[CANCER RESEARCH 58. 647-653, February 15, 1998]
a-Hydroxytamoxifen Is a Substrate of Hydroxysteroid (Alcohol) Sulfotransferase,
Resulting in Tamoxifen DNA Adducts1
Shinya Shibutani,2 Lakkaraju Dasaradhi, Isamu Terashima, Erden Banoglu, and Michael W. Duffel
Department of Pharmacological Sciences, State University of New York al Stony Brook, Stony Brook, New York 11794-8651 [S. S.. L. D., 1. T.], and Division of Medicinal and
Natural Products Chemistry, College of Pharmacy, The University of Iowa. Iowa City, Iowa 52242 [E. B., M. W. D.¡
ABSTRACT
When a-hydroxytamoxifen («-OHI AM) was incubated with rat liver
hydroxysteroid (alcohol) sulfotransferase a (STa) and 3'-phosphoad-
enosine 5'-phosphosulfate, (E)-a-OHTAM was found to be a better sub
strate for STa than (Z)-a-OHTAM. To explore the formation of tamoxifen
(TAM)-derived DNA adducts, DNA was incubated with STa and either
(E)-a-OHTAM or (Z)-a-OHTAM in the presence of 3'-phosphoadenosine
S'-phosphosulfate. Using 32P-postlabeling analysis, the amount of TAM-
DNA adducts resulting from (E)-a-OHTAM was 29 times higher than that
observed with (f)-a-OHTAM alone. Using (Z)-a-OHTAM and STa, some
TAM-DNA adducts were also detected but at levels 6.5 times lower than
that observed with (E)-a-OHTAM and STa. When compared with stand
ards of stereoisomers of 2'-deoxyguanosine S'-monophosphate-A^-tamox-
ifen, the major tamoxifen adduct was identified chromatographically as
an epimer of the trans form of a-(JV2-deoxyguanosinyl)tamoxifen, and the
minor adduct was identified as an epimer of the civ form. In the reaction
mixture, a conversion from (E)-a-OHTAM to (Z)-a-OHTAM through the
carbocation intermediate was also detected. These results show that sul-
fation of a-OHTAM catalyzed by STa results in the formation of TAM-
DNA adducts.
INTRODUCTION
TAM3 (structure in Fig. 1) is widely used in the treatment of breast
cancer (1) and is being considered as a prophylactic agent for healthy
women with a positive family history of breast cancer (2, 3). How
ever, this drug has been reported to be a potent hepatocarcinogen in
rats (4-6). A high frequency of mutations were found in the DNA
from livers of lambda//ac/ transgenic rats treated with TAM (7) and in
the rat p53 gene in hepatocarcinomas induced by TAM (8). An
increased incidence of endometrial cancer has been observed in breast
cancer patients treated with TAM (9-11). In 1996, TAM was listed as
a human carcinogen by the IARC (12).
TAM is activated in liver microsomes of rats and humans (13-15)
and gives rise to DNA adducts in the livers of rodents (16, 17). A
TAM-derived DNA adduct has been detected in the endometrial
tissues obtained from breast cancer patients treated with TAM (18).
Oxidative species such as 4-hydroxytamoxifen quinone methide have
been reported to promote the reaction with DNA (19). Alternatively,
a-hydroxylation of TAM and its metabolites, tamoxifen Af-oxide,
Af-desmethyltamoxifen, and 4-hydroxytamoxifen, respectively, are
Received 9/17/97; accepted 12/18/97.
The costs of publication of this article were defrayed in part by the payment of page
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18 U.S.C. Section 1734 solely to indicate this fact.
1 This research was supported in part by the Lilly W. Ammann Breast Cancer Research
Award, the School of Medicine, SUNY at Stony Brook (to S. S.), Grant ES04068 (to S.S.
and A. P. Grollman) from NIEHS, and Grants CA17395 (to A. P. G.) and CA38683 (to
M. W. D.) from NIH. I. T. was supported by a postdoctoral fellowship from the Uehara
Memorial Foundation, Japan.
2 To whom requests for reprints should be addressed, at Department of Pharmacolog
ical Sciences, State University of New York at Stony Brook, Stony Brook, New York
11794-8651. Phone: (516)444-8018; Fax: (516)444-3218.
