate that acute NaNO₂ intoxication provokes changes in the endogenous levels of Fe, Ca and Zn in mouse spleen. These findings suggest disruption of the ionic balance and impact on the activity of antioxidant defence enzymes.     

Transient postnatal fluoxetine leads to decreased brain arachidonic acid metabolism and cytochrome P450 4A in adult mice

Fetal and perinatal exposure to selective serotonin (5-HT) reuptake inhibitors (SSRIs) has been reported to alter childhood behavior, while transient early exposure in rodents is reported to alter their behavior and decrease brain extracellular 5-HT in adulthood. Since 5-HT_2A/2C receptor-mediated neurotransmission can involve G-protein coupled activation of cytosolic phospholipase A₂ (cPLA₂), releasing arachidonic acid (ARA) from synaptic membrane phospholipid, we hypothesized that transient postnatal exposure to fluoxetine would alter brain ARA metabolism in adult mice. Brain ARA incorporation coefficients k* and rates J_in were quantitatively imaged following intravenous [1-¹⁴C]ARA infusion of unanesthetized adult mice that had been injected daily with fluoxetine (10 mg/kg i.p.) or saline during postnatal days P4–P21. Expression of brain ARA metabolic enzymes and other relevant markers also was measured. On neuroimaging, k* and J_in was decreased widely in early fluoxetine- compared to saline-treated adult mice. Of the enzymes measured, cPLA₂ activity was unchanged, while Ca²⁺-independent iPLA₂ activity was increased. There was a significant 74% reduced protein level of cytochrome P450 (CYP) 4A, which can convert ARA to 20-HETE. Reduced brain ARA metabolism in adult mice transiently exposed to postnatal fluoxetine, and a 74% reduction in CYP4A protein, suggest long-term effects independent of drug presence in brain ARA metabolism, and in CYP4A metabolites. These changes might contribute to reported altered behavior following early SSRI in rodents.     

Alcohol ADME in Primates Studied with Positron Emission Tomography

Background and Purpose

The sensitivity to the intoxicating effects of alcohol as well as its adverse medical consequences differ markedly among individuals, which reflects in part differences in alcohol''s absorption, distribution, metabolism, and elimination (ADME) properties. The ADME of alcohol in the body and its relationship with alcohol''s brain bioavailability, however, is not well understood.

Experimental Approach

The ADME of C-11 labeled alcohol, CH₃ ¹¹CH₂OH, 1 and C-11 and deuterium dual labeled alcohol, CH₃ ¹¹CD₂OH, 2 in baboons was compared based on the principle that C–D bond is stronger than C–H bond, thus the reaction is slower if C–D bond breaking occurs in a rate-determining metabolic step. The following ADME parameters in peripheral organs and brain were derived from time activity curve (TAC) of positron emission tomography (PET) scans: peak uptake (C_max); peak uptake time (T_max), half-life of peak uptake (T_1/2), the area under the curve (AUC_60min), and the residue uptake (C_60min).

Key Results

For 1 the highest uptake occurred in the kidney whereas for 2 it occurred in the liver. A deuterium isotope effect was observed in the kidneys in both animals studied and in the liver of one animal but not the other. The highest uptake for 1 and 2 in the brain was in striatum and cerebellum but 2 had higher uptake than 1 in all brain regions most evidently in thalamus and cingulate. Alcohol''s brain uptake was significantly higher when given intravenously than when given orally and also when the animal was pretreated with a pharmacological dose of alcohol.

Conclusion and Implications

The study shows that alcohol metabolism in peripheral organs had a large effect on alcohol''s brain bioavailability. This study sets the stage for clinical investigation on how genetics, gender and alcohol abuse affect alcohol''s ADME and its relationship to intoxication and medical consequences.     

