TY - JOUR
T1 - Phenethyl isothiocyanate(PEIT) inhibits nitrosamine-mediated carcinogenesis in hamster buccal pouch epithelium(HBPE)
AU - Batrouni, Z.
AU - Chang, K. W.
AU - Solt, D.
PY - 1996/1/1
Y1 - 1996/1/1
N2 - The purpose of this study was to determine whether PEIT, a vegetable-derived cancer chemopreventive agent inhibits HBPE carcinogenesis mediated by N-methyl-N-benzylnitrosamine(M-BN). PEIT(50mM) in corn oil(CO) was topically applied to both buccal pouches of three hamsters(group 1), thrice-weekly for 2 weeks followed by twice-weekly(Monday/Thursday) topical treatments of a mixture of MBN and PEIT(both at 50mM) for 22 weeks. During the 22 weeks of MBN treatment, the group 1 hamsters also received PEIT(50mM) in CO, on Tuesdays and Fridays. Three group 2 hamsters were similarly treated with the vehicle CO, and MBN in CO, during the 24 week experiment. At the completion of the experiment, whereas the group 2(unprotected) hamsters exhibited a total of 60 epithelial neoplasms(23 ± 10 tumors/hamster), including squamous cell carcinomas, a total of only 4 epithelial neoplasms were observed in the group 1(PEIT protected) hamsters pouches. In a follow-up experiment, PEIT(25mM) in CO also strongly inhibited MBN-mediated induction of microscopic epithelial cell foci exhibiting either gamma-glutamyl transpeptidase(GGT) histochemical activity or immunohistochemical staining for the p53 tumor suppressor gene product. These presumptive precancerous foci were identified in HBPE whole mounts prepared after 8 to 13 weeks of topical MBN(25mM) treatment. We conclude that PEIT is a potent inhibitor of MBN-mediated HBPE carcinogenesis, and that early GGT and p53 foci are predictive of chemoprevention in this experimental model of oral carcinogenesis.
AB - The purpose of this study was to determine whether PEIT, a vegetable-derived cancer chemopreventive agent inhibits HBPE carcinogenesis mediated by N-methyl-N-benzylnitrosamine(M-BN). PEIT(50mM) in corn oil(CO) was topically applied to both buccal pouches of three hamsters(group 1), thrice-weekly for 2 weeks followed by twice-weekly(Monday/Thursday) topical treatments of a mixture of MBN and PEIT(both at 50mM) for 22 weeks. During the 22 weeks of MBN treatment, the group 1 hamsters also received PEIT(50mM) in CO, on Tuesdays and Fridays. Three group 2 hamsters were similarly treated with the vehicle CO, and MBN in CO, during the 24 week experiment. At the completion of the experiment, whereas the group 2(unprotected) hamsters exhibited a total of 60 epithelial neoplasms(23 ± 10 tumors/hamster), including squamous cell carcinomas, a total of only 4 epithelial neoplasms were observed in the group 1(PEIT protected) hamsters pouches. In a follow-up experiment, PEIT(25mM) in CO also strongly inhibited MBN-mediated induction of microscopic epithelial cell foci exhibiting either gamma-glutamyl transpeptidase(GGT) histochemical activity or immunohistochemical staining for the p53 tumor suppressor gene product. These presumptive precancerous foci were identified in HBPE whole mounts prepared after 8 to 13 weeks of topical MBN(25mM) treatment. We conclude that PEIT is a potent inhibitor of MBN-mediated HBPE carcinogenesis, and that early GGT and p53 foci are predictive of chemoprevention in this experimental model of oral carcinogenesis.
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U2 - 10.1016/S1079-2104(96)80250-2
DO - 10.1016/S1079-2104(96)80250-2
M3 - Article
AN - SCOPUS:33749108953
SN - 2212-4403
VL - 82
JO - Oral Surgery Oral Medicine and Oral Pathology
JF - Oral Surgery Oral Medicine and Oral Pathology
IS - 2
ER -
