PubMed Health⌕ Search

Biomedical subjects

F Jahn

Publications and source records attributed to F Jahn.

At least 19 recordsLinked to original sources
PubMed1998

Influence of 2-acetylaminofluorene (2-AAF) on biotransformation and lipid peroxidation in salivary glands and liver from male rats.

Salivary glands proved to be active in biotransformation. In microsomes of rat salivary glands 7-ethoxyresorufin O-deethylation (EROD) and 7-pentoxyresorufin O-depentylation (PEROD) were detectable, but with much lower activities than in the liver. Beside the well-known induction of EROD or PEROD in the liver by beta-naphthoflavone (BNF) or phenobarbital (PB), respectively, a marked rise in EROD rate of salivary glands was observed after BNF treatment. Administration of 2-AAF caused an increase in EROD rates in liver microsomes, but a decrease in microsomes of salivary glands. This decrease in EROD rate was accompanied by selective cytotoxic damages in the convoluted granulated tubules of the submandibular glands. No cytotoxic damage occurred in the submandibular glands after a combined administration of the inducer BNF and 2-AAF. This indicates relations between these toxic effects of 2-AAF and changes of 2-AAF-metabolism in BNF-induced rats, maybe in the liver and/or in the submandibular glands themselves.

2-Acetylaminofluorene↗
PubMed1993

Age dependent different influence of carbon tetrachloride on biotransformation of xenobiotics, glutathione content, lipid peroxidation and histopathology of rat liver.

15- and 60-day-old male rats were treated with different doses of CCl4 orally. 24 h later cytochrome P-450 (P450) concentration, 7-ethoxyresorufin O-deethylation (EROD) and 7-pentoxy-resorufin O-deethylation (PEROD) activities were determined. Whereas P450 and EROD are lowered to the same extent in both ages, PEROD shows a more pronounced inhibition in the livers of younger rats. The formation of endogenous lipid peroxides (measured as thiobarbituric acid reactive substances) is drastically increased only in the livers of young rats. The hepatic glutathione (GSH) content was unaffected by CCl4 treatment whereas oxidized glutathione is more increased in the livers of adult rats. This can be caused by a higher activity of GSH-peroxidase in the livers of adult rats. The changes in NADPH-induced lipid peroxidation and chemiluminescence correlate partially with the changes in P450 and biotransformation reactions. Histopathologically the liver damage is more extensive in suckling rats. The necrosis is localized predominantly in the perivenous tissue, which has normally the highest activities of toxification and detoxification enzymes.

Age Factors↗
PubMed1991

Nephrotoxic effects of diethylene glycol (DEG) in rats.

Diethylene glycol (DEG) is a widely used substance with various risks of intoxication. In adult rats influences of DEG on functional parameters are characterized, indicating early signs of nephrotoxicity. A dose dependent proteinuria, an oliguric effect, an increased excretion of free hydrogen ions and a compensated impairment of renal tubular transport processes can be stated (0.25, 0.5 and 0.75 ml DEG/100 g b.m. i.p.). Following a single dose of 0.5 ml DEG/100 g b.m. i.p. the maximally expressed nephrotoxic effect is measurable 4 to 8 days after administration.

Animals↗
PubMed1991

Influence of neonatal and postnatal administration of diethylstilbestrol on hepatic monooxygenase activities and lipid peroxidation in adult rats.

Treatment of adult male and female rats with DES caused a significant reduction of cytochrome P450 concentration, ethylmorphine N-demethylation and ethoxycoumarin O-deethylation. These decreases are not modified by a neonatal treatment with this hormone. In contrast to monooxygenase activities the NADPH-induced lipid peroxidation shows only a tendency to decrease if animals received DES as adults. But a decrease of about 50% is observed after "neonatal plus treatment of adults" with DES. The role of formation of reactive oxygen species characterized by chemiluminescence methods in connection with lipid peroxidation is discussed.

Animals↗
PubMed1991

[Contamination of breast milk with organochlorine compounds in comparison with cow's milk and selected milk products in the new federal districts].

400 human milk, 280 cowmilk, 56 milkpowder and 305 butter samples were examined concerning there content of chloroorganic compounds. In human milk the highest concentration had DDE, followed by PCB, DDT and HCB, the lowest values were measured for HCH. Only total DDT in human milk but no compound in the milk product samples was above the maximal tolerated limit. There is a strong reduction in comparison to the values measured in 1979 (ten times for total HCH, one half for total DDT and to one sixth for HCB) but the PCB concentration didn't change.

Animals↗
PubMed1990

Influence of age, phenobarbital and beta-naphthoflavone on hepatic microsomal lipid peroxidation in rats.

The NADPH-dependent lipid peroxidation is low in liver microsomes of newborns and increases to day 30 of life. Thereafter nearly no changes in lipid peroxidation occur. The relatively high rate of lipid peroxidation in fetal liver microsomes is of interest. The well known inducers of the monooxygenase system phenobarbital and beta-naphthoflavone change lipid peroxidation only in liver microsomes of newborns. Lipid peroxidation is connected with the formation of reactive oxygen species and organic radicals characterized by the chemiluminescence with the amplifiers luminol and lucigenin. Chemiluminescence increases with increasing age depending on the amplifier. Treatment of the animals with phenobarbital causes the most pronounced increase in chemiluminescence of the 10-day-old animals, independent of the amplifier used. beta-naphthoflavone leads to an increase in chemiluminescence in microsomes of all age groups investigated except the luminol chemiluminescence

Aging↗
PubMed1989

Influence of prenatal administration of cadmium on postnatal development and inducibility of hepatic monooxygenases in rats.

