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Biomedical subjects

V Scailteur

Publications and source records attributed to V Scailteur.

9 recordsLinked to original sources
PubMed1999

Human volunteer studies; a consumer products company view.

The term 'contact dermatitis' refers to a range of adverse effects whose causation is quite varied. Manufacturers of consumer products have an important responsibility to minimise the extent to which their products cause such skin reactions. In meeting this responsibility, use may be made of humans, e.g. in studies related to skin irritation, to try to ensure the highest possible safety standards are achieved. The purpose of this short review paper is to outline the principles that must be followed before initiating studies with human volunteers. In addition, these principles are considered in the context of European legislation on chemicals and preparations.

Dermatitis, Allergic Contact↗
PubMed1987

Dimethylformamide (DMF) hepatotoxicity.

Scattered case reports of accidental exposure and a few epidemiological studies have indicated that the liver is the main target organ following acute and chronic exposure to dimethylformamide (DMF). This has been confirmed in several animal species. In humans, ethanol intolerance is one of the earliest manifestations of (excessive) exposure to DMF, followed at higher exposure levels by various complaints (nausea, vomiting, abdominal pain) and the release of liver cytolytic enzymes in the plasma. The metabolic pathway of DMF has been recently clarified, but the primary cellular lesion responsible for its hepatotoxicity is still unknown.

Animals↗
PubMed1986

Subchronic oral toxicity testing in rats with a liquid hand-dishwashing detergent containing anionic surfactants.

A subchronic oral toxicity study on a model liquid dishwashing detergent containing anionic surfactants was performed to verify that the formulation, made up of a mixture of various ingredients, did not possess any toxicological properties that would not have been expected from available data for each separate ingredient. The product was administered to rats for 13 wk at dietary levels of 0, 0.025, 0.25 or 2.5% (w/w) in the diet. No adverse effects on gross or microscopic histopathology were apparent at any dose level, although increased relative liver weights at the 2.5% level suggested that this dose caused some adaptive changes.

Administration, Oral↗
PubMed1984

In vivo metabolism of dimethylformamide and relationship to toxicity in the male rat.

After in vivo administration of dimethylformamide (DMF) to male rats, about 50% of the dose is excreted in urine as N-hydroxymethyl-N-methylformamide (DMF-OH) and about 4% as N-methylformamide (NMF). NMF is not a product of DMF-OH biotransformation but is directly formed from DMF. Comparison of the acute toxicity of DMF, DMF-OH and NMF shows that NMF is more toxic than DMF-OH, which is itself more toxic than DMF. This study explains the different toxicity profile of DMF and NMF which until recently was believed to represent the main metabolite of DMF.

Animals↗
PubMed1984

In vivo and in vitro oxidative biotransformation of dimethylformamide in rat.

In rats and in humans, dimethylformamide (DMF) is mainly metabolized into N-hydroxymethyl-N-methylformamide (DMF-OH). The in vitro oxidation of DMF by rat liver microsomes is decreased in the presence of catalase and superoxide dismutase. The radical scavengers, dimethylsulfoxide (DMSO), tertiary butyl alcohol (t-butanol), aminopyrine, hydroquinone and trichloroacetonitrile reduce the oxidation of DMF to DMF-OH in vitro and in vivo. Conversely, DMF inhibits the demethylation of DMSO, t-butanol and aminopyrine. The addition of iron-EDTA to the incubation system induces the production of N-methylformamide (NMF) from DMF. These results support the hypothesis that the metabolic pathway leading from DMF to DMF-OH and NMF involves hydroxyl radicals. Superoxide radical and hydrogen peroxide take part in the metabolic process. DMF is preferentially metabolized into DMF-OH. NMF appears mainly when the production of hydroxyl radicals is stimulated, the methyl group being recovered as formic acid.

Animals↗
PubMed1984

Study on in vivo and in vitro metabolism of dimethylformamide in male and female rats.

The study of dimethylformamide (DMF) metabolism by rat tissues in vitro indicates that formaldehyde is not a metabolic product as previously reported [1]. Furthermore, no other monocarbon derivative (CO, CH3OH, HCOOH, CH4) was detected when DMF was incubated with a fortified liver preparation. One metabolic product is methylhydroxymethylformamide (DMF-OH) measured as N-methylformamide (NMF) due to the breakdown of the hydroxymethyl group during gas chromatography. It was usually believed that the main metabolite excreted in urine following administration of DMF to male and female rats was NMF. The results of this study indicate that DMF-OH constitutes the main metabolite in vivo. A quantitatively less important urinary metabolite, hydroxymethylformamide (NMF-OH), is determined as formamide (F) by gas chromatography. In male and female rats, partial hepatectomy reduces markedly the in vivo biotransformation of DMF. Following administration of DMF or NMF, the total amount of metabolites (DMF-OH and/or NMF-OH) excreted in urine is identical in both sexes, but female rats excrete more unchanged parent compound than male rats. The rate of NMF-OH excretion in urine following high doses of DMF supports the hypothesis that DMF may inhibit its own biotransformation.

Aminopyrine↗
PubMed1983

Potentiation of carbon-tetrachloride hepato-nephrotoxicity by phenobarbital in man, a case report.

A 47 year-old male epileptic who had been treated for eight years with variable doses of phenobarbital and valproate was hospitalized in the intensive care unit with the following clinical and biological features: coma grade 2, metabolic acidosis, acute renal and hepatic failure. The recent clinical history revealed that he had been using CCl4 to clean paintings for the last three days in a confined atmosphere. Upon admission, the recent absorption of CCl4 was confirmed by the detection of the solvent in blood and adipose tissue. Cellular lipoperoxidation was suggested by the presence of an increased concentration of pentane in expired air. Evidence of microsomal enzyme induction was provided by the relative preservation of aminopyrine demethylation as indicated by the 14C-aminopyrine breath test and also by the morphological evidence of endoplasmic reticulum proliferation at liver biopsy. Supportive therapy, repeated haemodialysis and administration of antioxidant drugs resulted in a complete recovery. The unusual severity of CCl4-induced liver and renal injury observed in this case is best explained by the induction of CCl4 microsomal activation due to phenobarbital therapy.

Barbiturates↗
PubMed1980

Tissue distribution of antitumor drugs associated with polyalkylcyanoacrylate nanoparticles.

Polymethylcyanoacrylate nanoparticles, polyethylcyanoacrylate nanoparticles, and free 3H-dactinomycin and 3H-vinblastine were studied with emphasis on their distribution pattern in rat tissues after intravenous administration. The adsorption of cytostatic drugs to polyalkylcyanoacrylate nanoparticles can modify drug distribution in tissues. Particularly with vinblastine, modification of drug disposition is important. Data are given concerning the formation and stability of nanoparticle--drug complexes. Polyalkylcyanoacrylate nanoparticles seem to be an interesting drug carrier owing to their size, structure, degradability, and drug sorptive properties.

Adsorption↗