-transparent.png){kind=logo}
Aflatoxin B1 (AFB1) is a potent carcinogen and mutagen. It requires metabolic activation to be converted to the DNA-binding product aflatoxin B1 epoxide (AFB1-epoxide). A model of this epoxide is aflatoxin B1 dichloride (AFB1Cl2). Both react at the N7 position of guanine to form large adducts. The major adduct formed can either be rapidly removed to leave an apurinic site or can undergo ring opening of the imidazole ring to form a chemically stable adduct. A number of Chinese hamster DNA repair-deficient mutants have been screened for their sensitivity to AFB1-epoxide and AFB1Cl2. Some of the mutants screened belong to different UV complementation groups. Human genes involved in nucleotide excision-repair correct deficiencies found in these complementation groups. The mutants which were found to be most sensitive to AFB1 (V-C4 and V-H1) were further investigated. Alkaline elution was used to measure AFB1-induced DNA single-strand break repair in the mutants. V-H1 repaired completely in 24 h whereas V-C4 displayed only partial repair.
E A Martin, and
R Waters
December 1989,
Cancer research,
E A Martin, and
R Waters
November 1996,
Carcinogenesis,
E A Martin, and
R Waters
January 1990,
Mutation research,
E A Martin, and
R Waters
February 1998,
Nucleic acids research,
E A Martin, and
R Waters
March 1989,
Cancer research,
E A Martin, and
R Waters
May 1985,
Mutation research,
E A Martin, and
R Waters
September 1992,
Radiation research,
E A Martin, and
R Waters
December 2000,
Proceedings of the National Academy of Sciences of the United States of America,
E A Martin, and
R Waters
September 2006,
The Journal of surgical research,
