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Biomedical subjects

J Kulcsár-Gergely

Publications and source records attributed to J Kulcsár-Gergely.

At least 19 recordsLinked to original sources
PubMed1997

Studies on the effect of ursodesoxycholic acid on rats with acute carbontetrachloride injury.

Bilirubin is a sensitive marker of toxic liver injury. Carbontetrachloride (CCl4) is used in some manufactures and laboratories. An acute intoxication is a peril. We have performed experiments to state total, indirect and direct bilirubin levels in rats exposed to a single CCl4 dose of 1.25 ml/kg. Total bilirubin in normal rats is 3.13 +/- 0.13 mumol/l. 58.6% is direct conjugated and 41.3% indirect unconjugated bilirubin. One hour after CCl4 administration bilirubin started to increase and reached its peak in the second hour. 24 h later a decrease began but even 72 h after intoxication it was not normalized. Ursodesoxycholic acid (UDCA, CAS 128-13-2, Ursofalk) treatment (25 mg/kg/dose) lowered bilirubin, returning to normal level 24 h after CCl4 administration. Hypothermia aggravates intoxications. In CCl4 lesion it develops 1 h after exposure. UDCA has not influenced low body temperature but liver function, conjugating capacity was restored. In CCl4 poisoning it is suggested to start UDCA treatment as early as possible and to continue it for some more days after improvement of serum bilirubin concentration.

Animals↗
PubMed1994

Metabolic actions of a single atenolol and metoprolol dose.

Atenolol (CAS 29122-68-7) and metoprolol (CAS 37350-58-6) are beta 1-selective adrenoceptor antagonists without intrinsic sympathomimetic activity. beta-Receptor blockers influence carbohydrate- and lipid metabolism. Liver is a central organ of these processes. The metabolic fate of a single oral atenolol and metoprolol dose and their actions on carbohydrate- and lipid parameters have been investigated. Healthy male rats received a dose reducing heart beat/min by 25% (atenolol: 6 mg/kg; metoprolol: 10 mg/kg). About 9% of atenolol is metabolized by cytochrome P-450 (P-450). P-450-dependent functions (aminopyrine-N-demethylase, hexobarbital biotransformation time) were not inhibited. Serum bilirubin was normal. Triglyceride (TG), total cholesterol and HDL-cholesterol levels of the plasma were not affected. Transient blood glucose increase was measured returning to initial value at 120 min. Metoprolol is metabolized by hepatic monooxygenases. P-450-dependent functions were inhibited correlating to the lowered P-450-content of the microsomes. High TG level and decreased HDL-cholesterol content were measured. Blood glucose was significantly high. The liposoluble metroprolol affected the hepatic functions more than the hydrophilic atenolol. The monitoring of blood glucose during beta-receptor antagonist treatment may be suggested.

Animals↗
PubMed1992

Metoprolol and propranolol treatment in carbon tetrachloride-induced hepatic injury.

The effects of beta 1-selective metoprolol (CAS 37350-58-6) and the nonselective beta-adrenoceptor antagonist propranolol (CAS 525-66-6) were investigated in healthy and CCl4 damaged male rats. Treatments were performed for 16 days, orally with dosages reducing heart beat/min by 25% (metoprolol 10 mg/kg, propranolol 1 mg/kg). Liver glycogen content was not influenced by either beta-blocker in healthy animals. CCl4-induced loss of glycogen was equally moderated by metoprolol and propranolol. Blood glucose increased in metoprolol treated healthy and liver damaged rats after a single dosage likewise following prolonged treatment. Propranolol was without effect on blood glucose level. Cytochrome P-450 decline in microsomal fraction was greater in metoprolol, than in propranolol treated healthy animals. However, the severe fall elicited by liver injury was moderated by metoprolol and normalised by propranolol. Cytochrome b5 seems to be involved in metoprolol metabolism. Cytochrome P-450-dependent aminopyrine-N-demethylase was impeded by metoprolol in animals with healthy liver. The serious inhibition caused by CCl4 was moderated by metoprolol and with a better result by propranolol. The high serum bilirubin level in liver lesion was lowered by metoprolol and particularly by propranolol. Neither phase I metabolic process aminopyrine-N-demethylation nor phase II glucuronidation were normalised. A comparison of this data with the results of a previous 12-day treatment schedule indicates that no changes in efficacy occurred with longer treatment. The present results pertain to the importance of the selection of beta-adrenoceptor blocker in liver lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine N-Demethylase↗
PubMed1991

Effects of tamoxifen and levonorgestrel treatment on carbon tetrachloride induced alterations in rats.

