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Biomedical subjects

F J Roe

Publications and source records attributed to F J Roe.

At least 73 records · Page 4Linked to original sources
PubMed1979

Milky spots (Taches laiteuses) as structures which trap asbestos in mesothelial layers and their significance in the pathogenesis of mesothelial neoplasia.

The UICC standard sample of asbestos, crocidolite, was injected subcutaneously into the flanks of CBA/lac mice. Asbestos fibres were found in milky spots in the serosal cavities more than 442 days after the injection, in the form of either naked fibres or asbestos bodies. Milky spots were the only structure in which asbestos fibres were observed in the mesothelial layer. The fact that asbestos fibres were found in the liver, spleen, kidney, brain, etc., in addition to milky spots, suggested that they were transported by the blood stream throughout the body. This assumption was confirmed by the similar distribution of asbestos after intravenous administration. The vascular and cellular structure of milky spots is such that they are particularly likely to trap blood-borne asbestos fibres. Hyperplastic changes were observed in milky spots after both subcutaneous and intravenous administration of asbestos in mice. The possible involvement of milky spots in the genesis of tumors of the mesothelium following exposure of animals to asbestos is discussed.

Animals↗
PubMed1979

Atherogenesis in the White Carneau pigeon. Further studies of the role of carbon monoxide and dietary cholesterol.

Two experiments are described. In the first, 3 pairs of groups of 20 female White Carneau pigeons were fed on diets containing 0.5%, 1% or 2% cholesterol. Birds in one group from each pair were exposed to 150 ppm carbon monoxide (CO) for 6 h on 5 days of each week for 52 weeks, sufficient to raise their carboxyhaemoglobin (COHb) levels to approximately 10%, while those in the other group were sham-exposed under similar conditions. In the second experiment, 3 groups of 40 female pigeons were each fed on a diet containing 1% cholesterol, one group being exposed to CO to give COHb levels of 20%, one to give COHb levels of 10% and one being sham exposed. In addition, 20 birds in the second experiment were fed on the 1% cholesterol diet but were neither exposed to CO nor sham-exposed. Cholesterol enriched diets caused mean plasma cholesterol values in each group to rise sharply within 4 weeks of starting them, but the levels reached were as high with diets containing 0.5% cholesterol as for diets containing 1% or 2% added cholesterol. Exposure to CO increased plasma and aortic cholesterol levels, though this increase was only statistically significant for aortic levels in the second experiment. In both experiments combined exposure to the 1% cholesterol diet and CO resulted in a significant decrease in aortic triglyceride content. The incidence and severity of coronary artery atherosclerosis was associated with increasing dietary cholesterol. It was also associated with exposure to CO in birds given 0.5% or 1%, but not 2%, dietary cholesterol; the increase in birds given 1% was related to the dose of CO. Possible mechanisms are discussed for this effect of CO, which is not found in normally fed birds.

Animals↗
PubMed1979

Food and cancer.

There are good reasons to suspect that the quantity and quality of food influence both the overall risk of development of many forms of cancer and the types of cancer which occur most commonly. The evidence is briefly reviewed and the kinds of mechanisms that may be responsible listed. The striking effects of dietary restriction on cancer risk in laboratory rats and mice and the possibility that dietary restraint may be beneficial in man are discussed. Recent laboratory evidence that carcinogens may be formed in food during cooking is mentioned. Finally, the importance of avoiding mineral imbalance when conducting animal studies designed to evaluate the safety of food constituents and additives is stressed in relation to urinary-calculus formation and bladder-tumour risk.

Animal Nutritional Physiological Phenomena↗
PubMed1978

Squamous lesions in lungs of rats exposed to tobacco-smoke-condensate fractions by repeated intratracheal instillation.