Diversity and Ecophysiology of New Isolates of Extremely Acidophilic CS2-Converting Acidithiobacillus Strains

Biofiltration of industrial carbon disulfide (CS₂)-contaminated waste air streams results in the acidification of biofilters and therefore reduced performance, high water use, and increased costs. To address these issues, we isolated 16 extremely acidophilic CS₂-converting Acidithiobacillus thiooxidans strains that tolerated up to 6% (vol/vol) sulfuric acid. The ecophysiological properties of five selected strains (2Bp, Sts 4-3, S1p, G8, and BBW1) were compared. These five strains had pH optima between 1 (2Bp) and 2 (S1p). Their affinities for CS₂ ranged between 80 (G8) and 130 (2Bp) μM. Strains S1p, G8, and BBW1 had more hydrophobic cell surfaces and produced less extracellular polymeric substance than did strains 2Bp and Sts 4-3. All five strains converted about 80% of the S added as CS₂ to S⁰ when CS₂ was supplied in excess. The rate of S⁰ consumption varied between 7 (Sts 4-3) and 63 (S1p) nmol O₂ min⁻¹ ml culture⁻¹. Low S⁰ consumption rates correlated partly with low levels of cell attachment to externally produced S⁰ globules. During chemostat growth, the relative amount of CS₂ hydrolase in the cell increased with decreasing growth rates. This resulted in more S⁰ accumulation during CS₂ overloads at low growth rates. Intermittent interruptions of the CS₂ supply affected all five strains. Strains S1p, G8, and BBW1 recovered from 24 h of starvation within 4 h, and strains 2Bp and Sts 4-3 recovered within 24 h after CS₂ was resupplied. We recommend the use of mixtures of Acidithiobacillus strains in industrial biofilters.     

Gallic acid modulates purine metabolism and oxidative stress induced by ethanol exposure in zebrafish brain

Gallic acid (GA) is a secondary metabolite found in plants. It has the ability to cross the blood-brain barrier and, through scavenging properties, has a protective effect in a brain insult model. Alcohol metabolism generates reactive oxygen species (ROS); thus, alcohol abuse has a deleterious effect on the brain. The zebrafish is a vertebrate often used for screening toxic substances and in acute ethanol exposure models. The aim of this study was to evaluate whether GA pretreatment (24 h) prevents the changes induced by acute ethanol exposure (1 h) in the purinergic signaling pathway in the zebrafish brain via degradation of extracellular nucleotides and oxidative stress. The nucleotide cascade promoted by the nucleoside triphosphate diphosphohydrolase (NTPDase) and 5′-nucleotidase was assessed by quantifying nucleotide metabolism. The effect of GA alone at 5 and 10 mg L^?1 did not change the nucleotide levels. Pretreatment with 10 mg L^?1 GA prevented an ethanol-induced increase in ATP and ADP levels. No significant difference was found between the AMP levels of the two pretreatment groups. Pretreatment with 10 mg L^?1 GA prevented ethanol-enhanced lipid peroxidation and dichlorodihydrofluorescein (DCFH) levels. The higher GA concentration was also shown to positively modulate against ethanol-induced effects on superoxide dismutase (SOD), but not on catalase (CAT). This study demonstrated that GA prevents the inhibitory effect of ethanol on NTPDase activity and oxidative stress parameters, thus consequently modulating nucleotide levels that may contribute to the possible protective effects induced by alcohol and purinergic signaling.

     

Tetrathiomolybdate(VI) as an antidote in acute intoxication by copper(II) and other toxic metal ions

Tetrathiomolybdate(VI), MoS₄^2?, has been found to act as an effective antidote for acute copper(II) intoxication in mice. Both (NH₄)₂MoS₄ and Na₂MoS₄ were used for this purpose with approximately the same results. The sodium salt is less toxic (LD50 = 537 mg/kg, ip) than the ammonium salt (LD50 = 176mg/kg, ip). The sodium salt was found to be an effective antidote for acute intoxication for some divalent metal ions (Zn²⁺ and Ni²⁺), but not for others (Hg²⁺, Cd²⁺. The sodium salt was also ineffective as an antidote in acute intoxication by arsenic(III), antimony(III) and bismuth(III), and methylmercuric chloride.     

Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice by upregulating visfatin expression

Ambient particulate matter (PM) exposure has been associated with atherosclerosis. However, research on the effect of real-world exposure to ambient PM in regulating visfatin expression in an animal model is very limited. The objective is to investigate whether Beijing ambient PM exposure could accelerate atherosclerosis in ApoE knockout (ApoE^−/−) mice by upregulating visfatin expression. Forty male ApoE^−/− mice were exposed to untreated ambient air (PM group, n = 20) or filtered air (FA group, n = 20), 24 h/day, 7 days/week, for 2 months. During the exposure, the mass concentrations of PM_2.5 and PM₁₀ in the two groups were continuously monitored. Moreover, a receptor source apportionment model was applied to apportion sources of PM_2.5. At the end of the exposure, visfatin in plasma and aorta, biomarkers of inflammation, oxidative stress and lipid metabolism in blood samples, and bronchoalveolar lavage fluid (BALF) were determined, and the plaque area of the atherosclerosis lesions was quantified. PM-exposed mice were significantly higher than FA-exposed mice in terms of plasma visfatin, OxLDL, MDA, serum TC, LDL, TNF-α as well as IL-6, TNF-α, OxLDL, and MDA in BALF, while SOD and GSH-Px activities in plasma and BALF were reduced in PM-exposed mice. Pathological analysis of the aorta demonstrated that the plaque area and visfatin protein in the PM group increased significantly compared to the FA group. Our findings indicate that ambient PM exposure could accelerate atherosclerosis, which is related to visfatin upregulation, as well as the activation of inflammation and oxidative stress.     

The effects of carbon disulphide on rat liver microsomal mixed-function oxidases, in vivo and in vitro

An intraperitoneal dose of CS₂ (500mg/kg) to male rats resulted in loss of liver microsomal mixed-function-oxidase activity (85% loss of biphenyl 4-hydroxylase), followed by denaturation of liver cytochrome P-450 to cytochrome P-420, and degradative loss of both cytochromes (50% loss). Losses of NADPH–cytochrome c reductase (20%) and cytochrome b₅ were considerably less. Intraperitoneal administration of CS₂ (100mg/kg) to rats pretreated wtih phenobarbitone or 3-methylcholanthrene resulted in similar losses, but the rate of destruction was greater with cytochrome P-450 than with cytochrome P-448. At 12h after intraperitoneal injection of CS₂ to non-pretreated rats, a new cytochrome (P-448) appeared. Rat liver microsomal preparations incubated with CS₂ in the presence of NADPH and O₂ resulted in loss of cytochrome P-450 and mixed-function-oxidase activity directly related to the concentration of CS₂ (10–100μm) and to the period of incubation. Addition of EDTA (1mm) completely inhibited this destruction of cytochrome P-450 by CS₂ in vitro. Addition of CS₂ to liver microsomal preparations resulted in moderate increases in the K_s values for type-I or type-II substrates, but these were insufficient to account for the inhibition of the mixed-function oxidases. We therefore suggest that desulphuration of CS₂ leads to binding of the S to cytochrome P-450, denaturation of cytochrome P-450 to cytochrome P-420, and ultimately to destruction of these cytochromes by autoxidation.     

Resveratrol Prevents Stress-Related Dysfunction of Mitochondria

This study was conducted to investigate the antistress potential of resveratrol, a natural polyphenol, in models that reproduce the conditions of acute hypobaric hypoxia and acute alcohol intoxication. Acute alcohol intoxication and acute hypobaric hypoxia induced an increase in the intensity of lipid peroxidation in the membranes of liver mitochondria from mice. Activation of lipid peroxidation was accompanied by swelling and variations in the levels of fatty acids with C₁₈ and C_20–22 in the composition of the total lipid fraction of mitochondrial membranes. The index of the unsaturation of fatty acids with C₁₈ was decreased by 7.5% (from 1.69 ± 0.01 to 1.52 ± 0.01). Furthermore, the (20:3ω6+20:5ω3)/22:6ω3 index decreased from 0.23 ± 0.02 to 0.13 ± 0.01 for fatty acids under acute hypobaric hypoxia conditions, suggesting a decrease in eicosanoid metabolism. The administration of 2 × 10^–5 mol/kg of resveratrol in animals for 5 days prevented changes in fatty acid composition, inhibiting activation of lipid peroxidation and swelling of mitochondria, thereby affecting physiological parameters. Thus, the adaptogenic properties of resveratrol may be ascribed to the prevention of lipid peroxidation in mitochondrial membranes, which probably affects the functional state of these organelles, contributing to the maintenance of cellular energy metabolism under stress conditions.