Oestrogens cause progression in liver lesion, and thus ovariectomy improves hepatic injury both functionally and histologically. In the present study the efficacy of the antioestrogen tamoxifen (CAS 10540-29-1) was examined in chronical carbon tetrachloride damage. The results were compared with the effect of the progestogen levonorgestrel. Male Wistar rats were treated for 16 days. Blood sampling and autopsy were performed 2 h after last tamoxifen resp. levonorgestrel and 1 h after last CCl4 dosage. Tamoxifen diminished water content of the healthy liver. By fairly the same ratio it decreased high water content of the damaged liver. Levonorgestrel moderated water imbibition in CCl4 impairment. Tamoxifen caused protein synthesis in healthy and in injured liver. Levonorgestrel could not prevent protein loss associated with CCl4 damage. Tamoxifen counteracted, levonorgestrel moderated glycogen loss in liver lesion. Blood glucose was normal in all examined groups. Cytochrome P-450 decrease in CCl4 injury was moderated but not normalised by tamoxifen. Levonorgestrel was less effective. Cytochrome b5 content diminished in CCl4 lesion and both treatments restored it. Aminopyrine-N-demethylase was impaired by liver injury. An improvement was measured correlating with microsomal cytochrome P-450 content. This was significant with tamoxifen but not following levonorgestrel administration. The pathological serum bilirubin level of CCl4 lesion was normalised by tamoxifen as well as levonorgestrel treatment. The progestogen levonorgestrel moderated liver injury in reducing high water content, glycogen loss and normalising serum bilirubin. The antioestrogen tamoxifen seems to be a promising treatment in chronic hepatic impairment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine N-Demethylase↗
PubMed1990

Correlations between hepatic monooxygenase system and glycogen storage.

In experiments performed on female Wistar rats we have stated that simultaneously with glycogen mobilisation occurring immediately after epinephrine injection the amount of cytochrome P-450 (cP-450) was reduced. A characteristic cP-450 dependent function hexobarbital biotransformation was inhibited. No changes in hepatic protein and water content and serum bilirubin were measured. Glycogen and cP-450 loss and functional impairment depend on the administered epinephrine dose and time of treatment. We have proven that reduced activity of mixed function monooxygenase is related only to diminished glycogen content of the liver. Restitution of glycogen stores as well as amount and function of cP-450 were parallel.

Animals↗
PubMed1989

Alpha-adrenergic receptors in the regulation of liver functions.

Rat liver contains 80% alpha 1 and 20% alpha 2 receptors. The role of adrenergic regulation of liver functions was studied by administration of antagonist and agonist pharmaca. Female rats were treated with the selective alpha 1 receptor blocker prazosin. A transitory inhibition of microsomal monooxygenases was observed after 5 days which was terminated at the 12 day. A 18.7% loss of glycogen was measured at this time indicating a slight adrenergic glycogenolytic effect. Dihyd 50-ergocryptime an equal lebocker of alpha 1 alpha 2 receptori preserved glycogen content and has not impaired liver functions. Agonist epinephrine inhibited monooxygenase functions and mobilised 75% of hepatic glycogen. Simultaneous administration of prazosin with epinephrine resulted into glycogen loss due to alpha 2 receptor stimulation. Dihydroergocryptine antagonised rather the metabolic actions of epinephrine. We have established that alpha 2 receptors are also involved in hepatic carbohydrate metabolism.

Animals↗
PubMed1989

[Beta receptor blockade and liver function].

The effects of propranolol on liver functions of healthy rats were studied administering daily doses of 1 mg/kg. Beta receptor blockade has been investigated in carbontetrachloride induced liver cirrhosis. Normal liver functions were unchanged with the exception of an increase in Glucos-6-Phosphatase. The severe cirrhotic injuries were counteracted or moderated when propranolol administration started the same day as CCl4 injection. The amount and function of mixed-function-monooxygenases were normalised. Carbohydrate and protein metabolism impairments were moderated. Serum triglyceride and HDL-cholesterin levels were however uninfluenced. The metabolic properties of propranolol seem to be advantageous in chronic liver impairments.

Animals↗
PubMed1989

Action of beta-adrenoceptor blockers on liver function of rats.

