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H Remmer

Publications and source records attributed to H Remmer.

At least 37 records · Page 2Linked to original sources
PubMed1983

Isolated intestinal cells of guinea pig: a suitable model for assessing direct toxic effects of ethanol on the mucosa of the upper small intestine.

The effects of acute ethanol (1-10%) on membrane transport and respiration in isolated jejunal cells of guinea pig were investigated. Three substrates with different transport mechanisms were employed: uridine (active, Na+-dependent transport), choline (saturable, Na+-independent transport), and chenodeoxycholate (simple diffusion). Uridine and choline transport were half-maximally inhibited by 3% ethanol; this inhibition was paralleled by a similar decrease in mitochondrial respiration and ATP production. Chenodeoxycholate uptake in contrast was virtually unaffected by up to 10% ethanol. It is concluded that acute ethanol inhibits active carrier-mediated absorption, but has no effect on transcellular diffusion of lipophilic compounds.

Adenosine Triphosphate↗
PubMed1982

Volatile alkanes produced by erythrocytes: an assay for in vitro studies on lipid peroxidation.

Lipid peroxidation in erythrocytes is currently studied by measuring the formation of malonyldialdehyde (MDA). A new and simple methodological approach to the measurement of the extend of lipid peroxidation is described here. Erythrocytes from freshly drawn human blood were washed and suspended in isoosmotic phosphate-buffered saline and incubated with sodium azide to inhibit the catalase. Oxidation of red cell lipids was induced by the addition of hydrogen peroxide. MDA formation was measured by the 2-thiobarbituric acid (TBA) reaction. After the same procedure of incubation the production of volatile alkanes (pentane, ethane, ethylene, n-butane, and propane) was estimated by gas chromatography. The total amount of pentane formation from red cells after 120 min of incubation with hydrogen peroxide was much higher than of the other alkanes. This assay provides a useful model to elucidate the role of lipid peroxidation of erythrocytes and is a simple method to study changes in their membrane lipid in diseases and red cell aging.

Alkanes↗
PubMed1982

First pass biotransformation of ethinylestradiol in rat small intestine in situ.

The intestinal absorption and biotransformation of ethinylestradiol and of ethinylestradiol glucuronide in rats were studied using a jejunal loop preparation in situ. Radioactivity associated with ethinylestradiol almost completely appeared in the venous outflow within 80 min. Forty two percent was present as unchanged compound, 56% in the glucuronide fraction and 2% as sulfate ester. Absorption of ethinylestradiol glucuronide was about 20 times slower than absorption of the nonconjugated molecule. The data indicate, that intestinal absorption of ethinylestradiol involves several superimposed kinetics and that glucuronidation in the gut may result in a decreased bioavailability of the compound.

Animals↗
PubMed1982

Further studies on adriamycin induced in vitro lipid peroxidation.

Adriamycin (AM)-induced lipid peroxidation was studied in rat liver microsomal system, measuring colour produced by thiobarbituric acid (TBA) reactive material and the development of volatile hydrocarbons. The onset of this degradative process is closely related to the AM content. This phenomenon appears to be highly influenced by the buffer used for the microsomal preparation. The effect of AM on FE--ADP-induced lipid peroxidation in liver microsomes has also been studied.

Adenosine Diphosphate↗
PubMed1982

Metabolic activation of carbon tetrachloride: induction of cytochrome P-450 with phenobarbital or 3-methylcholanthrene and its effect on covalent binding.

Anaerobic incubation of [14C]carbon tetrachloride with normal rat liver microsomes and microsomes from rats treated with the inducers phenobarbital (PB) and 3-methylcholanthrene (MC) reveals distinct differences in metabolic activation. While the increase in CO-binding pigment is comparable for both inducers, metabolism of CC14 is enhanced only by PB-induction; MC-induced microsomes are equivalent to microsomes from untreated animals. Sodium dodecyl sulphate (SDS)-electrophoresis of microsomal proteins confirms the expected increase at 52 000 daltons (cytochrome P-450 PB) on PB-induction, at 56 000 daltons (cytochrome P-450MC) on MC-induction; after anaerobic incubation with [14C]CC14 the electrophoretic pattern is largely unchange. The highly reactive radical intermediates of CC14-metabolism should attack the closest possible partner. Most of protein-bound radioactivity is located in the mass range between 47 000 and 54 000 daltons, indicating that cytochrome P-450PB is the isoenzyme mainly responsible for CC14-activation; cytochrome P-450MC plays virtually no role in metabolic activation. The direct participation of NADPH-cytochrome P-450 reductase appears unlikely, since the specific binding to proteins in the corresponding mass range is not elevated. A significant percentage of label is attached to proteins at 120 000 daltons and above, presumably oligomers of cytochrome P-450 apoprotein.

Anaerobiosis↗
PubMed1981

Uptake, accumulation and release of ouabain by isolated rat hepatocytes.

We investigated uptake of ouabain into isolated rat hepatocytes and release of ouabain from preloaded hepatocytes, thus assessing separately the two membrane transport steps, involved in biliary elimination of the drug. The following results were obtained: Uptake of ouabain was saturable (Km = 263 + 61 microM, V = 3.3 + 1.0 nmol/mgprot. x min), energy-dependent, sensitive to dinitrofluorobenzene and temperature-dependent (E = 80 - 96 kJ/mol). It had no pH-optimum in the physiological pH-range and was independent of the extracellular cation composition. Uptake of ouabain was competitively inhibited by the cardiac glycoside digitoxin (Ki = 0.3 microM). Uptake was not inhibited in the presence of the glycosidic sugar l-rhamnose, but it was competitively inhibited by the steroid taurocholate (Ki = 6.3 microM). Ouabain was accumulated within hepatocytes 170-fold. The predominant fraction of intracellular ouabain being unbound. Release of ouabain from preloaded cells was energy-independent, independent of the Na+-concentration and not susceptible to inhibition by dinitrofluorobenzene or taurocholate. It is concluded, first that hepatocellular uptake of ouabain is mediated by a carrier for steroids and second that the pathway of release is distinct from that of uptake. We assume, that the high bile/plasma concentration-gradient of ouabain in vivo is generated during active uptake into the cell and not during release into bile.

Animals↗
PubMed1980

Isobutene formation during halothane anaesthesia in man.

The concentrations of volatile hydrocarbons were studied in breath samples from patients before and after anaesthesia. In patients to whom halothane was administered, there was a significant increase in the concentration of isobutene (from 0.43 +/- 0.09 to 4.66 +/- 2.22 nmol litre-1). There was no change in the concentration of isobutene in six patients anaesthetized with ketamine and diazepam. The concentrations of ethane and pentane were not altered significantly in either group.

Adult↗
PubMed1979

An experimental model for the study of hepatic transport and metabolism of toxic compounds.

The usefulness of isolated liver cells for the study of hepatocellular transport and metabolism is demonstrated, using 1-naphthol and 2,2'-dichlorobiphenyl as model compounds. More than 60% of both substances is rapidly taken up by the cells. Naphthol is conjugated with sulphate and with glucuronic acid. These conjugates are released from the cells. Conjugation of dichlorobiphenyl and release of the conjugates is about 25 times slower than that of naphthol.

Animals↗