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Biomedical subjects

W Klinger

Publications and source records attributed to W Klinger.

At least 73 records · Page 4Linked to original sources
PubMed1989

Birch sap and birch leaves extract: screening for antimicrobial, phagocytosis-influencing, antiphlogistic and antipyretic activity.

Birch sap and birch leaves extract have been screened for antimicrobial, phagocytosis-influencing, anti-inflammatory and antipyretic activity. No antimicrobial effects could be detected in the agar-diffusion test with staphylococcus as test strain, whereas birch sap exhibited some inhibitory effect on phagocytosis, which exceeded that of the citric acid added to the birch sap as preservative. In rats, only the high doses of 1 and 2 ml/100 g b.m. birch sap had a weak and short-lasting anti-inflammatory activity against the Carrageenin edema, whereas birch leaves extract proved to be ineffective. Fever induced by baker's yeast in rats was inhibited by birch leaves extract in the high dose of 4 ml/100 g b.m. significantly, but not by birch sap, and only for a short period. Acetylsalicyclic acid had a much higher anti-inflammatory and antipyretic activity. Altogether despite of detectable anti-inflammatory, antipyretic and phagocytosis-inhibiting effects of these birch products no therapeutic activity of importance compared with classical and modern antipyretics-analgetics can be demonstrated.

Animals↗
PubMed1989

[Determination of the biliary excretion of reduced and oxidized glutathione].

An enzymatic method is presented for the detection of biliary excretion of reduced (GSH) and oxidized (GSSG) glutathione. The biliary excretion of GSH is 65.63 +/- 7.23 nmoles/kg b.w. x min and of GSSG 5.90 +/- 0.64 nmoles/kg b.w. x min in 55 day-old female rats, respectively. The recovery is 97.39 +/- 0.40% for GSH and 91.05 +/- 2.30% for GSSG. Cysteine which can be detected in bile, does not influence the accuracy of the results.

Animals↗
PubMed1989

[Anticonvulsive therapy and complications of pregnancy in epileptic patients].

During observation of 92 pregnancies, epileptic seizures, pregnancy complications and complications regarding the newborns were noticed with 67 women having epilepsy and correlated by means of following therapeutic aspects: without anticonvulsive therapy, monotherapy, combined therapy. Most of the attacks suffered women that were treated by combined therapy. Pregnancy and birth complications appeared nearly to the same extent more with patients under mono- and combined therapy than with patients without therapeutic treatment. Most frequently we saw complications and malformations with regard to the children in that group of mothers that had been treated by an anticonvulsive combined therapy.

Abnormalities, Drug-Induced↗
PubMed1988

Chlorinated drinking water is mutagenic and causes 3-methylcholanthrene type induction of hepatic monooxygenase.

Acid/neutral fractions of 4 chlorinated drinking water samples were tested for mutagenicity in the Ames' test and injected intraperitoneally to 10- and 20-day-old Wistar rats at doses of 200 and 100 liters of water/kg body weight. Cytochrome P-450 mediated enzyme activities of ethylmorphine-N-demethylase (EMND), 7-ethoxycoumarin-O-deethylase (ECOD), 7-ethoxyresorufin-O-deethylase (EROD) and 7-pentoxyresorufin-O-dealkylase (PEROD) were determined in the 9000 g supernatant fraction of liver homogenate. EROD was introduced by the concentrates. The induction was related to the mutagenic activity. About 4-fold increase in activity was observed with the most mutagenic sample. PEROD was also slightly enhanced. EMND and ECOD activities were not affected by the lower dose, but the higher dose caused inhibition of 30-40%. Although the extracts were not toxic to bacteria, they were unexpectedly toxic to rats. It is concluded that the samples contained 3-methylcholanthrene (3-MC) type inducer(s).

Animals↗
PubMed1988

Testing of dioxolan-methyl-metaacrylate (DMA) for hepatotoxicity and nephrotoxicity.