Three nonselective beta-adrenoceptor blockers, propranolol, cloranolol and talinolol, were examined in male rats. The amount and function of polysubstrate monooxygenase, serum bilirubin and carbohydrate metabolism were investigated. Doses producing a 25% reduction in heart beat/min were given orally. The effect of a single dose was compared to that of a 12-day treatment period. Propranolol in a single dose did not influence hepatic parameters. The 12-day treatment reduced the amount of cytochrome P-450 (cP-450) and prolonged hexobarbital biotransformation time. Cloranolol decreased cP-450, prolonged hexobarbital anaesthesia and inhibited aminopyrine-N-demethylation (AND) even in a single dose. No further impairment occurred with continued treatment. A single dose of talinolol led to cP-450 loss and inhibited cP-450 dependent liver functions. This inhibition progressed with continued treatment. High bilirubin levels were measured. Both cloranolol and talinolol elicited an initial rapid hyperglycaemia with normal liver glycogen content. At the end of the treatment blood glucose and liver glycogen values were normal. The reversible hyperglycemic reaction shows the necessity of controlling glucose tolerance. When talinolol is administered liver function parameters should be checked in appropriate time intervals.

Adrenergic beta-Antagonists↗
PubMed1988

Different mechanisms in the hepatic actions of estrogens.

Literary data proved evidence that uterine actions of estrogens develop through different receptor systems. We performed experiments to examine whether different mechanisms are also involved in the hepatic effects of estrogenic steroids. Female rats were treated with a single dose of 5 mg/kg estrone. Dry liver weight and protein content increased. Both responses were blocked by prior administration of natural antiestrogen progesterone. Increased wet organ weight and water content were measured as edematous reactions. They can be attributed to the depolymerisation of mucopolysaccharides. Progesterone could not prevent these effects. Estrone induced glycogen synthesis in the liver. This was counteracted by progesterone treatment. To elucidate the possible role of the adenylcyclase system the animals were treated with beta-receptor blocker propranolol which had no effect either on liver glycogen content or on estrone induced synthesis. Dihydroergocryptine, an equal blocker of alpha 1- and alpha 2-receptors, did not interfere with glycogenetic action of estrone either. The selective alpha 1-receptor blocker prazosin decreased the liver glycogen content and inhibited glycogenetic response to estrone. Our results proved that estrogens display their hepatic effects by several mechanisms that can be selectively blocked or moderated.

Animals↗
PubMed1984

Hepatic actions of progestogenic steroids.

The effects of two oral progestogens, norethisterone and d-norgestrel, were studied on hepatic functions in CFY female rats. In healthy animals both progestogens inhibited cytochrome-P-450 dependent nonspecific mixed function monooxygenases. Serum bilirubin and cholylglycin RIA values were normal. Protein and glycogen content of the liver remained intact after norethisterone, d-norgestrel reduced glycogen. The pathologic values characteristic for chronic carbon-tetrachloride damage improved on a highly significant grade when these progestogens were simultaneously administered. The progestogens inhibited mixed function monooxygenases. We may presume that in this way they inhibited the formation of hepatotoxic trichloromethyl free radical and improved several liver functions.

Aminopyrine N-Demethylase↗
PubMed1977

Short-term and prolonged treatment with oral contraceptives and liver function.

Experiments on female rats were performed to observe the effects of progesterone and two synthetic progestens: ethinodiol-diacetate and methylestrenolone on liver function. In acute experiments animals were treated for the duration of one sexual cycle. All three compounds prolonged the hexobarbital biotransformation time. This effect is reversible and normalised 48 h after stopping treatment. The testosterone inducement of microsomal mixed function oxydases remained at the level of controls after methylestrenolone pretreatments and was even higher in the ethinodiol-diacetate and progesterone pretreated animals. Subacute and chronical treatments lasting for two or more sexual cycles resulted in the same slight inhibition of hexobarbital biotransformation when performed with the two progestogens. Chronical progesterone administration prolonged significantly hexobarbital biotransformation time. This impairement is also reversible. Our results pertain to a moderate, transitive inhibition of hexobarbital metabolism during short-term and prolonged progesterone and progestogen treatment. This effect may be easily suspended by interrupting drug administration or inducing microsomal enzymes with a single dosage of testosterone. In our progesterone experiments the inhibition of liver function increased with dosage and exposition time. In case of the two examined progestogens exposition time has not been proven as a predisposing factor for impairing liver function.

Animals↗