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H Gjerde

Publications and source records attributed to H Gjerde.

30 records · Page 2Linked to original sources

Determination of serum tryptophan by isocratic high-performance liquid chromatography and ultraviolet detection.

A simple method for the determination of serum tryptophan is described. Serum proteins were precipitated using ethanol, and after a centrifugation, tryptophan concentrations were measured in the supernatant using isocratic high performance liquid chromatography with ultraviolet detection at 219 nm. All serum compounds absorbing at this wavelength were eluted within 6 min; the retention time for tryptophan was 3.95 min. This method is simpler and more rapid than previously published methods, and the results are reliable. The coefficient of variation of the analysis was found to be less than 6.5%.

Chemical Precipitation↗

The antiglucocorticoid RU486 inhibits the ethanol-induced increase of tryptophan oxygenase.

The effect of the glucocorticoid-antagonist RU486 (Roussel-Uclaf, France) on the increased activity of hepatic tryptophan oxygenase (TO) after administration of corticosterone and ethanol in rats was studied. RU486 (40 mg/kg per os) inhibited completely the effect of corticosterone (5-15 mg/kg injected intraperitoneally) on TO. Ethanol (4 g/kg) given intraperitoneally is followed by peak corticosterone concentrations comparable to those seen after the administration of 5-10 mg exogenous corticosterone, and increased the TO activity 3-fold 4 h after the injection. RU486 inhibited completely the ethanol-induced increase of TO, indicating that this increase is mediated by corticosterone.

Animals↗

11-Deoxycortisol induces hepatic tryptophan oxygenase in rats.

11-Deoxycortisol (cortexolone) has previously been used as a glucocorticoid antagonist in vitro and in adrenalectomized rats. Antiglucocorticoid properties of 11-deoxycortisol in intact rats were examined by studying the effect of 11-deoxycortisol on the induction of hepatic tryptophan oxygenase (TO) by corticosterone. No antiglucocorticoid effect was observed. When 11-deoxycortisol was injected into rats, the TO activity increased. This was probably mainly caused by an elevation of the serum corticosterone level. The induction of TO by 11-deoxycortisol was inhibited by metyrapone. However, 11-deoxycortisol (100 mg/kg) was still not a glucocorticoid antagonist even in presence of metyrapone.

17-Hydroxycorticosteroids↗

Determination of gamma glutamyltransferase in completely haemolysed blood samples.

A simple method for the determination of gamma glutamyltransferase (GGT) in completely haemolysed blood samples is described. Haemolysed blood was incubated in the presence of gamma glutamyl-p-nitroanilide and glycylglycine at 37 degrees C for 15 min, and the enzyme reaction was terminated by adding trichloroacetic acid. The pH in the supernatant was adjusted to 7.5 by using a buffer, and the amount of p-nitroaniline formed was measured spectrophotometrically. The correlation between this method and the GGT activity in serum as determined by the standard kinetic method was good, r = 0.982. The blood GGT activity (y) was related to the serum activity (x) as follows: y = 0.415x + 3.8. The effect of storage of blood at room temperature on the GGT activity was studied. The enzyme activity did not change during the first 12 days of storage.

Blood Chemical Analysis↗

Effect of warfarin on ATP content, viability, glycosylation and protein synthesis in isolated rat hepatocytes.

The effect of warfarin on ATP content, viability and incorporation of labelled glucosamine and leucine into protein was studied in suspensions of rat hepatocytes. When incubated with warfarin the synthesis of total protein and glycoprotein was equally inhibited, and the viability and ATP content of the cells were also lowered. These observations suggest that warfarin is not an inhibitor of glycosylation of proteins in isolated hepatocytes, however, the presence of warfarin leads to reduced ATP content of the cells which causes a decrease in protein synthesis and viability.

Adenosine Triphosphate↗

Impairment in drivers due to cannabis in combination with other drugs.

Blood samples from 425 suspected drugged drivers who were clinically impaired and negative for alcohol were analysed. Fifty-six percent of the samples were positive for tetrahydrocannabinol (THC). Tetrahydrocannabinol-positive blood samples were analysed for amphetamines, barbiturates, benzodiazepines, cocaine metabolites and opiates. Eighty-two percent of the samples were found to be positive for one or more drugs in addition to THC, and the concentrations of these drugs were often high. Thus, THC in combination with other drugs seems to be a much more frequent reason for impairment than THC alone among Norwegian drugged drivers.

