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Prostaglandin and Thromboxane Synthesis by Lewis Lung Carcinoma during Growth¹

Laboratories of Environmental Pharmacology and Toxicology [C. C., M. N. C., A. N., M. V., S. G., R. F.] and Cancer Chemotherapy "In Vivo" [M. B., M. G. D.], Mario Negri Institute for Pharmacological Research, via Eritrea 62, 20157 Milan, Italy

The five stable metabolites [prostaglandin F₂, prostaglandin D₂, prostaglandin E₂ (PGE₂), thromboxane B₂, and 6-keto-prostaglandin F₁] of arachidonic acid (AA) via the cyclooxygenase pathway were measured by high-resolution gas chromatography-mass spectrometry in Lewis lung carcinoma homogenates at various times after tumor implantation (11 to 25 days). Vegetating and necrotic sections of the primary tumor and lung metastases were examined. Vegetating tumor showed a very active AA metabolism. Synthesis of PGE₂, the most abundant product, markedly increased during tumor growth (up to 30 µg/g). A high and increasing synthetic capacity was also noted for prostaglandin D₂ (up to 9 µg/g). Minor time differences and lower levels (up to 1.4 µg/g) were found for the other AA metabolites. PGE₂ and prostaglandin D₂ were the major products in necrotic tumor, too, but synthesis was markedly less than in vegetating tumor, and no increase was noted over time. Metastatic tissue showed a different AA metabolic profile, as compared to primary tumor and surrounding lung tissue, with PGE₂ and 6-keto-prostaglandin F₁ being the main metabolites.

¹ This investigation was supported by the Italian Association for Cancer Research, Milan, Italy.

² To whom requests for reprints should be addressed.

Received 12/ 4/84. Revised 4/ 4/85. Accepted 4/12/85.

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