Abstract:
:Monocrotaline is a representative naturally occurring genotoxic pyrrolizidine alkaloid. Metabolism of monocrotaline by liver microsomes of F344 female rats generated (+/-)6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP) and monocrotaline-N-oxide as major metabolites. Metabolism in the presence of triacetyleandomycin, a P450 3A enzyme inhibitor, reduced the formation of DHP by 52% and monocrotaline N-oxide formation by 59%. Dexamethasone significantly induced microsomal monocrotaline metabolizing enzyme activities in rat liver and lung. Previously, we have identified a set of DHP-derived DNA adducts from DHP-modified calf thymus DNA by (32)P-post labeling/HPLC analysis. Metabolism of monocrotaline in the presence of calf thymus DNA resulted in a similar set of DHP-DNA adducts. These DHP-DNA adducts were also found in the liver DNA of rats treated with monocrotaline. The time course of the DHP-derived DNA adduct formation and removal in the liver of rats gavaged with a single dose (10mg/kg) of monocrotaline was similar to that of rats treated with riddelliine. The levels of DHP-DNA adducts in liver DNA of rats treated with monocrotaline were much lower than that of riddelliine-treated rats. Results from this study indicate that (i) DHP is a common reactive metabolite for retronecine-type of pyrrolizidine alkaloids, (ii) the formation of DHP-derived DNA adducts in the liver DNA of rats treated with monocrotaline suggests that monocrotaline-induced tumorigenicity is through a genotoxic mechanism.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Wang YP,Yan J,Beger RD,Fu PP,Chou MWdoi
10.1016/j.canlet.2004.11.039keywords:
subject
Has Abstractpub_date
2005-08-08 00:00:00pages
27-35issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(04)00933-4journal_volume
226pub_type
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