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¹ Department of Biochemistry and ² Department of Pharmacology, Meharry Medical College, Nashville, TN

Requests for Reprints:Salil K. Das, Department of Biochemistry, Meharry Medical College, 1005 David Todd Boulevard, Nashville, TN 37208. Phone: (615) 327-6988; Fax: (615) 327-6442. E-mail: sdas{at}mmc.edu

Cadmium (Cd) is an ubiquitous environmental carcinogen. Membrane phospholipids as well as fatty acid profile of membrane phospholipids are known to be altered in tumorigenicity and malignancy. Synthesis of cellular phosphatidylcholine (PC) has been used as a marker for membrane proliferation in the neoplastic mammary gland tissue. Cholinephosphotransferase (CPT), the terminal enzyme in de novo synthesis of PC, has an important role in regulating the acyl group of PC in mammalian cells. Our previous studies have shown that CPT is expressed differentially in the normal and cancerous mammary epithelial cell lines. In this study, we examined the effect of cadmium on CPT activity using normal (MCF-12A and MCF-12F) and cancerous (MCF-7, BT-549, and 11-9-1-4) human mammary epithelial cell lines. There was no consistent pattern of CPT activity in response to different doses of cadmium. The activity did not show a time-dependent variation at 5 µM concentration, except in MCF-7 and 11-9-1-4. CPT gene expression increased with cadmium as evident from slot blots. Mutation in the nucleotide sequence was also observed as the result of cadmium but this did not result into amino acid sequence changes.

Key Words: Cholinephosphotransferase • Cadmium • Breast cancer • Breast cell lines • Gene expression

Grant support:Department of Defense (Grant no. DAMD 17-03-1-0352 and Grant no. DAMD 17-99-9550) to S.K. Das and NIH (2S06GM-08037) to S.K. Das and S. Mukherjee.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 8/12/03; revised 11/14/03; accepted 11/26/03.