Dioxolan-methyl-metaacrylate (DMA) is applied as an adhesive for optical glasses and as a tooth filling material using the polymerisation properties. In rat LD50 was estimated at about 500 mg/100 g b.m. following i.p. or i.m. administration without distinct sex differences. DMA is less toxic following oral administration. Hypnotic or myorelaxing effects could be observed in a dose-dependent manner. DMA antagonized pentetrazole-induced convulsions. Prolongation of hexobarbital sleeping time without influence on awakening concentration of hexobarbital inhibition of biotransformation reactions, proved in vivo and in in vitro experiments measuring ethylmorphine-N-demethylation, ethoxycoumarin-O-deethylation and cytochrome P-450 content. There are no influences of DMA on urine concentrating ability. Oliguric effects of DMA might be caused by central depressive effects of DMA. There are no distinct effects of DMA on p-aminohippurate transport. Signs of a selective hepatotoxic or nephrotoxic effectiveness of DMA can be excluded because the respective functions were altered only following administration of extremely high doses of DMA (50% of LD50 values).

Animals↗
PubMed1988

Separation and characterization of hepatocytes from immature and adult rats into distinct subpopulations by centrifugal elutriation.

Hepatocytes were isolated from immature and adult rat liver by retrograde perfusion with calcium free buffer, followed by enzymic digestion, and separated into subpopulations by centrifugal elutriation. Several subpopulations with increasing cell diameters were distinguished. The smaller cells were attributed to the periportal area, the larger ones to the perivenous (centrilobular) region. Profiles of total cytochrome P-450 concentration, benzphetamine N-demethylation and ethoxyresorufin O-deethylation, NADPH-cytochrome c-reductase, glucose-6-phosphatase and glutamate-pyruvate-transaminase activities were determined in all subpopulations. With adult hepatocytes an increasing cytochrome P-450 concentration with increasing cell diameter (increasing from periportal to perivenous hepatocytes) could be observed, paralleled by increasing activities of benzphetamine N-demethylation and ethoxyresorufin O-deethylation activities. While NADPH-cytochrome c-reductase did not show a distinct zonation, glucose-6-phosphatase and glutamate-pyruvate-transaminase revealed increasing activities with increasing cell diameter. Immature hepatocytes (rats aged 11-15 days) were smaller, and more fragile. They could not be isolated with the same enzyme solution as adult hepatocytes and they did not show any zonation of cytochrome P-450 concentration, although the zonation of benzphetamine N-demethylation and ethoxyresorufin O-deethylation was almost fully developed. For NADPH-cytochrome c-reductase a zonation with higher activities in the perivenous cells could be demonstrated, in contrast to the lack of zonation in adult rats. Glucose-6-phosphatase activity showed a decline with increasing cell diameter in immature hepatocytes, whereas glutamate-pyruvate-transaminase activity did not show any zonation. In rats aged 20 days the zonation of these parameters in liver was in between that of younger and older animals. Zonation of the liver lobule develops postnatally with individual patterns for the different parameters.

Aging↗
PubMed1987

Interaction of induction, ontogenetic development and liver regeneration on the monooxygenase level.

2/3 Hepatectomy (HX), but also sham operation (SO) decreased liver dry mass for the first 3-4 days after operation both in 10- and 60-day-old male Wistar rats, whereas body mass development was not altered. Both SO and HX decreased ethylmorphine N-demethylation (EN) and ethoxycoumarin O-deethylation (EO), but distinctly more pronounced after HX. In 10-day-old rats EN and EO were in the normal range 14 days after SO and HX. After 3 weeks EN even exceeded the control level. In 60-day-old rats SO alone resulted in decreased EN and EO even 3 weeks after operation. Compared with SO-controls EN was lower but EO was in the same range in HX rats 14 days after operation. Neither in 10- nor in 60-day-old rats inducibility by phenobarbital (PB) could be demonstrated 24 h after HX with cytochrome P-450 concentration (P-450), EN and EO as parameters. But inducibility by betanaphthoflavone (BNF) was significant for P-450, EN and EO in 10-day-old rats and also for P-450 and EO in 60-day-old rats. In the young adult rats EN was depressed by BNF. In rats 10 days old at HX inducibility by PB was highest 3-7 days after HX, but inducibility by BNF after 14 days. In 60-day-old rats inducibility by PB was highest for EO 1 day after HX. These results indicate that ontogenetic development can be enhanced by induction, that during development regeneration can be superimposed and both induction and regeneration can superimpose ontogenetic development. During these processes different monooxygenases are under differential control.

Age Factors↗
PubMed1987

Influence of triiodothyronine and dexamethasone on the postnatal development of hepatic eosine transport in rats.

