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Biomedical subjects

P Grasso

Publications and source records attributed to P Grasso.

At least 109 records · Page 6Linked to original sources
PubMed1983

An investigation of the penetration of ingested asbestos into the normal and abnormal intestinal mucosa of the rat.

To characterize the tissue response associated with the presence of asbestos fibres in the gastro-intestinal wall, duodenal tissues of Wistar rats were examined by light microscopy following injection of a suspension containing amosite fibres into the wall of the duodenum. Intestinal tissues were also examined by light microscopy following oral administration of amosite for 5 days to healthy animals and for up to 7 days to animals with induced gastro-intestinal ulcers. Injection of amosite into the wall of the gastro-intestinal tract resulted in granulomatous lesions characterized by large numbers of macrophages containing crystals with the polarizing characteristics of amosite fibres. Examination by polarizing light microscopy following ingestion of asbestos revealed no such lesions or other histopathological abnormalities in the gut wall of the healthy animals and no intracellular fibres were observed in the animals with ulcers. Light microscopy, therefore, yielded no pathological evidence of widespread transmigration of asbestos from the gastro-intestinal tract of rats, even under conditions of mucosal loss. Further studies involving analysis by electron microscopy are under way.

Administration, Oral↗
PubMed1983

Endocrine study of anorexia nervosa.

The main objective of the study was to evaluate the endocrinological picture of anorexia. The sample consisted of 23 anorectic patients (20 females, 3 males) with a control group of 10 normal females and 5 normal males. All participants underwent a work-up which included testing for hypothalamic, hypophyseal, thyroidal, adrenal, gonadal functioning and glucose metabolism. Our results revealed a reduced urinary output and low serum levels of gonadotropins with different responses to LHRH correlating with the stage of the illness. We found reduced urinary estrogens and elevated testosterone levels in females. Males demonstrated a reduction of testosterone. While basal prolactinemia was normal in both sexes, males showed an exaggerated response to TRH. The thyroid function study in anorectic patients revealed a decrease in T3 and in free T3 and an increase in reverse T3. Free T4 was slightly increased with normal T4 levels. Basal TSH was normal with a delayed peak after TRH. We also noticed in the anorectic population reduced basal glucose levels with a flat glucose curve; reduced insulin levels with a slight increase after glucose administration; elevated basal GH with a fair response to L-Dopa; elevated serum cortisol with loss of circadian rhythm and slightly inhibited by dexamethasone. In addition, both noradrenalin and VMA were reduced. We concluded that the multiple endocrine abnormalities found are consistent with hypothalamic dysfunction. The etiology of this dysfunction remains for the endocrinologist highly controversial.

Adolescent↗
PubMed1982

Short-term toxicity study of carnauba was in rats.

Groups of 15 male and 15 female rats were fed diet containing 0 (control), 1, 5 or 10% carnauba wax or 10% cellulose powder for 13 wk and groups of five rats of each sex were given these treatments, except the 1% carnauba wax, for 2 or 6 wk. Rats given 10% carnauba wax or 10% cellulose consumed more food than the controls but showed no differences in body weight, an effect attributed to the dilution of the diet by non-nutrient test materials. The study showed no treatment-related differences in body weights, water intakes, haematological values, serum-enzyme activities, urinary concentration and 'dilution' tests, organ weights or histological findings. The no-untoward-effect level for carnauba wax in the diet was 10%, which represented a mean intake of approximately 8.8 and 10.2 g/kg body weight/day in males and females, respectively.

Animals↗
PubMed1981

Malnutrition, liver damage, and cancer.

There is no clear indication that malnutrition, per se, is a principal cause of cancer in man, but the prevalence of liver cancer in areas where malnutrition exists supports this hypothesis. Liver damage and liver cancer have been induced in laboratory rats by diets consisting of peanut meal and proteins deficient in some essential amino acids. However, liver damage, but not cancer, was produced when the diets contained no peanut meal but consisted of a mixture of amino acids deficient in methionine and cysteine, so that it is possible that aflatoxin, a contaminant of peanut meal, may have been responsible for the malignancies seen in the earlier experiments. Liver cancer developes in a high proportion of mice allowed to feed ad libitum or given a diet containing a high proportion of fat (groundnut oil) or protein (casein). Dietary restriction reduced the incidences of this cancer. This findings lends some support to current thinking that diet may be a factor in the development of cancer in man.

Aflatoxins↗
PubMed1980

Ortho-toluene sulphonamide and saccharin in the promotion of bladder cancer in the rat.

The importance of the contaminant OTS in the promoting activity of commercial saccharin on rat bladder neoplasia was investigated. OTS, OTS-free and OTS-contaminated saccharin were administered in the drinking water or diet for 2 years to groups of rats pretreated with an intravesical instillation of MNU; OTS alone and OTS-free saccharin were also given to groups of rats not pretreated with MNU. Administration of OTS was not associated with changes in urinary pH, crystalluria or calculus formation, had no effect on the histology of normal rat bladder, and did not increase the incidence of bladder hyperplasia or neoplasia elicited by pretreatment with MNU. No differences could be found between the effect of OTS-free or OTS-contaminated saccharin on bladders of rats pretreated with MNU. These results indicate that OTS contamination played no part in the reported promoting activity of saccharin on the rat bladder. Administration of saccharin did not increase urinary pH, crystalluria or calculus formation, and failed to promote bladder neoplasia after a carcinogenic dose of MNU, though the numbers of proliferative lesions in the bladder were increased.

Animals↗
PubMed1979

Liver growth and tumorigenesis in rats.

Liver enlargement is frequently reported in studies on the short-term toxicity of chemicals. In many such studies no histological evidence of damage is present but biochemically there is often an increased microsomal enzyme activity (MEA) which is interpreted to represent a type of work hypertrophy. In a few instances, the MEA in the enlarged liver is either normal or less than normal. In such instances histochemical evidence of liver damage (depression of G-6-Pase and autophagy) is found. A compound which produced the latter changes is Ponceau MX. When administered for up to 21 months at a dose-level which produces biochemical and histochemical evidence of liver injury, a series of changes were observed consisting of progerssive diminution of MEA, areas of glycogen accumulation and centrilobular fatty change and these were followed first by nodular hyperplasia and then by frank carcinoma. The protective effect of increased MEA in carcinogenesis was shown by the reduction in tumour incidence on the administration of phenobarbitone simultaneously with acetylaminofluorene, 4-dimethyl aminoazo benzene and diethylnitrosamine. But no such protective effect is seen if the phenobarbitone is administered after treatment with these carcinogens. In fact the number of tumours is enhanced presumably due to preferential stimulation of the growth of malignant cells.

Animals↗
PubMed1978

Suppression of Hela cell growth and increase in nuclear size by chemical carcinogens: a possible screening method.

HeLa cell monolayers were "pulse" treated with either carcinogenic or "non-carcinogenic" chemicals. Pre-carcinogens were added with a liver homogenate to provide an appropriate metabolizing system. All proximate carcinogens and a proportion of pre-carcinogens were able to inhibit cell division, and in all cases examined, this was accompanied by nuclear enlargement. Although several "non-carcinogenic" chemicals also arrested cell division, nuclear enlargment was not produced. The possibility that growth inhibition and nuclear enlargement in cells treated briefly with a chemical could provide a rapid indication of carcinogenic activity is discussed.

Carcinogens↗