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Biomedical subjects

A Arranto

Publications and source records attributed to A Arranto.

4 recordsLinked to original sources
PubMed1985

Initiation and promotion in young and old animals. Implications for human tumour formation.

The significance of ageing in experimental skin carcinogenesis and on the manifestation of tumour formation in man was studied. Initiation with the carcinogenic hydrocarbon 7,12-dimethylbenz [a]anthracene and promotion with croton oil in mouse skin showed that tumour formation was unchanged when promotion was delayed 3, 10, 23 or 43 weeks in comparison with that in untreated animals of the same age. The sensitivity to carcinogen treatment of animals over 71 weeks of age was less than that of animals 11-51 weeks of age; this finding affected the interpretation of data on animal groups treated 63 weeks after the start of the experiment. In a human autopsy study, the tumour incidence increased with age to the eighth decade; benign tumours of types not related to malignant tumours occurred in older age groups. The percentage of epithelial tumours was higher in humans aged 60-80 and in organs exposed to environmental agents, but lower in humans aged 80 and more.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Decrease in liver collagen accumulation in carbon tetrachloride-injured and normal growing rats upon administration of zinc.

Several attempts have been made to develop antifibrotic drugs for human use, but their success has been limited. The present data suggest that peroral zinc treatment has a direct and selective inhibitory effect on carbon tetrachloride-induced collagen accumulation in rat liver. Zinc did not normalize the carbon tetrachloride-induced increases in either liver relative weight, liver total protein content, fat accumulation, or the standard liver function tests, but it did efficiently inhibit liver collagen accumulation. It also reduced skin and liver collagen content and urinary hydroxyproline excretion in normal growing animals, indicating that the inhibition is not limited to the fibroproliferative inflammation associated with carbon tetrachloride injury. Neither inhibition of polysomal protein synthesis nor increased degradation of mature collagen fibers was found to play any major role in the effect of zinc. Instead, a plausible mechanism is inhibition of proline hydroxylation.

Animals↗
PubMed1982

Plasma high-density lipoproteins and hepatic microsomal enzyme induction. Relation to histological changes in the liver.

The relationship between high-density lipoproteins (HDL) in plasma and hepatic structure and microsomal function has been investigated in 54 patients undergoing diagnostic liver biopsy. Plasma HDL cholesterol and major apoproteins were correlated with hepatic histology and microsomal enzyme activity assessed directly as liver cytochrome P-450 concentration and indirectly by plasma antipyrine clearance rate. HDL cholesterol, the concentrations of apoproteins A-I and A-II, the HDL cholesterol/total cholesterol ratio and cytochrome P-450 were low in subjects with moderate or severe hepatic fatty infiltration or cirrhosis when compared with the values for subjects with a normal live. HDL cholesterol and apoprotein A-I and the HDL cholesterol/total cholesterol ratio were directly proportional to the amount of non-fatty parenchyma in the livers. Subjects with a normal liver undergoing treatment with enzyme-inducing drugs, such as phenytoin, phenobarbital and primidone, had higher HDL cholesterol, apoproteins A-I and A-II, HDL cholesterol/total cholesterol ratio, cytochrome P-450 and antipyrine clearance rate than subjects not receiving such therapy. Treatment with inducers appeared to have compensated for the effect of liver disease in lowering plasma HLD. In the entire population, and also in subjects not taking inducing drugs, when considered separately, plasma HDL cholesterol, apoproteins A-I and A-II and the HDL cholesterol/total cholesterol ratio were significantly correlated with cytochrome P-450 concentration. In subjects on enzyme inducers, HDL cholesterol and apoprotein A-I levels and the HDL cholesterol/total cholesterol ratio were proportional to the magnitude of the induction. Serum triglycerides were inversely proportional to the measures of liver microsomal enzyme activity. The lipoprotein pattern, high HDL cholesterol and apoproteins A-I and A-II, and high HDL cholesterol/total cholesterol ratio that accompany microsomal induction are characterized by a reduced risk of atherosclerotic vascular disease and a prolonged expectation of life. The plasma changes presumably reflect the effect of enzyme inducers, such as phenytoin and phenobarbital on hepatic lipids and proteins.

Adult↗