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Biomedical subjects

V J Feron

Publications and source records attributed to V J Feron.

At least 109 records · Page 6Linked to original sources
PubMed1985

Respiratory tract tumors in hamsters after severe focal injury to the trachea and intratracheal instillation of benzo[a]pyrene.

Two groups of male and female Syrian golden hamsters, of which the trachea was severely injured by electrocoagulation, received 6 weekly intratracheal instillations of benzo[a]pyrene (BaP) + ferric oxide in saline or saline alone. Two comparable groups of hamsters were similarly treated but had an undamaged trachea. The experiment was terminated in week 82. Treatment with BaP resulted in hyper- and metaplastic lesions and tumours of the laryngeal, tracheal, bronchial and pulmonary epithelium. There was no evidence of an increased incidence of BaP-induced tumours in the injured trachea.

Animals↗
PubMed1985

Pulmonary response of hamsters to fibrous glass: chronic effects of repeated intratracheal instillation with or without benzo[a]pyrene.

Syrian golden hamsters were given intratracheal instillations of glass fibres with or without benzo[a]pyrene suspended in saline, once a fortnight for 52 weeks. The experiment was terminated at week 85. 'Silicotic granulomas' consisting of tightly packed, iron-positive macrophages filled with glass fibres and surrounded by a layer of alveolar epithelial cells were the predominant pulmonary lesion. No mesotheliomas or other tumours of the respiratory tract were observed in hamsters treated with glass fibres alone. There was no indication that glass fibres enhanced the development of respiratory tract tumours induced by benzo[a]pyrene. In hamsters similarly exposed to crocidolite fibres with or without benzo[a]pyrene no mesotheliomas or other respiratory tract tumours were observed either. An explanation for the absence of pulmonary tumours might be that repeated administration of fibres over a period of 52 weeks entails an acute pulmonary reaction after each administration with the implication that the fibres cannot settle down well enough to be able to induce tumours. Another possible explanation is the relatively short duration of the experimental period.

Animals↗
PubMed1985

Glass fibers and vapor phase components of cigarette smoke as cofactors in experimental respiratory tract carcinogenesis.

Syrian golden hamsters were given intratracheal instillations of glass fibers with or without BP suspended in saline, once a fortnight for 52 weeks; the experiment was terminated at week 85. No tumors of the respiratory tract were observed in hamsters treated with glass fibers alone. There was no indication that glass fibers enhanced the development of respiratory tract tumors induced by BP. In another study Syrian golden hamsters were exposed to fresh air or to a mixture of 4 major vapor phase components of cigarette smoke, viz. isoprene (800----700 ppm), methyl chloride (1000----900 ppm), methyl nitrite (200----190 ppm) and acetaldehyde (1400----1200 ppm) for a period of at most 23 months. Some of the animals were also given repeated intratracheal instillations of BP or norharman in saline. Laryngeal tumors were found in 7/31 male and 6/32 female hamsters exposed only to the vapor mixture, whereas no laryngeal tumors occurred in controls. The tumor response of the larynx most probably has to be ascribed entirely to the action of acetaldehyde. Simultaneous treatment with norharman or BP did not affect the tumor response of the larynx. Acetaldehyde may occur in the vapor phase of cigarette smoke at levels up to 2000 ppm. Chronic inhalation exposure of rats to acetaldehyde at levels of 0 (controls), 750, 1500 or 3000----1000 ppm resulted in a high incidence of nasal carcinomas, both squamous cell carcinomas of the respiratory epithelium and adenocarcinomas of the olfactory epithelium. It was discussed that acetaldehyde may significantly contribute to the induction of bronchogenic cancer by cigarette smoke in man. No evidence was obtained for a role of isoprene, methyl chloride or methyl nitrite in the induction of lung cancer by cigarette smoke.

Acetaldehyde↗
PubMed1984

Inhalation toxicity of acetaldehyde in rats. II. Carcinogenicity study: interim results after 15 months.