     

Isolation of a carbon disulfide utilizing <Emphasis Type="Italic">Thiomonas</Emphasis> sp. and its application in a biotrickling filter

The carbon disulfide (CS₂)-oxidizing bacterium Thiomonas sp. WZW was enriched and isolated using activated sewage sludge as inoculum. Growth of Thiomonas sp. WZW was observed on CS₂, thiosulfate, dimethylsulfide (DMS), dimethyldisulfide (DMDS), and H₂S. No growth occurred on dimethylsulfoxide, methanol, acetate, and on complex media with glucose, yeast extract, or tryptone. DMDS-grown cells respired CS₂, DMS, and DMDS, while thiosulfate-grown cells did not respire CS₂. Chemostat cultures growing on thiosulfate could be rapidly adapted to growth on CS₂. Growth was observed between pH 6 and 8. The K _s values for CS₂, thiosulfate, and sulfide of CS₂-grown cells were between 5 and 10 μM. CS₂ was inhibitory above 0.3 mM. A lab-scale biotrickling filter with lava stone as carrier material for treatment of CS₂-polluted air was inoculated with Thiomonas sp. WZW. A rapid start up (95% removal in 1 week) was obtained at an inlet CS₂ concentration of 2 cmol l⁻¹ and an initial space velocity (SV) of 54 h⁻¹. Subsequent thiosulfate addition for a week during start up increased the removal to 99%. The step-wise increase of SV to 130 h⁻¹ and a CS₂ concentration to 3 μmol l⁻¹ resulted in a stable performance with a removal efficiency of 95%. Feeding mixtures of volatile sulfur compounds showed simultaneous conversion of H₂S, CS₂, dimethyldisulfide (DMDS), and DMS, with a preference in this order.     

Effects of acute hypoxia on incorporation of [1-14C]arachidonic acid into glycerolipids of rat brain

The effects of 1 min of acute hypoxic treatment (1% O₂ in N₂) on incorporation of [1-¹⁴C]arachidonic acid into brain lipids of 16-day-old rats were investigated at 3, 6, and 12 min after intracerebral injection of the labeled fatty acid. The hypoxic-hypoxia condition associated with convulsive seizures caused a decrease in the conversion of labeled arachidonate to its acyl-CoA as well as incorporation of the label into the brain phospholipids. Among the phospholipids, there was a specific decrease in the labeling of diacylglycerophosphoinositol (GPI), and this change was accompanied by an increase in labeling of the diacylglycerols. These results indicate that metabolism of the long-chain fatty acids and some glycero-lipids in brain are vulnerable to acute hypoxic treatment.     

Effect of selenium on thyroid hormone metabolism in filial cerebrum of mice with excessive iodine exposure

The effects of supplementing selenium on thyroid hormone metabolism were studied on mice with excessive iodine exposure. The serum concentrations of thyroxine (T₄) and triiodothyronine (T₃) and the activities of iodothyronine 5′ and 5-deiodinase (D2, D3) were measured in the brain of filial mice to study the influence of selenium on thyroid hormone metabolism. Measurements were carried out on postnatal day 0, 14, and 28. It was found that selenium supplementation alleviated the adverse effects of excessive iodine on progeny. The serum TT₄ level as well as TT₄ and TT₃ concentrations and D3 activity in cerebrum of progeny decreased, whereas D2 activity increased in the cerebrum of progeny on postnatal day 0 and 14. Selenium supplementation exerted some favorable effects on thyroid hormone metabolism in cerebrum of progeny of dam with excessive iodine intake.     

An evaluation of carbon disulphide as a sulphur fertilizer and as a nitrification inhibitor

