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Embryonic prostaglandin H synthase‐2 (PHS‐2) expression and benzo[ α ]pyrene teratogenicity in PHS‐2 knockout mice 1
Author(s) -
PARMAN TOUFAN,
WELLS PETER G.
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.01-0140com
Subject(s) - benzo(a)pyrene , embryo , chemistry , fetus , pyrene , embryogenesis , andrology , knockout mouse , atp synthase , prostaglandin , prostaglandin e2 , organogenesis , medicine , microbiology and biotechnology , endocrinology , biology , pregnancy , biochemistry , enzyme , genetics , receptor , gene , organic chemistry
The developmental role of prostaglandin H synthase‐2 (PHS‐2), which converts xenobiotics such as benzo[ a ]pyrene (B[ a ]P) to toxic free radical intermediates, is poorly understood. In this study, we determined the embryonic expression and teratological relevance of PHS‐2 in pregnant CD‐1 and B6/129S7 PHS‐2 knockout mice. Wild‐type (+/+) B6/129S7 dams given B[ a ]P on gestational day (GD) 10 had three times more fetal malformations than did +/‐PHS‐2deficient dams ( P <0.05). GD 10–13 CD–1 embryos had high PHS–2 protein expression, and both + /+ and +/–GD 19 B6/129S7 fetuses had more B[ a ]P‐initiated malformations and postpartum lethality than did ‐/‐littermates ( P <0.05). Thus, embryonic PHS–2 is expressed constitutively during organogenesis and contributes substantially to B[ a ]P teratogenicity.—Parman, T., Wells, P. G. Embryonic prostaglandin H synthase‐2 (PHS‐2) expression and benzo[ a ]pyrene teratogenicity in PHS‐2 knockout mice. FASEB J. 16, 1001–1009 (2002)