The modifying potential of capsaicin (CAP) on lesion development was examined in a rat multiorgan
carcinogenesis model. Groups 1 and 2 were treated sequentially with diethylnitrosamine (DEN) (100
mg/kg, ip, single dose at commencement), N-methylnitrosourea (MNU) (20 mg/kg, ip, 4 doses at days
2, 5, 8, and 11), and N,N-dibutylnitrosamine (DBN) (0.05% in drinking water during weeks 3 and 4).
Group 3 received vehicles without carcinogens during the initiation period. Group 4 served as the
untreated control. After this initiating procedure, Groups 2 and 3 were administered a diet containing
0.01% CAP. All surviving animals were killed 20 weeks after the beginning of the experiment and the
target organs examined histopathologically. The induction of GST-P+ hepatic foci in rats treated
with carcinogens was significantly inhibited by treatment with CAP. CAP treatment significantly
decreased the incidence of adenoma of the lung but increased the incidence of papillary or nodular
(PN) hyperplasia of the urinary bladder. The tumor incidence of other organs, such as the kidney
and thyroid, was not significantly different from the corresponding controls. These results
demonstrated that concurrent treatment with CAP not only can inhibit carcinogenesis but can
also enhance it depending on the organ. Thus, this wide-spectrum initiation model could be used
to confirm organ-specific modification potential and, in addition, demonstrate different modifying
effects of CAP on liver, lung, and bladder carcinogenesis.
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