Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells

David L. Mitchell; Ronald M. Humphrey; Gerald M. Adair; Larry H. Thompson; Judith M. Clarkson

doi:10.1016/0167-8817(88)90007-7

Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells

David L. Mitchell, Ronald M. Humphrey, Gerald M. Adair, Larry H. Thompson, Judith M. Clarkson

Research output: Contribution to journal › Article

44 Scopus citations

Abstract

Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defectiev in the UV-sensitive cells. In contrast, only 20--60% of antibody-binding sites specific for cylcobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair pf (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude thtat a consequences of DNA repair in CHO cells is modification rather that reemoval of cylobutane dimers.

Original language	English (US)
Pages (from-to)	53-63
Number of pages	11
Journal	Mutation Research DNA Repair Reports
Volume	193
Issue number	1
DOIs	https://doi.org/10.1016/0167-8817(88)90007-7
State	Published - 1988
Externally published	Yes

Keywords

(6-4)Photoproducts
Cyclobutane dimers
DNA excision repair
Split-dose recovery

ASJC Scopus subject areas

Medicine(all)

Access to Document

10.1016/0167-8817(88)90007-7

Fingerprint Dive into the research topics of 'Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells'. Together they form a unique fingerprint.

Cite this

Mitchell, D. L., Humphrey, R. M., Adair, G. M., Thompson, L. H., & Clarkson, J. M. (1988). Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells. Mutation Research DNA Repair Reports, 193(1), 53-63. https://doi.org/10.1016/0167-8817(88)90007-7

@article{eff0a291f1924dacafdf22907cc0f00e,

title = "Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells",

abstract = "Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defectiev in the UV-sensitive cells. In contrast, only 20--60% of antibody-binding sites specific for cylcobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair pf (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude thtat a consequences of DNA repair in CHO cells is modification rather that reemoval of cylobutane dimers.",

keywords = "(6-4)Photoproducts, Cyclobutane dimers, DNA excision repair, Split-dose recovery",

author = "Mitchell, {David L.} and Humphrey, {Ronald M.} and Adair, {Gerald M.} and Thompson, {Larry H.} and Clarkson, {Judith M.}",

year = "1988",

doi = "10.1016/0167-8817(88)90007-7",

language = "English (US)",

volume = "193",

pages = "53--63",

journal = "Mutation Research DNA Repair Reports",

issn = "0167-8817",

publisher = "Elsevier BV",

number = "1",

}

TY - JOUR

T1 - Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells

AU - Mitchell, David L.

AU - Humphrey, Ronald M.

AU - Adair, Gerald M.

AU - Thompson, Larry H.

AU - Clarkson, Judith M.

PY - 1988

Y1 - 1988

N2 - Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defectiev in the UV-sensitive cells. In contrast, only 20--60% of antibody-binding sites specific for cylcobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair pf (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude thtat a consequences of DNA repair in CHO cells is modification rather that reemoval of cylobutane dimers.

AB - Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defectiev in the UV-sensitive cells. In contrast, only 20--60% of antibody-binding sites specific for cylcobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair pf (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude thtat a consequences of DNA repair in CHO cells is modification rather that reemoval of cylobutane dimers.

KW - (6-4)Photoproducts

KW - Cyclobutane dimers

KW - DNA excision repair

KW - Split-dose recovery

UR - http://www.scopus.com/inward/record.url?scp=0023882323&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023882323&partnerID=8YFLogxK

U2 - 10.1016/0167-8817(88)90007-7

DO - 10.1016/0167-8817(88)90007-7

M3 - Article

C2 - 3275879

AN - SCOPUS:0023882323

VL - 193

SP - 53

EP - 63

JO - Mutation Research DNA Repair Reports

JF - Mutation Research DNA Repair Reports

SN - 0167-8817

IS - 1

ER -