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PubMedDate not supplied

[Liver disease in toxic oil syndrome. Clinical and enzymatic course].

One-hundred and fifty-nine patients intoxicated with adulterated oil in the province of Salamanca, Spain, were followed-up for 2 years from the onset of the syndrome, in 1981. Four alcoholic patients were excluded from the study. In the remaining 155 patients the liver involvement at the onset took different forms. It was acute in 12 (7%), with jaundice and/or hepatomegaly associated with cytolysis and/or cholestasis; 21 patients (13%) had evidence of cytolysis and/or cholestasis without clinical symptoms, and 29 (18%) only showed a rise in gamma-glutamyltranspeptidase with normal transaminase and alkaline phosphatase levels. Liver enlargement and/or jaundice subsided within 1 month in the 12 patients with clinical symptoms. However, high gamma-glutamyltranspeptidase levels persisted in 4 of them and in 5 of the 21 patients with laboratory abnormalities only. At the end of the study, this enzyme remained elevated in 6 and 7 patients respectively of these two groups and in 5 of the 29 patients with no other abnormality than a rise in gamma-glutamyltranspeptidase.

Adult↗

PubMedDate not supplied

Screening for illicit heroin use in patients in a heroin-assisted treatment program.

The aim of this study was to investigate the use of illicit heroin among patients in a heroin-assisted treatment program. In this program, pharmaceutical-grade heroin was administered to heroin-addicted patients. Monitoring of illicit heroin use was considered important for the evaluation of this treatment program. Acetylcodeine and codeine, common adulterants of "street" heroin, were used as markers for illicit heroin. A liquid chromatography method with tandem mass spectrometric detection (LC-MS-MS) was developed, for quantitative analysis of heroin and methadone, their metabolites, and the simultaneous detection of acetylcodeine. One-hundred patients in a heroin-assisted treatment program were screened for acetylcodeine in plasma. Furthermore, patients were interviewed about illicit heroin use, and they were tested for alcohol and cocaine use. In plasma samples of 16% of the patients, acetylcodeine was detected. Overall agreement between self-report and plasma samples was 95% (kappa: 0.81). Patients who tested positive for acetylcodeine had visited the outpatients' clinics significantly less frequently than the patients who tested negative. Alcohol and cocaine use was more common in patients who tested positive for acetylcodeine. Illicit heroin use was observed in a limited percentage of patients. Overall agreement between self-report and markers of illicit heroin use was good.

Adult↗

PubMed1992

Comparative lethality of methanol, ethanol and mixtures in female rats.

The lethalities of pure methanol and pure ethanol were compared to two mixtures of ethanol/methanol with the following percentages (95/5% and 65/35% v/v). This study was conducted to simulate situations of human exposure to denaturated alcohol (by 5% methanol) or adulterated alcohol (by 35% methanol). Four groups of female adult virgin albino rats were treated with the four mixtures. A fifth group was used as a vehicle control. Graded oral doses were given to eight animals per dose. Lethality over 24 h was used as an end-point. The LD50 was calculated for each of the four treatments on a molar basis. A dose-response function for each mixture was plotted of percentage lethality vs. mmol kg-1 equivalent to the given ml kg-1 dose. Results showed a significantly different LD50 estimates (P less than 0.03) for the four mixtures. The order of lethal toxicity was as follows: 95/5% methanol/ethanol, pure methanol, pure ethanol then 65/35% methanol/ethanol. Slope comparisons indicated two pairs: 65/35% ethanol/methanol and pure ethanol yielding a steep slope, and 95/5% ethanol/methanol and pure methanol yielding a shallow slope. These data indicated that the acute lethality of ethanol/methanol mixtures is a complex unpredictable function. This toxicity presumably depends in a complicated way on the differences in the effective molecular weights of the two alcohols in each of the mixtures.

Animals↗

PubMed2004

Analysis of nitrite in adulterated urine samples by capillary electrophoresis.

