Modulation of dihydroxy-di-n-propylnitrosamine-induced liver lesion development in Opisthorchis-infected syrian hamsters by praziquantel treatment inassociation with butylated hydroxyanisole or dehydroepiandrosterone administration

Citation
Ma. Moore et al., Modulation of dihydroxy-di-n-propylnitrosamine-induced liver lesion development in Opisthorchis-infected syrian hamsters by praziquantel treatment inassociation with butylated hydroxyanisole or dehydroepiandrosterone administration, JPN J CANC, 89(11), 1998, pp. 1113-1117
Citations number
30
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
JAPANESE JOURNAL OF CANCER RESEARCH
ISSN journal
09105050 → ACNP
Volume
89
Issue
11
Year of publication
1998
Pages
1113 - 1117
Database
ISI
SICI code
0910-5050(199811)89:11<1113:MODLLD>2.0.ZU;2-X
Abstract
The effects of praziquantel coupled with dehydroepiandrosterone (DHEA) or b utylated hydroxyanisole (BHA) administration 16 weeks subsequent to dihydro xy-di-n-propylnitrosamine (DHPN) treatment and infection with Opisthorchis viverrini (OV) on lesion development in the liver of Syrian hamsters were i nvestigated. Animals were given 80 OV metacercariae and then two i.p. injec tions of DHPN (500 mg/kg body weight) 4 and 5 weeks thereafter, At week 16, groups received praziquantel (250 mg/kg, i.g.) and were placed on normal d iet or diet supplemented with BHA (1%) or DHEA (0.6%) until they were kille d at week 24, Histopathological assessment revealed that, whereas antihelmi nthic treatment alone resulted in a clear reduction in hepatocellular lesio n development, effects on cholangiocellular lesions were equivocal, BHA and DHEA, in contrast, were both associated with a significant reduction in fr equency of cholangiofibrosis and cholangiocellular carcinoma, The former ch emical, however, increased the numbers of liver nodules while the hormone b rought about a decrease as well as a shift in the phenotype of the lesions, The results thus indicate that although cholangiocellular lesion developme nt may, unlike generation of hepatocellular nodules, be to a certain extent independent of the continued presence of parasite, it can be influenced by exogenous treatments.