Male and female Wistar rats were exposed to acetaldehyde vapour at concentrations of 0, 750, 1500 and 3000/1000 ppm during 6 h/day, 5 days/week for up to 27 months. The present paper deals with the results obtained during the first 15 months of the study, including interim kills after 13, 26 and 52 weeks. Major compound-related lesions occurred in the nose and larynx. The nasal lesions comprised: (1) degenerative changes of the olfactory epithelium at all dose levels, frequently accompanied by focal hyperplasia of basal cells and thickening of the submucosa with loss of Bowman's glands and nerve bundles in the dorsomedial region, (2) stratified squamous metaplasia of the respiratory epithelium lining the caudoventral part of the nasal septum and the inner aspect of the ventral endoturbinates often accompanied by severe keratinisation and occasionally by papillomatous hyperplasia, almost exclusively observed at the top-dose level, and (3) malignant tumours (squamous cell carcinomas and adenocarcinomas) at all dose levels. Hyperplasia and keratinised stratified squamous metaplasia of the laryngeal epithelium were seen at the 2 highest dose levels.

Acetaldehyde↗
PubMed1984

Sub-acute versus sub-chronic oral toxicity study in rats: comparative study of 82 compounds.

Toxicity data of 82 compounds, tested in both a sub-acute and a sub-chronic study, were evaluated to find out whether it is possible to substitute a sub-acute for a sub-chronic study without losing quantitative information. The no-effect level (NEL) and the minimal-effect level (MEL) were used as the basis for comparison. For each of the compounds, the sub-acute and sub-chronic studies were performed under similar conditions, with the same strain of rats and with a comparable range of dietary levels. It appeared that the NEL in the sub-acute study was equal to the NEL in the sub-chronic study for 56% of the compounds. For 44% of the compounds reviewed, the NEL in the sub-chronic test was lower than the NEL in the sub-acute test, indicating that a sub-chronic study cannot simply be replaced by a sub-acute study. However, it may be acceptable to use the NEL obtained in a sub-acute study as a basis for establishing acceptable daily intakes or permissible exposure levels for humans if an additional safety factor of 10 is applied. Furthermore, it was concluded that the conventional sub-acute study, including some selected haematological and biochemical parameters, seems extremely useful to obtain quick and reliable information on the toxicity of the numerous non-regulated chemicals which have to be investigated in the years to come.

Administration, Oral↗
PubMed1984

Restoration of the hamster tracheal wall following injury by electrocoagulation.

The trachea of Syrian golden hamsters was injured by electrocoagulation. The lesions induced as well as the repair process were studied by light and scanning electron microscopy. The changes observed were considered to create the proper conditions for studying the significance of severe focal damage to the respiratory tract for the formation of tumors at the site of injury. Electrocoagulation caused deep crater-like injuries measuring 2 to 3 mm in diameter. Not only the mucosa, but also the submucosal tissues and cartilage rings were damaged. The repair process of the epithelium followed the pattern of covering the defect by squamous epithelium, hyperplasia, and stratified squamous metaplasia and finally differentiation into normal tracheal epithelium. The recovery of the epithelium was strikingly slow; even after a recovery period of 10 weeks regeneration of the epithelium was still incomplete in some animals. This relatively slow process of repair was ascribed to the depth and severity of the injuries involving a large mass of damaged tissues other than epithelium. Regeneration of the cartilage rings comprised three processes, viz removal of necrotic cartilage, growth of fibroblasts into the necrotic cartilage, and deposition of new cartilage along the necrotic rings.

Animals↗
PubMed1984

General toxicity testing: sense and non-sense, science and policy.

The dramatic increase in the number and variety of industrial chemicals in addition to natural compounds, and the increased public concern about their health effects, has in the last few decades led to a remarkable development in number and types of toxicity tests employed to assess safety of chemicals. Not too many years ago, toxicity tests were relatively simple in design and conduct. They were sometimes inadequate in a number of aspects. Toxicity testing has now become an unbalanced mixture of sound science and policy. Many times companies wishing to market products internationally are faced with a plethora of different national regulatory requirements. In this presentation attention is given to requirements for toxicity data and the need for harmonization in guidelines while avoiding rigid protocols. The wisdom and necessity of conducting all currently required tests will be considered. The relevance of certain biochemical, hematological, and pathological parameters is discussed as is the relevance of Good Laboratory Regulation for toxicity testing. The importance of a scientific evaluation of all chemical biological data derived from modern sensibly designed toxicity tests with respect to extrapolation and safety assessment is emphasized. Future development in certain areas of toxicity research is stressed and examples are given.