Twice-weekly intratracheal instillations in rats of up to 24 mg of Fraction (R + P)G suspended in either infusine (I) or buffered saline/gelatine (BS/G) gave rise to foci of squamous metaplasia of alveolar epithelium (SqM) and squamous neoplasms (SqN). Fraction (R + P)G, which is a fraction of cigarette-smoke condensate almost as tumorigenic for mouse skin as the nearly 30 × larger mass of condensate from which it is derived, could be given in this way for up to 40 weeks without excessive mortality or any marked effect on the rate of body-weight gain. By contrast, similar treatment with Fraction N(QG), a fraction having very low tumorigenic activity for mouse skin, induced no SqN and barely any excess of SqM over that induced by either vehicle alone.The effects of Fraction (R + P)G on the incidence of SqM and SqN were both time and dose related, the effect on SqM incidence being already evident after 10 weeks of treatment. No SqN seen were unequivocally malignant, though, due to the design of the experiment, only 5 rats exposed to Fraction (R + P)G were observed more than 60 weeks after the start of the experiment.Other changes in the lung, including aggregates of alveolar macrophages laden with golden-brown pigment (GBM) and foci of cuboidal/columnar metaplasia of alveolar epithelium (CCM), were frequently seen in response to both fractions. Fraction (R + P)G administered in I was more effective in causing SqM and SqN than the same fraction administered in BS/G. The implications of the findings are discussed, particularly the possibility that the intratracheal/instillation technique might be useful as a rapid bioassay for comparing the tumorigenicity of different cigarette-smoke condensates.

Animals↗
PubMed1978

Hydrazine.

Explore the source record for details and available documents.

Adult↗
PubMed1976

Chromatin-bound and free forms of poly(adenylic acid) polymerase in rat hepatic nuclei.

Isolated rat hepatic nuclei were shown to contain poly(A) polymerase in two distinct physiologically active forms. One form was associated with the chromatin fraction and was dependent on endogenous RNA, presumably mRNA. The other activity was localized in the nuclear sap in a 'free' form and was stimulated almost 30-40-fold by exogenously added poly(A). Isolated nucleoli were devoid of significant poly(A)-synthesizing activity.

Animals↗
PubMed1975

The carcinogenicity of polycyclic hydrocarbon epoxides in newborn mice.

Benz(a)anthracene injected subcutaneously during the first 3 days of life caused a dose related increase in the incidence of liver and lung tumours in Swiss mice but over a similar dose range, the K region epoxide of benz(a)anthracene was less effective. Neonatally injected 7-methylbenz(a) was considerably more active than its K region epoxide in increasing the incidence of liver tumours in males. Both the parent compound and the epoxide slightly raised the incidence of lung tumours. Both chrysene and its K region epoxide increased liver tumour incidence but not lung tumour incidence. The K region epoxides of dibenz(a,h)-anthracene and 3-methylcholanthrene were without apparent effect on the incidence of liver, lung or other tumours despite indications from previously reported studies that the parent hydrocarbons are active at the same dose levels. The K region epoxide of phenanthrene had no effect on the incidence of any kind of neoplasm.

Animals↗
PubMed1975

Cancer and ageing in mice and men.

In an experiment involving 950 mice with a normal lifespan of 2-3 years, in laboratory conditions, regular benzpyrene application to the skin was started at 10, 25, 40 or 55 weeks of age. The incidence rate of malignant epithelial tumours among the survivors in each group increased steeply with time. This increase was associated directly with duration of exposure but, given duration, was independent of age at the start of exposure, as were the growth rates of already established tumours. In our experiment, although age per se was irrelevant, the cancer incidence rate increased approximately as a power of the duration of exposure to benzpyrene. This shows that the observed approximate power-law increase of most human adult cancer incidence rates with age could exist merely because age equals duration of exposure to background and spontaneous carcinogenic stimuli. Thus, no intrinsic effects of ageing (such as failing immunological surveillance or age related hormonal changes) whatever need to postulated to explain the vast increases in old age of the incidence rates of such human cancers. This result can greatly simplify speculation about mechanisms of carcinogenesis.

Age Factors↗
PubMed1975

Response of rat lung to 3,4-benzpyrene administered by intratracheal instillation in infusine with or without carbon black.

In a controlled experiment groups of SPF Wistar rats were give 18 once-fortnightly doses of 0-5, 1-0 or 2-0 mg 3,4-benzpyrene (BP) suspended in infusine (I) or in carbon black (CB) + I by intratracheal instillation. Of rats examined post mortem, 1/16 given I+CB only, 0/16 given I only, 15/51 given BP in I+CB and 24/48 given BP in I developed squamous neoplasms of the lung. The incidence of tumours was significantly related to dose of BP. At the 1 or 2 mg dose levels BP in I only was more productive of tumours than BP in I+CB. Other changes encountered included squamous metaplasia of alveolar and bronchiolar epithelium (Sq.M), but not of bronchial epithelium, and cuboidal and columnar metaplasia of alveolar epithelium in the vicinity of terminal bronchioles (CCM). Sq.M was associated with exposure to BP or I+CB. CCM was strongly associated with exposure to I+CB but only weakly with exposure to BP.

