S. Okazaki et al., MODIFICATION OF HEPATOCARCINOGENESIS AND RENAL CARCINOGENESIS BY CATECHOL AND ITS ISOMERS IN RATS PRETREATED WITH N-ETHYL-N-HYDROXYETHYLNITROSAMINE, Teratogenesis, carcinogenesis, and mutagenesis, 13(3), 1993, pp. 127-137
Modifying effects of catechol, resorcinol, and hydroquinone on second
stage hepato- and renal carcinogenesis was investigated in rats pretre
ated with N-ethyl-N-hydroxyethynitrosamine(EHEN). Groups of twenty 6-w
eek-old Wistar/Crj male rats were treated with 0.1% EHEN in the drinki
ng water for 3 weeks. Starting 1 week after the termination of EHEN tr
eatment, they were given a diet containing 0.8% catechol, 0.8% resorci
nol, or 0.8% hydroquinone or basal diet for 36 weeks. Further groups o
f 15 rats were each treated with the same doses of phenolic compounds
or basal diet alone without EHEN pretreatment. All surviving animals w
ere killed at the end of week 40 when histopathological assessment rev
ealed significant reduction of the numbers per rat of hepatocellular a
denomas and hepatocellular carcinomas by resorcinol, whereas hydroquin
one significantly enhanced the numbers per rat of renal microadenomas
and renal cell tumors. On the other hand, the number of alpha2u-globul
in positive tubules in the animals treated with hydroquinone was signi
ficantly lower than controls, without any alteration in bromodeoxyurid
ine (BrdU) incorporation. Lipid peroxidation, as evaluated by thiobarb
ituric acid reactive substance (TBARS), was at control levels in the k
idneys of rats treated with hydroquinone throughout the experiment. Th
e results showed that the known renal carcinogen hydroquinone potently
enhances the second stage of EHEN-induced renal carcinogenesis, while
its isomer resorcinol inhibited hepatocarcinogenesis. Alpha2u-Globuli
n and lipid peroxidation may not play roles in hydroquinone-associated
promotion of renal carcinogenesis.