Animals↗
PubMed1983

Tissue damage and nutritional factors in experimental respiratory tract (Co-)carcinogenesis.

Cofactors involved in respiratory tract carcinogenesis were studied in Syrian golden hamsters or in rats using benzo(a)pyrene as the carcinogenic agent. These factors included severe tissue damage induced by electro-coagulation, glass fibers administered by intratracheal instillation, acetaldehyde as irritant vapor, food restriction, and nutrients such as vitamin A and saturated and unsaturated fats. In addition, the effects of a combined exposure to four different major gaseous cigarette smoke components--methyl nitrate, isoprene, methyl chloride and acetaldehyde--and to one solid cigarette smoke component--norharman--were examined in short- and long-term inhalation studies. An interesting finding was the carcinogenicity of acetaldehyde, of which the possible mechanism is briefly discussed. Another conspicuous observation was the substantial increase in number and size of lipid droplets in alveolar fibroblasts of hamsters fed a high vitamin A diet.

Acetaldehyde↗
PubMed1982

Respiratory tract tumours in hamsters exposed to acetaldehyde vapour alone or simultaneously to benzo(a)pyrene or diethylnitrosamine.

Syrian golden hamsters were exposed to 0 or 2500-1650 ppm acetaldehyde vapour, 7 hr/day, 5 days/week for a period of 52 weeks. A proportion of the animals was given, simultaneously, either intratracheal instillations of benzo(a)pyrene (BP) or subcutaneous injections of diethylnitrosamine (DENA). All treatments were stopped after 52 weeks. The study was terminated after 81 weeks. Major effects attributed to acetaldehyde exposure included growth retardation, rhinitis, hyperplasia and metaplasia of the nasal, laryngeal and tracheal epithelium, nasal and laryngeal carcinomas, and a markedly increased incidence of BP-initiated tracheobronchial carcinomas. There was no evidence of acetaldehyde enhancing the development of DENA-initiated tumours of the respiratory tract. It was concluded that acetaldehyde is an irritant, as well as a carcinogen, for the respiratory tract of Syrian golden hamsters. Possible mechanisms of the carcinogenicity of this aldehyde are briefly discussed.

Acetaldehyde↗
PubMed1982

Inhalation toxicity of acetaldehyde in rats. I. Acute and subacute studies.

The 4-h LC50 of acetaldehyde in rats was determined and found to be 13,300 ppm (24.0 g/m3 air). In a 4-week study groups of 10 male and 10 female rats were exposed to 0, 400, 1000, 2200 or 5000 ppm acetaldehyde for 6 h/day, 5 days/week. Treatment-related changes observed at the 5000 ppm level included dyspnoea and excitation during the first 30 min of each exposure, yellow-brown fur, severe growth retardation, more neutrophils and less lymphocytes in the blood, a reduced production of urine with a high density, increased lung weights, and severe degenerative, hyperplastic and metaplastic changes of the nasal, laryngeal and tracheal epithelium. Major lesions seen at 1000 and 2200 ppm comprised growth retardation and an increased production of urine in males, slight to moderate degeneration with or without hyper- and metaplasia of the nasal epithelium, and only at 2200 ppm, minimal epithelial changes in the larynx and trachea. The only change observed at the 400 ppm level that could be attributed to acetaldehyde was slight degeneration of the nasal olfactory epithelium seen as loss of microvilli and thinning and disarrangement of the layer of epithelial cells.

Acetaldehyde↗
PubMed1981

Ultrastructural changes in the kidneys of rabbits treated with lead acetate.

Electron microscopical studies were carried out on the kidneys of rabbits given s.c. injections of 0 (control), 0.25 or 0.50 mg lead acetate/kg b.w. 3 times a week during 14 weeks. At the end of the experimental period the animals had lead blood levels of 60, 500 and 600 micrograms/l whole blood respectively. Treatment-related renal changes were found in the proximal tubules; they consisted of a dose-related increase in the amount of lysosomes in epithelial cells of the convoluted part, and of severely damaged cells and loss of brush border in the straight part. There was also an increase in lysosomal tubular inclusions, which are considered characteristic of lysosomes of the proximal tubular cells of the rabbit kidney. The significance of these findings for assessing the risk of occupational exposure to lead is briefly discussed.

Animals↗