Cadmium inhibits hepatic monooxygenases in rats of different ages. But also in the offspring of dams which had received cadmium during pregnancy changes in biotransformation activities and their inducibilities could be observed. In the 30- and 60-day-old offspring a decrease in the inducibility of ethoxyresorufin O-deethylation by the specific inducer beta-naphthoflavone could be demonstrated, whereas cytochrome P-450 concentration, ethylmorphine N-demethylation and ethoxycoumarin O-deethylation were not influenced.

7-Alkoxycoumarin O-Dealkylase↗
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↗
PubMed1987

Hemodynamic parameters and renal blood flow following stimulation of renal tubular transport processes by treatment with thyroid hormones.

In adult rats, renal excretion of p-aminohippurate (PAH) can be stimulated by repeated administration of thyroid hormones. Data on renal cortical slices show clearly that a stimulation of active, carrier-mediated tubular transport processes is the most important cause. In vivo experiments also show an influence of treatment with thyroid hormones on various hemodynamic parameters. The diminution of vascular resistance in cortical and medullary regions of the kidney might contribute to the increased PAH excretion in thyroid hormone-treated rats.

Animals↗
PubMed1987

Increase of 14C-leucine uptake following stimulation of renal tubular transport processes.

Following treatment with cyclopenthiazide, triiodothyronine or dexamethasone the renal excretion of p-aminohippurate (PAH) as well as the accumulation of PAH in renal cortical slices from adult rats and from rats with immature kidney function are increased. There are differences with respect to the age of the rats as well as in dependence on the substance used for treatment. In 10- and 60-day-old rats the [14C]leucine uptake following such a stimulation of kidney function is increased, that means active tubular transport of amino acids can also be stimulated. Furthermore, the [14C]leucine content in the protein fraction of homogenized kidney tissue is increased, indicating a higher degree of incorporation of amino acids in kidney tissue following treatment with cyclopenthiazide, triiodothyronine or dexamethasone.

Animals↗
PubMed1983

Effect of cadmium in vitro on benzphetamine-N-demethylation and ethoxyresorufin-O-deethylation in rats of different age.

The in vitro influence of CdSO4 on the liver microsomal benzphetamine-N-demethylation and ethoxyresorufin-O-deethylation activities in male Wistar rats/age 10, 30, 60 and 240 days/as well as the type of inhibition were studied after phenobarbital or beta-naphthoflavone pretreatment. Both reactions were inhibited by CdSO4 in dependence on concentration in all age groups. After phenobarbital pretreatment the inhibition of N-demethylation was slightly pronounced in 10-day old rats. In 10 and 30-days old rats the type of inhibition was competitive while in 60 and 240-days old rats a non-competitive type of inhibition was observed. O-deethylation of ethoxyresorufin was inhibited also in 10-day old rats, the inhibition type was non-competitive in all age groups. After beta-naphthoflavone pretreatment N-demethylation was inhibited competitively in all age groups. The inhibition of O-deethylation was more pronounced in 30-day old rats, in other age groups the inhibition was weak but concentration dependent. The type of inhibition was noncompetitive for all age groups studied.

Aging↗
PubMed1982

Influence of age on in vitro effect of cadmium on rat liver cytochrome P-450 concentration and monooxygenases activity.

Cadmium++ added in vitro destroys rat liver cytochrome P-450 (cyt. P-450) with increasing age by 25-50%. Ethylmorphine N-demethylation is inhibited only in rats 30-days old and thereafter. Ethoxycoumarin 0-deethylation is inhibited even in newborn rats, and the maximal inhibition appears to increase with age. It is concluded that in all age groups cadmium resistant cyt. P-450 subspecies are present. Ethoxycoumarin 0-deethylase activity possibly indicates the cadmium sensitive P-450 fraction.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1982

The influence of cadmium on the biliary excretion of eosine and bromsulphthalein and on microsomal monooxygenase activities in the rat.

Cadmium sulfate x 8/3 H2O (0.3, 0.6, 1.5 and 2.0 mg/kg) administered simultaneously with eosine and bromsulphthalein (120 mumol/kg i.v.) did not significantly change the biliary excretion of the dyes. After a 3 days pretreatment with 2.0 mg/kg CdSO4 i.p. a body weight loss and an increase in the relative liver weight when calculated on body weight were observed together with an enhanced bile flow, but the excretion of the dyes was not markedly influenced. Ethylmorphine N-demethylation and ethoxycoumarin O-deethylation activities as well as microsomal cytochrome P-450 concentration were diminished by about 50%. It can be concluded that in male rats the hepatic microsomal monooxygenase system is more sensitive towards cadmium than the hepatic transport system for organic anions.

Animals↗
PubMed1972

[Not Available].

Explore the source record for details and available documents.

History, Modern 1601-↗