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Metabolism of Ether-linked Glycerolipids in Cultures of Normal and Neoplastic Rat Respiratory Tract Epithelium¹

Medical and Health Sciences Division, Oak Ridge Associated Universities [C. C. S., F. S.], and Biology Division, Oak Ridge National Laboratory [C. C. S., C. A. H., P. N.], Oak Ridge, Tennessee 37830

To study the mechanism of ether lipid accumulation which is characteristic of many tumors, we have compared the metabolism of lipids in primary rat tracheal epithelial cells and in a cell line derived from a benzo(a)pyrene-induced tumor. Growth of the primary epithelial cells in vitro resulted in the accumulation of alkyldiacylglycerols at levels (10% of total lipid) comparable to those found in the tumor cell line (B2-1). This class of ether lipids could not be detected in normal rat tracheal epithelium in vivo. A double isotope labeling method using [³H]- and [¹⁴C]palmitic acid was used to study metabolic stability of lipid classes in the cell cultures. Primary cells and B2-1 cells labeled with palmitic acid showed the greatest loss of label from triacylglycerols and free fatty acids during incubation in unlabeled media. A slight loss of label from the ester linkages of the alkyldiacylglycerols was observed in the primary epithelial cells but not the B2-1 cells. No label was lost from the ether linkages of the alkyldiacylglycerols of either the B2-1 or primary cells. With the exception of diradylglycerophosphocholine, phospholipids of primary and B2-1 cells labeled with palmitic acid accumulated label during incubation in unlabeled media. Similar results were observed with the B2-1 cells using labeled glycerol as the lipid precursor. The results demonstrate that alkyldiacylglycerols can be induced in nontumorigenic cells by growth in culture and can thus provide a useful model for studying the regulation of ether lipid metabolism.

¹ The work performed at Oak Ridge Associated Universities was supported by United States Department of Energy Contract EY-76-C-05-0033, American Cancer Society Grant BC-701, and National Cancer Institute Grant CA-11949-09. The work performed at Oak Ridge National Laboratory (operated by Union Carbide Corporation) was supported by United States Department of Energy Contract WR-7405-eng-26 and National Cancer Institute Training Grant in Carcinogenesis Research [C.C.S.], Grant CA-05296.

² To whom requests for reprints should be addressed.

Received 1/ 9/78. Accepted 10/13/78.