Photocarcinogenesis and persistent hyperplasia in UV-irradiated SENCAR mouse skin

Research output: Contribution to journalArticle

Abstract

Susceptibility to photocarcinogenesis has been examined in several mouse strains and stocks including SENCAR, CD-1, BALB/c, C3H, C57BL, and NZB. SENCAR mice are hypersusceptible to tumorigenesis caused by single high dose exposures to ultraviolet (UV) radiation but not by chronic low-dose exposures. SENCAR mice also exhibit an exaggerated and persistent epidermal hyperplasia in response to UV-induced tissue damage. The persistent hyperplasia is apparently due to a sustained proliferation of the epithelial basal cells, rather than to delayed cell differentiation. SENCAR mice did not inhibit persistent hyperplasia following other forms of tissue damage (surgical or thermal). In related studies, the levels of thymine dimers induced in SENCAR epidermis by UV radiation were comparable to those observed in BALB/c epidermis. In addition, no differences were found in the tissue distribution or persistence of thymine dimers in SENCAR and BALB/c skin.

Original languageEnglish (US)
Pages (from-to)131-134
Number of pages4
JournalEnvironmental Health Perspectives
VolumeVol. 68
StatePublished - 1986
Externally publishedYes

Fingerprint

Inbred SENCAR Mouse
Hyperplasia
Pyrimidine Dimers
skin
Skin
ultraviolet radiation
Tissue
Epidermis
Ultraviolet radiation
Radiation
damage
Tissue Distribution
Cell Differentiation
Carcinogenesis
persistence
Hot Temperature
Epithelial Cells
Cells
tissue
dose

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Public Health, Environmental and Occupational Health

Cite this

Photocarcinogenesis and persistent hyperplasia in UV-irradiated SENCAR mouse skin. / Strickland, Paul Timothy.

In: Environmental Health Perspectives, Vol. Vol. 68, 1986, p. 131-134.

Research output: Contribution to journalArticle

@article{e6291206440a4895ab0b8af40c76798d,
title = "Photocarcinogenesis and persistent hyperplasia in UV-irradiated SENCAR mouse skin",
abstract = "Susceptibility to photocarcinogenesis has been examined in several mouse strains and stocks including SENCAR, CD-1, BALB/c, C3H, C57BL, and NZB. SENCAR mice are hypersusceptible to tumorigenesis caused by single high dose exposures to ultraviolet (UV) radiation but not by chronic low-dose exposures. SENCAR mice also exhibit an exaggerated and persistent epidermal hyperplasia in response to UV-induced tissue damage. The persistent hyperplasia is apparently due to a sustained proliferation of the epithelial basal cells, rather than to delayed cell differentiation. SENCAR mice did not inhibit persistent hyperplasia following other forms of tissue damage (surgical or thermal). In related studies, the levels of thymine dimers induced in SENCAR epidermis by UV radiation were comparable to those observed in BALB/c epidermis. In addition, no differences were found in the tissue distribution or persistence of thymine dimers in SENCAR and BALB/c skin.",
author = "Strickland, {Paul Timothy}",
year = "1986",
language = "English (US)",
volume = "Vol. 68",
pages = "131--134",
journal = "Environmental Health Perspectives",
issn = "0091-6765",
publisher = "Public Health Services, US Dept of Health and Human Services",

}

TY - JOUR

T1 - Photocarcinogenesis and persistent hyperplasia in UV-irradiated SENCAR mouse skin

AU - Strickland, Paul Timothy

PY - 1986

Y1 - 1986

N2 - Susceptibility to photocarcinogenesis has been examined in several mouse strains and stocks including SENCAR, CD-1, BALB/c, C3H, C57BL, and NZB. SENCAR mice are hypersusceptible to tumorigenesis caused by single high dose exposures to ultraviolet (UV) radiation but not by chronic low-dose exposures. SENCAR mice also exhibit an exaggerated and persistent epidermal hyperplasia in response to UV-induced tissue damage. The persistent hyperplasia is apparently due to a sustained proliferation of the epithelial basal cells, rather than to delayed cell differentiation. SENCAR mice did not inhibit persistent hyperplasia following other forms of tissue damage (surgical or thermal). In related studies, the levels of thymine dimers induced in SENCAR epidermis by UV radiation were comparable to those observed in BALB/c epidermis. In addition, no differences were found in the tissue distribution or persistence of thymine dimers in SENCAR and BALB/c skin.

AB - Susceptibility to photocarcinogenesis has been examined in several mouse strains and stocks including SENCAR, CD-1, BALB/c, C3H, C57BL, and NZB. SENCAR mice are hypersusceptible to tumorigenesis caused by single high dose exposures to ultraviolet (UV) radiation but not by chronic low-dose exposures. SENCAR mice also exhibit an exaggerated and persistent epidermal hyperplasia in response to UV-induced tissue damage. The persistent hyperplasia is apparently due to a sustained proliferation of the epithelial basal cells, rather than to delayed cell differentiation. SENCAR mice did not inhibit persistent hyperplasia following other forms of tissue damage (surgical or thermal). In related studies, the levels of thymine dimers induced in SENCAR epidermis by UV radiation were comparable to those observed in BALB/c epidermis. In addition, no differences were found in the tissue distribution or persistence of thymine dimers in SENCAR and BALB/c skin.

UR - http://www.scopus.com/inward/record.url?scp=0022558835&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022558835&partnerID=8YFLogxK

M3 - Article

C2 - 3780624

AN - SCOPUS:0022558835

VL - Vol. 68

SP - 131

EP - 134

JO - Environmental Health Perspectives

JF - Environmental Health Perspectives

SN - 0091-6765

ER -