In male Wistar rats of different ages the influence of a three days pretreatment with triiodothyronine (T3, 100 micrograms/kg b.m.s.c.) or dexamethasone (0.4 mg/kg b.m.i.p.) on eosine accumulation of rat liver in vitro and biliary excretion of eosine in vivo was investigated. T3 stimulated the eosine accumulation in liver slices. This in vitro effect was not paralleled by higher serum elimination rates of eosine in vivo. Neither T3 nor dexamethasone could accelerate the maturation of the rate limiting excretion process for organic anions in developing rats.

Age Factors↗
PubMed1987

Effects of allopurinol, (+)-cyanidanol-3 and dihydroquinoline-type antioxidants on rat hepatic microsomal cytochrome P-450 and monooxygenases.

The cytochrome P-450 system is a sensitive indicator in different forms of experimental liver diseases in the rat. Both CCl4 and ethanol produce a liver damage by free radical mechanisms causing a lesion of liver cell endoplasmic reticulum. Protective effects of antioxidants on CCl4 or ethanol induced liver damage were investigated on this basis in adult Wistar rats. The strongest protective effect in CCl4 treated animals was shown to be exerted by allopurinol. The other three antioxidants (cyanidanol, MTDQ monomer and MTDQ dimer) could not prevent the CCl4 induced changes, measured by liver/body mass quotient, P-450 concentration, ethylmorphine N-demethylation and ethoxycoumarin O-deethylation. Ethanol in the given doses did not produce any distinct effect on the test parameters. The most sensitive parameter was the ethylmorphine N-demethylation. In conclusion CCl4 intoxication is a suitable model for studying radical initiated liver injuries. The mechanisms of the hepatoprotective effects of the four substances are different.

Allopurinol↗
PubMed1986

Functional hepatocellular heterogeneity determined by the hepatotoxins allyl alcohol and bromobenzene in immature and adult Fischer 344 rats.

Adult (male, 75-90 days old) and immature rats (both sexes, 11-12 days old) were treated with allyl alcohol or bromobenzene to induce periportal or centrilobular hepatic injury, respectively. Histologically confirmed liver lesions were produced in adult rats with both treatments. In adult rats, allyl alcohol decreased hepatic cytochrome P-450, benzphetamine N-demethylation, and ethoxyresorufin O-deethylation activities all by about 30%, whereas bromobenzene influenced these parameters differently: cytochrome P-450 was lowered by 55%, benzphetamine N-demethylation by 80%, and ethoxyresorufin O-deethylation by 90%. Cytochrome c reductase, 5'-nucleotidase, glucose-6-phosphatase, and glutamate-pyruvate transaminase activities were not significantly influenced. In immature rats, allyl alcohol did not produce histopathological alterations in liver, but did lower both cytochrome P-450 concentration (30%) and ethoxyresorufin O-deethylation (75%). Benzphetamine N-demethylation was not significantly affected. Bromobenzene produced typical centrilobular liver damage and a decrease of both cytochrome P-450 (20%) and ethoxyresorufin O-deethylation (50%). Benzphetamine N-demethylation was increased slightly, but not significantly. The differences in effects of the two hepatotoxins in adult vs immature rats seem to indicate that the hepatocellular heterogeneity of xenobiotic metabolism which is seen in adult liver (perivenous vs periportal areas) is not well developed in the immature animal.

1-Propanol↗
PubMed1986

Monooxygenase activity of fish liver in biomonitoring aquatic environment.

The hepatic biotransformation activity of four cultivated freshwater fish, Amur carp (Ctenopharyngodon idella), carp (Cyprinus carpio), rainbow trout (Salmo gairdneri) and tench (Tinca tinca) were studied one day after catching the fish from ponds and a river in the south of GDR and in fish kept for two weeks in clean filtrated and deacidified water. Aryl hydrocarbon hydroxylase, 7-ethoxycoumarin O-deethylase and 7-ethoxyresorufin O-deethylase activities fell to about 20% during the stay in clean water in rainbow trout liver microsomes. The reductions were smaller in the other species studied.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1986

Influence of age, hexobarbital, and aniline on NADPH/NADH dependent hydrogen peroxide production in rat hepatic microsomes.