There was little release of extractable SO₄-S during four weeks from CS₂ applied by injecting into two S-deficient soils. In this incubation experiment, the rate of CS₂ was 30 μg S g⁻, placement was injection at 9 cm depth, soil temperature was 20°C, and soil moisture tension was 33 kPa. The yield of barley forage after seven weeks in the greenhouse showed only small increases from 10 or 30 μg S g⁻¹ of CS₂ as compared to Na₂SO₄, on the two soils. While CS₂ supplied little plant available S in the short term, it was an effective inhibitor of nitrification. In the laboratory, or in the field, the injection of CS₂ (with N fertilizers) at a point 9 cm into the soils either stopped or reduced nitrification. In one laboratory experiment, 35 μg of CS₂ g⁻¹ of soil with urea reduced nitrification for at least four weeks; and in another experiment 20 μg of CS₂ g⁻¹ of soil with aqua NH₃ nearly or completely inhibited nitrification at 20 days. In two field experiments, 3 and 12 μg of CS₂ g⁻¹ of soil (or 6 and 24 kg ha⁻¹) with aqua NH₃ inhibited nitrification from October to the subsequent May. In addition, CS₂ reduced the amount of ammonium produced from the soil N, both in these two field experiments and in the laboratory experiments. That is to say, CS₂ injected at a point, inhibited both nitrification and ammonification. In other field experiments, CS₂ at a rate of 10 kg ha⁻¹ was injected in bands 9 cm deep with urea in October, and by May there was still reduced nitrification. Less than half of the fall-applied urea alone was recovered as mineral N, but with the application of CS₂ the recovery was increased to three-quarters. The yield and N uptake of barley grain was increased where fall-applied banded urea or aqua NH₃ received banded CS₂, (NH₄)₂CS₃, or K₂CS₃. The average increase in yield from fall-applied fertilizer, from inhibitor with fall-applied fertilizer, and from spring-applied fertilizer was 800, 1370, and 1900 kg ha⁻¹, respectively. In the same order, the apparent % recovery of fertilizer N in grain was 24, 42, and 60.     

Role of Thiobacillus thioparus in the biodegradation of carbon disulfide in a biofilter packed with a recycled organic pelletized material

This study reports the biodegradation of carbon disulfide (CS₂) in air biofilters packed with a pelletized mixture of composted manure and sawdust. Experiments were carried out in two lab-scale (1.2 L) biofiltration units. Biofilter B was seeded with activated sludge enriched previously on CS₂-degrading biomass under batch conditions, while biofilter A was left as a negative inoculation control. This inoculum was characterized by an acidic pH and sulfate accumulation, and contained Achromobacter xylosoxidans as the main putative CS₂ biodegrading bacterium. Biofilter operation start-up was unsuccessfully attempted under xerophilic conditions and significant CS₂ elimination was only achieved in biofilter A upon the implementation of an intermittent irrigation regime. Sustained removal efficiencies of 90–100 % at an inlet load of up to 12 g CS₂ m^?3 h^?1 were reached. The CS₂ removal in this biofilter was linked to the presence of the chemolithoautotrophic bacterium Thiobacillus thioparus, known among the relatively small number of species with a reported capacity of growing on CS₂ as the sole energy source. DGGE molecular profiles confirmed that this microbe had become dominant in biofilter A while it was not detected in samples from biofilter B. Conventional biofilters packed with inexpensive organic materials are suited for the treatment of low-strength CS₂ polluted gases (IL <12 g CS₂ m^?3 h^?1), provided that the development of the adequate microorganisms is favored, either upon enrichment or by inoculation. The importance of applying culture-independent techniques for microbial community analysis as a diagnostic tool in the biofiltration of recalcitrant compounds has been highlighted.     

Neuropathological Responses to Chronic NMDA in Rats Are Worsened by Dietary n-3 PUFA Deprivation but Are Not Ameliorated by Fish Oil Supplementation

Background

Dietary long-chain n-3 polyunsaturated fatty acid (PUFA) supplementation may be beneficial for chronic brain illnesses, but the issue is not agreed on. We examined effects of dietary n-3 PUFA deprivation or supplementation, compared with an n-3 PUFA adequate diet (containing alpha-linolenic acid [18:3 n-3] but not docosahexaenoic acid [DHA, 22:6n-3]), on brain markers of lipid metabolism and excitotoxicity, in rats treated chronically with NMDA or saline.

Methods

Male rats after weaning were maintained on one of three diets for 15 weeks. After 12 weeks, each diet group was injected i.p. daily with saline (1 ml/kg) or a subconvulsive dose of NMDA (25 mg/kg) for 3 additional weeks. Then, brain fatty acid concentrations and various markers of excitotoxicity and fatty acid metabolism were measured.

