Catechol (CAS: 120-80-9), given in
drinking water to rats, was the most effective of 5
phenols in enhancing [3H]
thymidine incorporation [( 3H]dThd-l) into esophageal
DNA. To test for esophageal
cocarcinogenesis, groups of 30 male MRC-Wistar rats received 3 weekly ip
injections of 25 mg
methyl-n-amylnitrosamine [(MNAN) CAS: 13256-07-0]/kg. From the time of the first MNAN injection, each group also received
catechol,
tannic acid (CAS: 1401-55-4), dried leaves of Bidens pilosa L., or
croton oil (CAS: 8001-28-3) (respectively, 2, 10, 50, and 2 g/kg semipurified diet), or were given 20 ip
injections of 6 mg
phorbol (CAS: 17673-25-5)/rat. The rats were killed after 20-45, 46-52, or 53-72 weeks (subgroups A, B, and C). In the group given MNAN alone, most esophageal
papillomas developed during the first 45 weeks. Both
catechol and B. pilosa significantly increased the esophageal
papilloma multiplicity (No. of
papillomas/rat) induced by MNAN, with a maximum
tumor yield of 2.2 times that in the corresponding subgroup treated with MNAN alone.
Papilloma multiplicity increased from subgroup A to subgroup C in the MNAN plus B. pilosa group but not in the MNAN plus
catechol group. No
tumors were induced by the test cocarcinogens given without MNAN. We concluded that a) an increased esophageal [3H]dThd-I indicates potential cocarcinogenicity and b)
catechol and B. pilosa were weak esophageal cocarcinogens. These results support the view that
catechol in cigarette
smoke and B. pilosa as eaten in South Africa contribute to the etiology of human
esophageal cancer.