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E D Rees

Publications and source records attributed to E D Rees.

33 records · Page 2Linked to original sources

Changes in chromosomes of bone marrow after intravenous injections of 7,12-dimethylbenz(a)anthracene and related compounds.

Multiple intravenous injections of an emulsion containing 7,12-dimethylbenz(a)anthracene (DMBA) or 7,8,12-trimethylbenz(a)anthracene (TMBA) induce a high incidence of leukemia in rats. Twenty-four hours after a single injection, about half of the metaphase cells in the marrow have chromosomes with breaks. Although breaks were inflicted on chromosomes of various sizes and morphology, these aberrations were nonrandom in that members of the nos. 1 and 2 chromosome pairs were involved to an extent greater than expected on the basis of their size and number. Distinctive karyotypic abnormalities involving the no. 2 chromosome were observed in half of the leukemic rats, whereas these abnormalities were not observed in nonleukemic, DMBA-treated rats. Benzo(a)pyrene and benzo(e)pyrene, polycyclic aromatic hydrocarbons which did not induce leukemia, produced fewer breaks of the no. 2 (and other) chromosomes than did DMBA or TMBA.

Animals↗

Lipid composition of rat mammary carcinomas, mammary glands, and related tissues: endocrine influences.

The lipids of mammary glands and mammary carcinomas from rats in various hormonal states were studied and compared with each other, with adipose tissue, and with a new transplantable sarcoma derived from cultured mammary carcinoma cells. When large doses of estradiol-17 Beta were administered to the host, cells of a few carcinomas became engorged with triglyceride containing an increased proportion of C(10)-C(14) fatty acids-a characteristic of milk fat. Cancers capable of fatty transformation must retain in latent form the enzyme system for fatty acid synthesis possessed by mammary epithelium; estradiol-17 Beta apparently activates this system. The lipid composition of retroperitoneal adipose tissue resembled that of the mammary tissue of virgin rats; this indicates similarity between retroperitoneal fat and the adipose component of mammary gland. Relative to the dry nonfat material present, the phospholipid content of adipose tissue was greater than that of the other tissues. Generally, differences in lipid composition between tissues were in amounts of triglyceride present and proportions of fatty acids in the triglyceride fraction. The ratios of cholesterol and cholesterol ester to phospholipid were similar in normal and neoplastic tissues. The amounts of free fatty acid, monoglyceride, and diglyceride were roughly proportional to the amount of triglyceride present.

Adipose Tissue↗

Comparison of the clastogenic and carcinogenic effects of intravenous beta-propiolactone and benzo(a)pyrene in rats.

Scored at 24 hours, the LD-50 of a solution of beta-propiolactone administered intravenously to young rats was 225 +/- 55 mg/kg. Twenty-four hours after a single intravenous injection (100 mg/kg = 1.4 m mole/kg) of beta-propiolactone into male and female rats of both the Long-Evans and Sprague-Dawley strains, the incidence of breaks found in the chromosomes of metaphase marrow cells was low (8.8 percent vs. 5.0 percent in controls). The s5 chromosomes were preferentially damaged. A 200 mg/kg dose increased the incidence modestly to 11.3 percent. In comparison, a single intravenous dose of benzo(a)pyrene (40 mg/kg = 0.16 m mole/kg) produced a break incidence of 19 percent. In long-term experiments multiple (five) intravenous injections (100 mg/kg each) of beta-propiolactone given in a 6 week period elicited only two neoplasms (a chloro-leukemia and a mammary fibroadenoma) among 37 animals during the following 12-13 months. In contrast, four injections of benzo(a)pyrene (40 mg/kg) produced a 14-times greater mammary tumor incidence in the Sprague-Dawley female rat than did beta-propiolactone. Marrow cell chromosome examination indicated no significant chromosomal changes due to the earlier beta-propiolactone treatment except for one animal with a consistent 43-chromosome karyotype resulting from S1 trisomy; no neoplasm was evident in that animal. Earlier treatment with benzo(a)pyrene produced a persistent and significant elevation in break incidence. Both the carcinogenic and clastogenic effects of intravenous beta-propiolactone are low in rats and are not comparable in magnitude to those produced by benzo(a)pyrene.

Animals↗