Results

Compared to the diet-adequate group, brain DHA concentration was reduced, while n-6 docosapentaenoic acid (DPA, 22:5n-6) concentration was increased in the n-3 deficient group; arachidonic acid (AA, 20:4n-6) concentration was unchanged. These concentrations were unaffected by fish oil supplementation. Chronic NMDA increased brain cPLA₂ activity in each of the three groups, but n-3 PUFA deprivation or fish oil did not change cPLA₂ activity or protein compared with the adequate group. sPLA₂ expression was unchanged in the three conditions, whereas iPLA₂ expression was reduced by deprivation but not changed by supplementation. BDNF protein was reduced by NMDA in N-3 PUFA deficient rats, but protein levels of IL-1β, NGF, and GFAP did not differ between groups.

Conclusions

N-3 PUFA deprivation significantly worsened several pathological NMDA-induced changes produced in diet adequate rats, whereas n-3 PUFA supplementation did not affect NMDA induced changes. Supplementation may not be critical for this measured neuropathology once the diet has an adequate n-3 PUFA content.     

Degradation of carbondisulphide by a Thiobacillus isolate

During experiments investigating the purification of waste gas a bacterium capable of using carbon disulphide (CS₂) als sole energy source was isolated. It could be identified as a Thiobacillus sp.; however, the species remains unclear. Both the properties of T. thioparus and T. thiooxidans have been observed. Since the organism could be used for removing CS₂ in the environment, the degradation kinetics have been investigated by different methods. Substrate concentrations of up to 100 mg CS₂·l^–1 were oxidized at maximum rates of 2.5 mg CS₂·g^–1 protein·min^–1 at pH 7.0 and at 30°C. CS₂ levels above 150 mg CS₂·l^–1 caused termination of degradative activity. Correspondence to: Ch. Plas     

Do CS-US Pairings Actually Matter? A Within-Subject Comparison of Instructed Fear Conditioning with and without Actual CS-US Pairings

Previous research showed that instructions about CS-US pairings can lead to fear of the CS even when the pairings are never presented. In the present study, we examined whether the experience of CS-US pairings adds to the effect of instructions by comparing instructed conditioning with and without actual CS-US pairings in a within-subject design. Thirty-two participants saw three fractals as CSs (CS⁺1, CS⁺2, CS⁻) and received electric shocks as USs. Before the start of a so-called training phase, participants were instructed that both CS⁺1 and CS⁺2 would be followed by the US, but only CS⁺1 was actually paired with the US. The absence of the US after CS⁺2 was explained in such a way that participants would not doubt the instructions about the CS⁺2-US relation. After the training phase, a test phase was carried out. In this phase, participants expected the US after both CS⁺s but none of the CS⁺s was actually paired with the US. During test, self-reported fear was initially higher for CS⁺1 than for CS⁺2, which indicates that the experience of actual CS-US pairings adds to instructions about these pairings. On the other hand, the CS⁺s elicited similar skin conductance responses and US expectancies. Theoretical and clinical implications are discussed.     

Metabolic effects of CO2 anaesthesia in Drosophila melanogaster

Immobilization of insects is necessary for various experimental purposes, and CO₂ exposure remains the most popular anaesthetic method in entomological research. A number of negative side effects of CO₂ anaesthesia have been reported, but CO₂ probably brings about metabolic modifications that are poorly known. In this work, we used GC/MS-based metabolic fingerprinting to assess the effect of CO₂ anaesthesia in Drosophila melanogaster adults. We analysed metabolic variation of flies submitted to acute CO₂ exposure and assessed the temporal metabolic changes during short- and long-term recovery. We found that D. melanogaster metabotypes were significantly affected by the anaesthetic treatment. Metabolic changes caused by acute CO₂ exposure were still manifested after 14 h of recovery. However, we found no evidence of metabolic alterations when a long recovery period was allowed (more than 24 h). This study points to some metabolic pathways altered during CO₂ anaesthesia (e.g. energetic metabolism). Evidence of short-term metabolic changes indicates that CO₂ anaesthesia should be used with utmost caution in physiological studies when a short recovery is allowed. In spite of this, CO₂ treatment seems to be an acceptable anaesthetic method provided that a long recovery period is allowed (more than 24 h).