Adenocarcinoma↗
PubMed1975

Response of rat lung to tobacco smoke condensate or fractions derived from it administered repeatedly by intratracheal instillation.

The repeated intratracheal instillation of cigarette smoke condensate (SWS) in rats at close to maximum tolerated dose levels failed to induce squamous neoplasms in the lungs although such treatment was associated with an increased incidence of cuboidal/columnar metaplasia (CCM) and squamous metaplasia (Sq.M) of alveolar epithelium. With one exception, various fractions of SWS had no effect on lung tumour incidence though some were more effective than SWS in increasing the incidence of CCM and Sq.M. The exceptional fraction, Fraction P, which contains most of the polycyclic aromatic hydrocarbons of smoke and is the most effective of the fractions tested in producing tumours in mouse skin, gave rise to 4 squamous tumours of doubtful malignancy and one metastasizing squanmous carcinoma among 3 groups of 18 animals exposed at 3 different dose levels. The results are discussed in relation to the possible development of a method for comparing condensates for relative lung carcinogenicity.

Animals↗
PubMed1975

Response of rat lung to inhaled vapour phase constituents (VP) of tobacco smoke alone or in conjunction with smoke condensate or fractions of smoke condensate given by intratracheal instillation.

In a controlled experiment, 6 groups of SPF rats were given cigarette smoke condensate (SWS) in solid form without a vehicle once fortnightly by intratracheal instillation, at 3 dose levels with or without additional exposure to the vapour phase of smoke (VP) from 10 plain cigarettes each week. Treatment continued for life. Six other groups were similarly treated with one of 3 fractions of condensate with or without VP. Exposure to VP was associated with a significant reduction in body weight, but not signficantly with the incidence or severity of any observed pathological change in the lungs. A significant dose-related assoication was seen between SWS or its fractions and the incidence and degree of chronic respiratory disease (CRD), cuboidal or columnar metaplasia (CCM) and squamous metaplasia of alveolar epithelium (Sq.M) produced. No neoplasms, however, were elicited. A significant correlation was found between the degrees of CCM and of Sq.M produced in the 24 groups exposed to SWS or fractions. The results are discussed in the light of studies in which rats were exposed to tobacco smoke by inhalation and of studies in which the same condensate and fractions were applied to mouse skin.

Animals↗
PubMed1975

Response of rat lung to inhaled tobacco smoke with or without prior exposure to 3,4-benzpyrene (BP) given by intratracheal instillation.

SPF rats were exposed to the smoke from 10 cigarettes per week from the age of 10 weeks until they died. Survival, body weight, tumour incidence and histopathological appearances of the lungs were compared with those for untreated sham exposed rats. Two further groups were given a single dose of 3,4-benzyprene (BP) by intratracheal instillation. One of these was then exposed to the smoke of 10 cigarettes per week till death. Compared with untreated or sham exposed rats, exposure to smoke was associated with a significant reduction in incidence of mammary tumours. Exposure to smoke was associated with an increasing incidence of collections of macrophages laden with golden-brown pigment (GBM) and of areas of cuboidal or columnar metaplasia (CCM) or squamous metaplasia (Sq.M) of alveolar epithelium. In control rats there was virtually no GBM, a low incidence of CCM and Sq.M. Four out of 406 smoke exposed rats which came to post mortem had squamous neoplasms in the lungs, 3 having lesions of doubtful malignancy and one having a squamous carcinoma. In contrast, no squamous neoplasms were seen in 197 control rats. This difference was not statistically significant. The findings in rats given a single dose of BP were, in all the above respects, similar to those in untreated rats, except that one developed a squamous carcinoma of the lung. The effects of a single dose of BP followed by smoke exposure were in general similar to those of smoke exposure only. Three rats on this treatment regimen developed squamous cancers of the lung. None of the treatments increased the incidence of adenomata of the lungs. The results are discussed in relation to other studies of the effects of smoke exposure on rats and other species.

Adenoma↗