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PubMed1981

Hepatotoxicological studies of pyrazolone derivatives on rats. Part 3: Quantitative immunologic determination of serum concentration of transferrin, IgG, alpha 2-acute phase protein and VLDL.

At present no sufficiently sensitive liver function tests are available to exactly detect small liver impairments caused by drugs. In this respect immunological quantitation of serum proteins could be useful. We have determined quantitative alterations of four serum proteins (IgG, transferrin, alpha 2-AP = alpha 2-acute phase protein, VLDL = very low density lipoprotein) from rats treated with aminophenazone, phenazone and propyphenazone (each 1,55 mmol/kg body mass/d). The serum concentration of the four proteins examined is temporarily elevated immediately after onset of treatment. In chronic treatment transferrin is increased by the influence of all drugs investigated. Propyphenazone treatment increased the amount of VLDL whereas aminophenazone had the opposite effect, phenazone is without influence in the same period. The alpha 2-AP serum level is decreased in long time treatment, IgG remains unchanged. The observed alterations indicate disturbances of liver function in the investigated rats. Among the drugs used, aminophenazone has the strongest, propyphenazone the smallest liver damaging effect. The results reported support the importance of serum protein quantitation in connection with the search for possible liver damage due to drug action.

Animals↗
PubMedDate not supplied

[Nature of the interaction of voltaren and other pyrazolone and aniline derivatives with prostaglandin endoperoxide synthetase].

A study was made of the nature and mechanism of interaction of voltaren, butadion, analgin, phenacetin and paracetamol with endoperoxide prostaglandin synthetase (PGH-synthetase) of sheep vesicular glands. Activity of the enzyme was measured by polarography with the aid of a Clark's electrode. Butadion and analgin reversibly inhibited PGH-synthetase at concentrations of the order of 10(-4) M, whereas voltaren at those of the order of 10(-6) M. As regards the mechanism of action, butadion and analgin are competitive inhibitors of PGH-synthetase in respect to arachidonic acid and uncompetitive inhibitors in respect to the electron donor adrenaline. Phenacetin administered at concentrations up to 4 X 10(-2) M did not inhibit PGH-synthetase, whereas paracetamol (10(-3)-10(-2) M) increased its catalytic activity, apparently due to the electron donor properties.

Acetaminophen↗
PubMed1981

[Hepatotoxicological studies of pyrazolone derivatives on rats. Part 1: The study of aminophenazone (author's transl)].

After oral application of aminophenazone to animals (170 and 340 mg/kg daily, over up to 17 weeks), the authors investigated the effect of this drug on some liver functions and performed also a morphological study. They found that aminophenazone produces an increase of the smooth ER, peripheral fatty degradation and reactive-inflammatory responses of the liver, the intensity of these phenomena being dependent upon the dose and time of application. The increase of the smooth ER is the expression of the inductive effect which persists throughout the whole experimental period and manifests itself by accelerated degradation of hexobarbital, increased N-demethylation, increased ascorbic acid synthesis and increased liver weight. The increase in body weight is reduced in the animals treated. The enzyme activities in the plasma lie within the range observed with control animals; they are no indicator of the slight live changes stated. Reactive metabolites and/or the impairment of other metabolic reactions may be considered to be the cause of the hepatotoxic effect of aminophenazone.

Aminopyrine↗
PubMed1981

[Hepatotoxicological studies of pyrazolone derivatives on rats. Part 2: The study of propyphenazone and phenazone (author's transl)].

In female rats the administration of 1,5 mmol/kg of, respectively, propyphenazone and phenazone over a period of 12 weeks produces a histologically detectable fatty degeneration and reactive-inflammatory changes of the liver, presumably caused by reactive metabolites. These slight morphological alterations do not lead to an increase in plasma enzyme activities. Only in case of phenazone administration, reduced increases in body weight are indicative of a toxic effect. The acceleration of hexobarbital degradation and N-demethylation and the increase in liver weight testify to the inductive activity of both these compounds.

Aminopyrine N-Demethylase↗