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Biomedical subjects

T Ekström

Publications and source records attributed to T Ekström.

52 records · Page 3Linked to original sources
PubMed1988

Recovery of malondialdehyde in urine as a 2,4-dinitrophenylhydrazine derivative analyzed with high-performance liquid chromatography.

Malondialdehyde (MDA) in urine was measured as a 2,4-dinitrophenylhydrazine (DNPH) derivative using high-performance liquid chromatography (HPLC) for the analysis. MDA standard coeluted with a peak obtained from rat urine after i.p. administration of MDA standard. This peak was also the only peak containing 14C after injection of a [14C]MDA standard, and was shown by mass spectrometry to contain 1-(2,4-dinitrophenyl)pyrazole, the derivative formed when MDA is treated with DNPH. Depending on the amount given (0.3-5.5 mumol), the recovery (after 24 h sampling period) in urine was 0.7-2.6%. This apparent non-linear kinetics may relate to several factors, such as dose-dependent metabolism. However, the peak urinary concentration approached the expected plasma concentration and reproducible recovery data were obtained, suggesting that MDA was passively excreted in a reasonably stable form. These data indicate that monitoring MDA excretion in urine can give useful information about lipid peroxidation in vivo.

Animals↗
PubMed1988

Recovery of malondialdehyde in urine as a 2,4-dinitrophenylhydrazine derivative after exposure to chloroform or hydroquinone.

Malondialdehyde (MDA) excretion in urine as an index for toxicological effects of chloroform and hydroquinone was evaluated. In a first series of experiments three groups of rats were used: non-pretreated rats (group I), starved rats (group II) and starved plus phenobarbital pretreated rats (group III). Chloroform (0.15 or 0.30 ml/kg, p.o.) was given as a single dose. The MDA excretion was related to the pretreatment, and in group III to liver damage. In a second series of experiments control rats were administered hydroquinone (100 or 200 mg/kg, p.o.), which induced a dose-related MDA excretion. These data indicate that the MDA assay was a selective and accurate marker for toxicological effects induced by the tested compounds.

Alanine Transaminase↗
PubMed1988

Gastro-oesophageal reflux and nocturnal asthma.

Gastro-oesophageal (GO) reflux is believed to be a possible cause of nocturnal asthma. The aim of this study was to see if there is any correlation between the incidence of GO-reflux at night and nocturnal asthma. Thirty-seven adult patients with a history of nocturnal asthma for more than one hundred days a year and of reflux disease were evaluated using 24 h pH-monitoring of the oesophagus and measurement of peak expiratory flow (PEF) rate every hour when awake. Half of the patients suffered from severe GO-reflux at night, whilst the other half had no nocturnal reflux. Respiratory symptoms and inhalation of beta-2 agonists were recorded during the night and PEF was recorded when the patients awoke in the morning. A significant correlation was found between reflux at night and the degree of bronchial obstruction in the early morning, but not between night-time reflux and nocturnal respiratory symptoms. It would appear that GO-reflux in most asthmatics is neither a strong nor immediate trigger factor in nocturnal asthma, although it does seem to influence bronchial obstruction during the night as was demonstrated by a low morning-PEF value.

Asthma↗
PubMed1987

Gastro-oesophageal reflux and triggering of bronchial asthma: a negative report.

The aim of this study was to investigate whether a direct causal relationship exists between gastro-oesophageal (GO) reflux episodes and bronchial asthma. Forty-two patients with moderate or severe asthma and pathological GO-reflux were examined using a 24-h pH test at a proximal and a distal level of the oesophagus. Respiratory symptoms and the use of extra beta-2 agonist metered dose inhaler were recorded in a standardized protocol, and peak expiratory flow (PEF) was recorded once an hour until the patient went to bed. No association was found between reflux at either the proximal or the distal level of the oesophagus and bronchial symptoms or PEF reductions. We conclude that GO-reflux does not play an important role as an immediate trigger factor in bronchial asthma.

Adult↗
PubMed1986

Lipid peroxidation in vivo monitored as ethane exhalation and malondialdehyde excretion in urine after oral administration of chloroform.