Amphetamines↗

Screening for cannabinoids in blood using EMIT: concentrations of delta-9-tetrahydrocannabinol in relation to EMIT results.

The EMIT d.a.u. cannabinoid assay of methanolic extracts of blood was found to be usable as a screening method in cases of suspected impairment by cannabis, when delta-9-tetrahydrocannabinol (THC) was analysed in the subsequent assay. A prerequisite is that the blood sample is taken some time after cannabis smoking. When a cut-off limit corresponding to 50 nM delta-9-tetrahydrocannabinol carboxylic acid (17 ng/ml) was used, 86% of the EMIT positive blood samples contained THC concentrations above the cut-off limit of 1 nM (0.3 ng/ml). A high EMIT result gave a high probability of finding a high THC concentration in the subsequent confirmation analysis.

Cannabinoids↗

Ethanol increases rat liver tryptophan oxygenase: evidence for corticosterone mediation.

Acute administration of ethanol (4.0 g/kg) intragastrically or intraperitoneally induced rat liver tryptophan oxygenase (TO) activity 3-4 fold 4-5 hr later. Ethanol administration increased the concentration of plasma free tryptophan and free fatty acids. Pretreatment with a beta-receptor blocker, propranolol, modified the latter responses without affecting the TO induction due to ethanol. The rise of the level of plasma free tryptophan due to ethanol was too small to influence TO activity. Liver tryptophan concentration and TO half-life was unchanged after ethanol administration. Ethanol administration increased the concentration of plasma corticosterone sufficiently to increase TO activity. Pretreatment with a glucocorticoid antagonist blocked this TO response to ethanol. The increased TO activities found after ethanol or corticosterone treatment were influenced in the same manner and to the same extent by cycloheximide. Taken together it is concluded that ethanol induces TO through a rise of glucocorticoid hormones and not by a tryptophan-linked mechanism.

Animals↗

Determination of amphetamine and methamphetamine in blood by derivatization with perfluorooctanoyl chloride and gas chromatography/mass spectrometry.

A relatively simple method for quantitation of amphetamine and methamphetamine in blood was developed. Blood samples were extracted with cyclohexane, and the extracts were derivatized with perfluorooctanoyl chloride prior to gas chromatography/mass spectrometry. Selected ions were monitored at m/z 118 and 440 for amphetamine, m/z 118 and 454 for methamphetamine, and m/z 121 and 443 for the internal standard amphetamine-d3. The imprecision was less than 5% for amphetamine and less than 9% for methamphetamine. Limits of detection were 11 micrograms/L for amphetamine and 13 micrograms/L for methamphetamine, while limits of quantitation were 22 and 34 micrograms/L, respectively. Calibration curves were linear in the ranges 14-2700 micrograms/L and 15-3000 micrograms/L, respectively. Some drugs that were known or suspected to interfere with immunological or chromatographic methods for amphetamine and methamphetamine were tested for interference. None of the drugs tested interfered, except for a substance in putrefied blood samples, which was found to interfere with one ion (m/z 118) for amphetamine but not with the second ion.

Amphetamine↗

Heavy drinking among Norwegian male drunken drivers: a study of gamma-glutamyltransferase.

The distributions of blood alcohol concentrations (BACs) of different age groups of drunken drivers suggested that a large number of the drunken drivers above 29 years of age had high tolerance to alcohol, and many of these might be heavy drinkers. In order to study the extent of heavy drinking, gamma-glutamyltransferase (GGT) activities were measured in 269 blood samples from male drunken drivers using a new method suitable for hemolyzed blood samples. Of the drunken drivers above 29 years of age, 40% had elevated GGT activities, indicating that roughly one-third of these drivers might be heavy drinkers (consuming more than 80 g of alcohol/day). Of the drunken drivers above 29 years of age with BACs above 55 mmol/liter (250 mg/100 ml), 63% had elevated GGT, indicating that a large majority of these drivers were heavy drinkers. Fewer of the younger drivers had elevated GGT activities. The GGT activities of the repeating offenders indicated that the percentage of heavy drinkers in this group was approximately the same as in the total population of apprehended drunken drivers.

Adult↗