3 The abbreviations used are: TAM, tamoxifen; dG, 2'-deoxyguanosine; dG3'P, 2'-
deoxyguanosine 3'-monophosphate; STa, hydroxysteroid (alcohol) sulfotransferase a; (£)-
and (Z)-a-OHTAM, trans and cii forms of a-hydroxytamoxifen, respectively; dG-N2-
TAM, a-(/V2-deoxyguanosinyl)tamoxifen; PEI, poly(ethyleneimine); PAP, adenosine
3',5'-diphosphate; PAPS, 3'-phosphoadenosine 5'-phosphosulfate; HPLC, high-perfor
mance liquid chromatography; hHST, human hydroxysteroid sulfotransferase.
likely candidates, capable of forming DNA adducts with nucleosides
(20-23). However, a-OHTAM has only a low level of reactivity with
DNA in vitro (21). Because the formation of TAM-DNA adducts was
inhibited by sulfotransferase inhibitors (24), the a-hydroxyl moiety of
TAM was expected to be O-sulfonated prior to reaction with DNA
(24, 25). Recently, one of us found that a-sulfate TAMs are highly
reactive with DNA, forming four diastereoisomers of dG-N2-TAM
(26). Similar results were observed for a model activated form,
a-acetoxytamoxifen (25, 26). We also found that these dG-N2-TAM
adducts display a high miscoding potential, predicting G —>T and
G —>C transversions and deletions in mammalian cells (27).
Hydroxysteroid sulfotransferases have been purified to homogene
ity (28), and the substrate specificities of these enzymes led to their
designation as both hydroxysteroid and alcohol sulfotransferases.
Many hydroxymethyl polycyclic aromatic hydrocarbons are activated
to carcinogenic and/or mutagenic sulfuric acid esters through reac
tions catalyzed by these enzymes (29, 30). Because STa catalyzes the
sulfation of xenobiotic alcohols, including benzylic alcohols (31),
a-OHTAM is likely a substrate for this enzyme. In this study, we
report that dG-N2-TAM adducts are formed through the sulfation of
a-OHTAM catalyzed by STa.
MATERIALS AND METHODS
Chemicals. [•y-32P]ATP (specific activity, 6000 Ci/mmol) was obtained
from Amersham Corp. (Arlington Heights. IL). PEI-cellulose plates were
purchased from Machery-Nagel (Duren, Germany). Calf thymus DNA, pro-
teinase K, potato apyrase, alkaline phosphatase (type III), dGVP, PAP, and
PAPS were purchased from Sigma Chemical Co. (St. Louis, MO). RNase A,
RNase Tl, micrococcal nuclease, and spleen phosphodiesterase were obtained
from Worthington Biochemical Co. (Freehold, NJ). T4 polynucleotide kinase
was purchased from Stratagene (La Jolla, CA). HPLC analysis was performed
on a Waters 990 HPLC instrument, equipped with a photodiode array detector.
Purification of STa. STa was purified to apparent homogeneity from
female Sprague Dawley rats (9-10 weeks of age), using a modification (31) of
a procedure published previously (32, 33). The resulting STa was homogene
ous by SDS-PAGE gel electrophoresis with Coomassie Blue staining. Protein
concentrations were determined using a modified Lowry procedure (34), with
BSA as a standard. Hydroxysteroid sulfotransferase activity was determined in
assay mixtures containing 0.25 M potassium phosphate (pH 7.0), 8.3 mM
mercaptoethanol, 200 /J.MPAPS, and 40 /¿M dehydroepiandrosterone. Enzyme
units are expressed as nanomoles of sulfuric acid ester product formed per
minute. The specific activity of the STa was 99.2 units/mg protein.
Kinetic Studies of STa with a-OHTAM. (E)-a-OHTAM or (Z)-a-OH-
TAM was synthesized by the established protocol (35). PAPS was prepared
according to a published procedure (36). Both (£)-a-OHTAM and (Z)-a-
OHTAM were evaluated as substrates of purified STa using a published HPLC
procedure for determination of the concentration of PAP formed in the reaction
(37). Reaction mixtures (30 jil total volume) contained 0.25 M potassium
phosphate buffer (pH 7.0), 8.3 mM 2-mercaptoethanol, 0.3 mM PAPS, and
various concentrations of the alcohols in acetonitrile (final concentration of
acetonitrile in the assay was no more than 5% v/v). Reactions were initiated by
the addition of 2.4 fig of STa, incubated at 37°Cfor 15 min, and terminated by
the addition of 30 ¿ilof methanol. The substrate-dependent concentration of
PAP formed in the reaction was determined by HPLC (37), and linear standard
curves directly relating the area of HPLC peaks to the concentrations of PAP
were determined daily. Apparent Km and Vmax values for a-OHTAM as a
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