In vivo lipid peroxidation was studied in phenobarbital pretreated rats exposed for chloroform. Lipid peroxidation was monitored as ethane exhalation or malondialdehyde (MDA) excretion in urine. A single oral dose of chloroform (0.7 ml/kg b.wt.) showed a marked increase in ethane exhalation in animals starved for 48 hours prior to chloroform treatment. This increase became evident after a lag-period of about 100 min. Pretreatment with diethylmaleate (1 ml/kg b.wt.) 1 hour prior to chloroform treatment gave a similar result. MDA excretion in urine from non-starved animals, exposed to chloroform, markedly increased after 4 hours and after 24 hours 115 nmol/kg had been excreted. In animals starved for 48 hours prior to chloroform treatment about 270 nmol/kg excreted within 24 hours. Small molecular weight thiols were measured in liver, kidneys and lungs. Chloroform decreased the thiol content of the liver by 43.2% within 100 min. while the concentration in the kidneys and the lungs were less affected. It is suggested that chloroform may act as a potent inducer of lipid peroxidation in vivo. The synergistic effects of the pretreatments and the lag phase indicate that glutathione depletion in the liver was an essential factor in this response.

Administration, Oral↗
PubMed1986

The effect of inhaled clonidine in patients with asthma.

To study the effect of inhaled clonidine on broncho-obstruction in asthmatics, 10 patients with extrinsic asthma were broncho-provoked twice with an allergen that had been shown to give positive skin prick test results. Before the provocations, saline or clonidine (75 micrograms) was inhaled via a DeVilbiss no. 40 nebulizer. Clonidine slightly improved the basal respiratory function without significantly influencing the blood pressure. There was a reduction in the allergen-evoked broncho-obstruction by 42 to 65% after pretreatment with clonidine. The eosinophilic leukocytes in peripheral blood had a slight tendency to leave the circulatory system during the provocation preceded by the clonidine treatment. These data add further evidence to the finding that clonidine may be of interest in the treatment of broncho-obstructive diseases.

Administration, Intranasal↗
PubMed1982

Biosynthesis of dolichol and dolichylphosphate in rat hepatocytes in vivo.

The biosynthesis of dolichol and dolichylmonophosphate in rat liver was studied using [3H]mevalonate as precursor. The radioactive precursor was either injected into the portal vein of the rat or added to the incubation medium containing isolated hepatocytes, followed by the isolation of microsomes and mitochondria from the liver or the hepatocytes. In both systems dolichol in microsomes was highly labeled after a short labeling period followed by a rapid decrease. During this period the labeling of mitochondrial dolichol was low. The specific radioactivity of dolichyl-P in microsomes of both systems was higher in the initial phase than in dolichol and increased further with time. The mitochondrial labeling was also increased but was at a much lower level.

Animals↗
PubMed1982

Enrichment of the intracellular dolichol pool in isolated liver cells.

Isolated hepatocytes were incubated with egg lecithin liposomes containing dolichol(C55), dolichol(C95), and dolichol phosphate(C55) in order to enrich intracellular membranes with these polyprenols. After incubation, the lipids were recovered from various membrane fractions and from the supernatant. The highest concentration was found in the microsomes. A part of the dolichol in microsomes, as well as in other fractions, was phosphorylated. This phosphorylation is mediated by the CTP-specific kinase that is present only on the outer surface of the microsomes and uses alpha-saturated polyprenols as substrates. The isolated microsomes enriched with dolichol in vivo exhibited increased lipid and protein glycosylation upon incubation with nucleotide sugars and it was demonstrated that the increased lipid glycosylation was due to transfer of the sugar to the exogenous incorporated dolichol.

Animals↗
PubMed1980

Metabolism of toxic substances in isolated hepatocytes.

Chloroform and selenite toxicity have been studied in isolated hepatocytes. Two different toxic mechanisms, which lead to cellular lysis after distinct lag periods, are compared. Chloroform toxicity can be divided into 2 phases, a first phase characterized by chloroform metabolism and a second phase characterized by lipid peroxidation. GSH depletion during the first phase is claimed to be a prerequisite for lipid peroxidation in the second phase. Selenite metabolism leads to cofactor depletion as well. Selenite reduction via a GSH reductase dependent pathway exhausts the cells of NADPH and this effect can be related to cellular lysis.

Animals↗