A simple method for analyzing nitrite in urine has been developed to confirm and quantify the amount of nitrite in potentially adulterated urine samples. The method involved separation of nitrite by capillary electrophoresis and direct UV detection at 214 nm. Separation was performed using a bare fused silica capillary and a 25 mM phosphate run buffer at a pH of 7.5. Sample preparation consisted of diluting the urine samples 1:20 with run buffer and internal standard, and centrifuging for 5 min at 2500 rpm. The sample was hydrodynamically injected, then separated using -25 kV with the column maintained at 35 degrees C. The method had upper and lower limits of linearity of 1500 and 80 microg/mL nitrite, respectively, and a limit of detection of 20 microg/mL. The method was evaluated using the National Committee for Clinical Laboratory Standards (NCCLS) protocol (Document EP10-A2), and validated using controls, standards, and authentic urine samples. Ten anions, ClO-, CrO4(-2), NO3-, HCO3-, I-, CH3COO-, F-, SO4-, S2O8(-2), and Cl-, were tested for potential interference with the assay. Interferences with quantitation were noted for only CrO4(-2) and S2O8(-2). High concentrations of Cl- interfered with the chromatography. The method had acceptable accuracy, precision, and specificity.

Buffers↗

PubMed2007

Seizure prophylaxis in an animal model of epilepsy by dietary fluoxetine supplementation.

Clinical and animal model evidence suggests that selective serotonin reuptake inhibitors (SSRIs) act as anticonvulsants. The present studies tested the possibility that the El mouse model of genetically predisposed/handling-triggered epilepsy would exhibit fewer seizures following SSRI treatment via dietary fluoxetine adulteration. In particular, potential bioenergetic and neural mechanisms for anticonvulsant efficacy of fluoxetine were explored using food intake/body weight monitoring and quantification of brain serotonin transporter protein. El mice consuming a chow diet ad libitum or yoked in quantity to fluoxetine diet intake exhibited seizure incidence of 40% in response to tail-suspension handling, whereas seizures were abolished (0%) among El mice consuming a fluoxetine-adultered diet over 7 days. A 3 day period of fluoxetine administration was insufficient to exert anticonvulsant efficacy and all treatment groups exhibited the same circadian locomotor activity patterns at the time of seizure susceptibility testing. Bioenergetic factors could not account for the anticonvulsant efficacy of fluoxetine since yoked diet controls with matched food intake, body weight change and blood glucose levels exhibited the same 40% seizure incidence as ad libitum chow controls. Importantly, the 7 day period of dietary fluoxetine exposure was effective in selectively reducing cell density in the parietal cortex and increasing serotonin transporter protein content in the nucleus accumbens. Taken together, these results suggest that dietary fluoxetine supplementation abolishes handling-induced seizure susceptibility in El mice via a neural remodeling mechanism independent of energy balance.

Animal Feed↗

PubMed1994

Impurities, adulterants and diluents of illicit heroin. Changes during a 12-year period.

Changes in the content of impurities, adulterants and diluents are described for 383 samples of illicit heroin seized in the western part of Denmark during the 12-year period 1981 through 1992. A wide range in purity was found within each year, whereas the average purity did not vary much from one year to another. The average purity of wholesale samples (45%) was only slightly higher than the purity of retail samples (36%). The SW Asian type of heroin, containing high concentrations of noscapine, predominated from the mid-eighties. Heroin base and heroin hydrochloride each accounted for approximately half of the samples during the eighties. However, in recent years the base form has become predominant. During the early eighties caffeine and procaine were the most frequent additives next to sugars. During the middle and late eighties an increasing number of heroin samples were cut with phenobarbital and methaqualone. During the early nineties the occurrence of phenobarbital and methaqualone has decreased, whereas paracetamol in combination with caffeine has become predominant. Re-analyses of samples which had been kept in storage for several years showed that most samples had not changed after being stored in the dark for a couple of years at room temperature. However, storage for more than 5 years often resulted in decomposition, particularly in samples consisting of the SW Asian type of heroin.

Acetaminophen↗

PubMed1997

Effects of in utero and lactational exposure of the laboratory rat to 2,4,2',4'- and 3,4,3',4'-tetrachlorobiphenyl on dopamine function.