Hepatic microsomal H2O2 production (oxidase function of microsomal cytochrome P-450) is strongly dependent on NADPH or NADH concentration. NADH increases H2O2 production after the addition of a supraoptimal concentration of NADPH to the incubation mixture in all age groups. Maximum activities are found in 60-day-old male Wistar rats. Hexobarbital increased in a dose dependent manner both NADPH, NADH, and NADPH/NADH dependent H2O2 production. Aniline had no effect or slightly decreased H2O2 production. Hexobarbital enhanced NADPH/NADH dependent H2O2 production in all age groups (5-240 days of age) to the same degree. Hence it is concluded that H2O2 production is due to the decay of the peroxycytochrome P-450 complex after the second reduction step via cytochrome b5 and that in all age groups reducibility of cytochrome P-450, which is enhanced by hexobarbital, is rate limiting. As the age course of H2O2 production is similar to that of ethylmorphine N-demethylation, it is concluded that the phenobarbital-inducible cytochrome P-450 subspecies predominantly catalyse H2O2 production.

Aging↗
PubMed1986

Action of different doses of I-131 on thyroid gland, its tissue distribution and elimination in adult male rats.

Adult male Wistar rats were administered 0.1, 1, 2 or 5 mCi/kg I-131 i.p. Activities were measured in the thyroid gland or region, blood plasma (total and protein bound), salivary gland, cerebral cortex (= brain), skin, liver, spleen, small intestine, kidney, heart and skeletal muscle after 1-30 (36) days. Beginning 8 days after radiothyroidectomy the remaining or possibly regenerated thyroid function was tested with a test dose of 5 microCi/kg i.p. After administration of 0.1 mCi/kg I-131 the thyroid gland shows a regeneration within 30 days, but not after treatment with the higher doses. The time course of tissue distribution of activity is dose dependent: after 0.1 mCi/kg I-131 increasing activities after the 3rd-8th day are observed in skin, brain, salivary gland, intestine, spleen, kidney, heart and skeletal muscle. After 1 mCi/kg I-131 only in skin, brain, liver and intestine increasing activities between the 8th and 30th day have been observed. After 5 mCi/kg I-131 only in skin, spleen and intestine increasing activities after the 15th day were measured. Thyroid gland activity 24 hs after administration of 5 microCi/kg I-131 showed during the experimental period of 50 days considerable variation with a factor of 4 for thyroid gland, 8 for protein bound and about 10 for total plasma I-131 activity.

Animals↗
PubMed1986

Hepatic elimination kinetics of organic anions in rats: developmental aspects and influence of phenobarbital.

Maturation and phenobarbital inducibility of hepatic uptake of the organic anions indocyanine green (ICG) and eosine were studied in rats of different ages. Bile duct ligation reduced the ICG and eosine liver concentration in young rats. Therefore, bile duct ligation cannot be recommended for uptake investigations in rats of different ages. The longest elimination half life time (12.4 min) was found in 10-day-old rats within the first 15 min after i.v. administration of 38 mumol ICG/kg. In 20-day-old rats the ICG half life was significantly shorter than in adult 110-day-old rats (5.8 versus 9.6 min). Phenobarbital pretreatment did not alter the ICG elimination half lives in 10-, 20- and 110-day-old rats. The shortest elimination half life time of eosine was found in 60-day-old rats (33.0 min versus 80.3 min in 10-day-old rats and 62.4 min in 240-day-old ones). Phenobarbital pretreatment did not influence eosine serum concentrations. Our results indicate for ICG that uptake comes to maturity earlier than biliary excretion. Differences between ICG and eosine in maturation of the two transport steps support the assumption of more than one carrier for exogenous organic anions. Dye uptake was not altered after phenobarbital and, consequently, cannot be responsible for enhanced biliary dye excretion in differently aged rats.

Aging↗
PubMed1986

Influence of new estrogens on liver transport function in rats.

Ethinylestradiol (EE), administered to male Wistar rats for 5 or 14 days, decreased bile flow and biliary excretion of ICG in bile fistula rats in dependence on dose. The bile acid excretion rate was not constantly influenced. EE pretreatment of rats also diminished the in vitro accumulation of eosine in liver slices. The new estrogens STS 651 and STS 661 decreased bile flow, ICG excretion and in vitro eosine accumulation to nearly the same extent as did EE pretreatment; bile acid excretion was not influenced significantly. Evidently the 14 alpha-15 alpha-methylen structure in STS 651 and STS 661 as well as the additional methoxygroup in C3 position did not protect against cholestatic effects of estrogens. The new 17 beta-trimethyl-silyloxy-estrogen J 303 did not show cholestatic effects in rats. This structure is able to prevent the formation of toxic estrogen metabolites in rats.

Animals↗