The Kinetics of<i>in Situ</i>Repair in Rat Mammary Cells

Mahler, Peter A.; Gould, Michael N.; Clifton, Kelly H.

doi:10.1080/09553008314551421

Cited by 6 publications

(2 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…. 1981, with normal rat mammary epithelial cells (Mahler et al 1983), and with parenchymal hepatocytes (Jirtle et al . 1984a, b, Gould et al 1984 .…”

Section: Repair and Fixation Of Pld May Affect Survival Of Cells Irmentioning

confidence: 96%

Radiation-induced Potentially Lethal Damage: DNA Lesions Susceptible to Fixation

Iliakis

1988

International Journal of Radiation Biology

131

View full text Add to dashboard Cite

The various postirradiation incubation conditions reported to uncover potentially lethal damage (PLD) induced by ionizing radiation are outlined and critically discussed. The process of damage fixation is the most characteristic determinant in distinguishing between PLD and other forms of damage (lethal or non-lethal). The results compiled indicate the induction of two forms of PLD (termed alpha- and beta-PLD). Evidence is presented that repair and fixation of alpha-PLD may underlie the variation in radiosensitivity observed through the cycle. Beta-PLD appears to be sensitive only to postirradiation treatment in anisotonic sale solutions. Results obtained at the DNA and chromosome level, under conditions allowing repair or causing fixation of PLD, are reviewed and combined together to devise a qualitative model that outlines a possible sequence of events from damage fixation at the DNA level, to damage fixation at the chromosome level and, ultimately, to cell death. It is suggested that damage uncovered at the cellular level as potentially lethal, comprises DNA dsb (single, pairs or groups) and that fixation is mediated by forces transmitted to the double helix through alteration (local or general) in chromatin conformation. Changes in chromatin conformation are caused either as a result of the cell's progression through the cycle or in response to a postirradiation treatment. The fixation process leads to the induction of chromosome aberrations. The validity of the concept of PLD in in vivo systems is shown, and the possible importance of PLD repair in radiation therapy is reviewed. The concept of PLD is compared to the concept of sublethal damage, and the possibility that similar molecular lesions underlie both types of damage is discussed.

show abstract

“…. 1981, with normal rat mammary epithelial cells (Mahler et al 1983), and with parenchymal hepatocytes (Jirtle et al . 1984a, b, Gould et al 1984 .…”

Section: Repair and Fixation Of Pld May Affect Survival Of Cells Irmentioning

confidence: 96%

Radiation-induced Potentially Lethal Damage: DNA Lesions Susceptible to Fixation

Iliakis

1988

International Journal of Radiation Biology

131

View full text Add to dashboard Cite

show abstract

“…Third, quantitative transplantation assays of cells prepared from x-irradiated mammary glands in which the formation of AU is used as the end point have shown that the capacity of such cells to form AU decreases with the x-ray dose according to the relationship to be expected if AU are derived from single cells (3,4). Furthermore, the recovery of AU-forming capacity after radiation exposure in vivo follows the kinetic pattern typical of repair of potentially lethal intracellular damage in irradiated mammalian cells in culture as measured by clonal colony-forming capacity (5). Fourth, as reaffirmed herein, the number of grafted cells required to produce at least one AU in 50% of the graft sites, the alveolar dose-50% (ADSo) is remarkably constant in cells prepared from the glands of normal young adult female rats of both Fischer (F344) and W/Fu strains.…”

mentioning

confidence: 96%

Differential Control of Alveolar and Ductal Development in Grafts of Monodispersed Rat Mammary Epithelium

Kamiya¹,

Gould²,

Clifton³

1991

Experimental Biology and Medicine

View full text Add to dashboard Cite

Multicellular secretory alveolar units (AU) develop in grafts of monodispersed mammary cells in intact recipient rats co-grafted with mammotropic hormone-secreting pituitary tumor (MtT). The cumulative evidence is consistent with a postulated clonal origin of these structures. Small numbers of multicellular structures of a second type, mammary ductal units (DU), were found in mammary cell grafts in intact Wistar/Furth recipients co-grafted with MtT W10 but not in intact F344 recipients co-grafted with MtT F4. Studies in (Wistar/Furth x F344) F1 hybrid recipients grafted with mammary cells from either parent strain demonstrated that this difference in DU formation is dependent on the strain of grafted MtT, and is not a genetic characteristic of the rat strain. DU formation is stimulated and AU formation is inhibited by elevation of mammotropic hormones from MtT coupled with glucocorticoid deficiency induced by adrenalectomy. cortisol treatment reverses this effect. Finally, in mammary glands in situ in intact rats, the total numbers of AU-forming clonogens decrease during 6 weeks after MtT transplantation. In contrast, during the same period, elevated mammotropins from grafted MtT coupled with glucocorticoid deficiency from adrenalectomy cause an increase in the total number of cells that are capable of AU formation when transplanted to intact recipients co-grafted with MtT. Thus, the same hormonal combination that stimulates DU formation in mammary cell grafts and has previously been shown to promote cancer in mammary glands in situ also stimulates an increase in the glandular content of assayable AU-forming cells in situ.

show abstract

The Clonogenic Cells of the Rat Mammary and Thyroid Glands: Their Biology, Frequency of Initiation, and Promotion/Progression to Cancer

Clifton¹

1990

Scientific Issues in Quantitative Cancer Risk Assessment

View full text Add to dashboard Cite

The Kinetics ofin SituRepair in Rat Mammary Cells

Cited by 6 publications

References 8 publications

Radiation-induced Potentially Lethal Damage: DNA Lesions Susceptible to Fixation

Radiation-induced Potentially Lethal Damage: DNA Lesions Susceptible to Fixation

Differential Control of Alveolar and Ductal Development in Grafts of Monodispersed Rat Mammary Epithelium

The Clonogenic Cells of the Rat Mammary and Thyroid Glands: Their Biology, Frequency of Initiation, and Promotion/Progression to Cancer

Contact Info

Product

Resources

About