Offspring of Sprague-Dawley derived dams were exposed to either 2,4, 2',4'-tetrachlorobiphenyl (TCB) (1, 10, or 20 mg/(kg.day)) or 3,4,3', 4'-TCB (0.1 or 1 mg/(kg.day)) from gestational Day 6 through weaning by providing the dams with cookies adulterated with the appropriate amount and type of PCB. Male and female offspring were sacrificed on postnatal Days 35, 60, and 90, and brain concentrations of dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, were determined in the frontal cortex, caudate nucleus and substantia nigra by high-performance liquid chromatography with electrochemical detection. In utero and lactational exposure to 3,4,3',4'-TCB resulted in significant elevations in concentrations of dopamine in the frontal cortex, and of dopamine and its metabolites in the substantia nigra that persisted into adulthood. In contrast, in utero and lactational exposure to 2,4,2',4'-TCB resulted in significant decreases in concentrations of dopamine in the frontal cortex and caudate nucleus that also persisted into adulthood. We suggest that the reductions in brain dopamine concentrations are a consequence of ortho-substituted PCB congener-induced inhibition of the synthesis of dopamine during critical periods of development acting, perhaps, in concert with PCB-induced changes in cholinergic receptor function. On the other hand, the persistent elevations in brain dopamine and metabolite concentrations following perinatal exposure to 3,4,3',4'-TCB may be mediated by alterations in steroid hormone function during key developmental periods.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2000

Reduced levels of 1,25-dihydroxyvitamin D(3) in rat dams and offspring after exposure to a reconstituted PCB mixture.

Previous studies revealed effects of polychlorinated biphenyls (PCBs) and other polyhalogenated hydrocarbons on steroid hormone levels and hormone-dependent functions including behavior. In the present study serum concentrations of the vitamin D(3) metabolites 25-hydroxycholecalciferol (25-D) and 1,25-dihydroxycholecalciferol (1,25-D) were determined in rat dams and offspring after exposure to a PCB mixture that was reconstituted according to the congener pattern found in human breast milk. Unmated females were exposed to diets adulterated with 0; 5; 20; or 40 mg PCBs/kg diet. Exposure started 50 days prior to mating and was terminated at birth. Gestational exposure reduced serum concentrations of 1,25-D in dams in a dose-dependent manner. Concentration of 25-D was also decreased at the time of delivery, but not at weaning. Determination of 1,25-D in offspring at weaning revealed reductions in both high-exposure groups. Levels of 25-D were diminished only at the highest exposure level. Internal PCB concentrations in adipose tissue and brains exhibited a linear relation to dosages in diet. Concentrations of PCBs in brains were similar in dams and offspring at birth, but decreased at the end of lactation in dams. In offspring, values increased during this period because of continued exposure via the milk. In the adipose tissue, PCB levels were much lower in offspring than in dams. To our knowledge, this is the first report of PCB-induced effects on vitamin D(3) metabolites. In dams, reductions were seen even at the lowest exposure level used. Further studies are needed to evaluate the biological significance of these reductions in pregnant dams and possible consequences for the developing offspring.

Adipose Tissue↗

PubMed2004

Unequivocal evidence of genotoxic potential of argemone oil in mice.

Consumption of mustard oil adulterated with argemone oil leads to a clinical condition, commonly referred to as "Epidemic Dropsy." Since in vitro studies have shown that sanguinarine, an active benzophenanthridine alkaloid of argemone oil, intercalates DNA molecule, the in vivo clastogenic and DNA damaging potential of argemone oil was investigated in mice. Swiss albino mice were intraperitoneally administered 0.5, 1.0, 2.0 and 4.0 ml/kg body wt. of argemone oil to analyze chromosome aberrations and micronucleus test, while 0.25, 0.5, 1.0 and 2.0 ml/kg body wt. were given for alkaline comet assay. The frequencies of chromosomal aberrations and micronucleated erythrocytes formation in mouse bone marrow cells increased in a dose-dependent manner following argemone oil treatment. However, significant induction in chromosomal aberrations (83%) and micronucleated erythrocytes formation (261%) were observed at a minimum dose of 1.0 ml/kg. The results of comet assay revealed DNA damage in blood, bone marrow and liver cells following argemone oil treatment. Olive tail moment (OTM) and tail DNA showed significant increase in bone marrow (35-44%) and blood cells (25-40%) even at a dose of 0.25 ml/kg body wt. of argemone oil. In liver cells, OTM was significantly increased (20%) at a dose of 0.25 ml/kg, while all the comet parameters including OTM, tail length and tail DNA showed significant increase (31-101%) at a dose of 0.5 ml/kg. These results clearly suggest that single exposure of argemone oil even at low doses produces genotoxic effects in mice.

Animals↗