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L C Satterfield

Publications and source records attributed to L C Satterfield.

14 recordsLinked to original sources

Strain-dependent susceptibility to radiation-induced mammary cancer is a result of differences in epithelial cell sensitivity to transformation.

Variations in sensitivity to radiation-induced mammary cancer among different strains of mice are well known. However, the reasons for these variations have not been determined. In the present study, the cell dissociation assay was used to determine the radiation-induced transformation frequencies in sensitive BALB/c mice and resistant C57BL mice as well as the resistant hybrid B6CF1 independent of host environment. The influence of host environment on the progression of transformed cells to the neoplastic phenotype was also examined. Results demonstrated that the variations in sensitivity among these sensitive and resistant mice are a result of inherent differences in the sensitivity of the mammary epithelial cells to radiation-induced transformation. Under the conditions used, host environment played no role in the initiation of transformed cells by radiation or in the progression of these cells to the neoplastic phenotype.

Animals↗

Induction of phenotypically altered mammary epithelial cells by neutrons and gamma rays.

These studies have examined alterations in the in vivo growth properties of mammary epithelial cells isolated at 1, 4, and 16 weeks after in vivo irradiation with -137Cs gamma rays or fission-spectrum neutrons. Altered in vitro growth potential was characterized by the proliferation of epithelial foci (EF) from irradiated animals under conditions in which mammary cells from nonexposed animals senesced. These EF were further characterized based on their ability to be subcultured. Both gamma and neutron irradiation resulted in the appearance of cells capable of forming EF. Further, with increased time in situ between irradiation and cell isolation, the frequency of EF which were capable of being subcultured indefinitely (EFs) increased. Reducing the gamma-ray dose rate resulted in fewer EFs while reducing the neutron dose rate resulted in increased frequencies of EFs. These data confirm earlier observations following gamma irradiation and show these cellular changes are also observed following neutron irradiation. In addition, these data indicate that changes in dose rate primarily influence the emergence of immortalized cell populations.

Animals↗

Radiation carcinogenesis: time-dose relationships.

The present studies were undertaken to examine the time-dose relationships for the induction of lung adenocarcinomas and mammary adenocarcinomas in female BALB/c mice following gamma irradiation. Twelve-week-old female BALB/c/An NBd mice were irradiated with 137Cs gamma rays, and lifetime tumor incidences following high-dose-rate, low-dose-rate, or fractionated exposure regimens were compared. Analysis of the results indicated that the data could be fitted by linear-quadratic dose-response models for the induction of both tumors following acute doses and a linear model with a slope similar to that for the linear portion of the linear quadratic following low-dose-rate exposure regimens. When doses were fractionated the response was dependent upon the dose per fraction. If the dose per fraction was a dose which was predominantly on the linear portion of the acute dose response curve, then the response was linear and similar to that after low-dose-rate exposures. If the dose per fraction was in a region where the quadratic portion of the acute dose-response was significant, then the tumor incidence was higher than that following low-dose-rate exposures.

Adenocarcinoma↗

Long-term effects of repeated exposure to 3-methylfuran in hamsters and mice.

Male and female Syrian golden hamsters were exposed for 2 h once a week for 10 consecutive weeks to 344 mumol/l of 3-methylfuran (3MF), an agent known to produce acute Clara-cell necrosis. Ten months later their respiratory function was evaluated. No functional differences were found between control and treated animals, and histopathologic evaluation of the lungs did not reveal any major treatment-related alterations. Male and female BALB/c mice were exposed for 1 h to 26.8 mumol/l of 3MF once weekly for 10 wk. After 2 yr the tumor incidence in exposed animals was not increased when compared to controls. It is concluded that the acute Clara-cell necrosis produced by 3MF at the doses used is of little long-term consequence.

Air Pollutants↗

Effects of the antioxidant butylated hydroxytoluene (BHT) on mortality in BALB/c mice.

Butylated hydroxytoluene (BHT) was given in the feed to determine its effect on life span in genetically well-defined, barrier-derived BALB/c mice. Both sexes received 0.75% BHT for three different treatment periods: (A) 8 to 11 weeks of age; (B) for life, beginning at 11 weeks; (C) for life, beginning at 8 weeks of age. The control group (D) was untreated. All BHT treatment groups had mean survival times which exceeded that of controls. The order of survival was B greater than C greater than A greater than D (Males: 890, 832, 726, 684 days; Females: 875, 798, 759, 701 days). Most of the increases in mean survival time were related to a reduction in early deaths (350--600 days) in BHT-treated mice. The reason for the life-lengthening effect on BHT was not identified, but it may relate to alterations in specific disease incidences.

Aging↗

Diseases of aging untreated virgin female RFM and BALB/c mice.

Diseases of untreated, virgin female barrier-maintained RFM and BALB/c mice used as controls in a large radiation aging experiment were necropsied after natural death. The spectrum and incidence of neoplastic and nonneoplastic diseases were somewhat different in the two strains. Both strains show a high incidence of neoplasma (largely reticulum cell sarcomas and lung tumors) and of glomerulosclerosis. A wide variety of other diseases was noted in much lower incidence. The findings in the RF were briefly compared with those in earlier experiments with that strain in this laboratory.

Aging↗

Selective sex-related modification of diethylnitrosamine-induced carcinogenesis in BALB/c mice by concomitant administration of butylated hydroxytoluene.

Tumor induction in BALB/c mice by diethylnitrosamine (DENA) was shown to be sex related. Female mice killed 13.5 months after DENA exposure generally had higher incidences of forestomach and lung tumors than did males and also had higher numbers of lung tumors per tumor-bearing mouse. Although neither sex developed stomach tumors spontaneously, males had higher incidences of spontaneous lung tumors than did females (45 vs. 26%). When butylated hydroxytoluene (BHT) was given concomitantly with DENA treatment, females had an increased survival (68 vs. 43%) and a reduced incidence of forestomach squamous cell carcinomas (77 vs. 100%) compared with females given DENA alone. No such protective effect on survival or on the occurrence of stomach tumors was seen in males given BHT and DENA or on lung tumorigenesis in either sex. In males, BHT given alone increased survival of treated mice over that of untreated controls, but it had no such effect on the females. The results of this study suggested an as yet unexplained hormonal influence and/or dependence for this BHT modification of DENA tumorigenesis.

Animals↗