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Thromboxane (TX)A 3 and prostaglandin (PG)I 3 are formed in man after dietary eicosapentaenoic acid: Identification and quantification by capillary gas chromatography–electron impact mass spectrometry
Author(s) -
Fischer Sven,
Weber Peter C.
Publication year - 1985
Publication title -
biomedical mass spectrometry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.475
H-Index - 121
eISSN - 1096-9888
pISSN - 0306-042X
DOI - 10.1002/bms.1200120905
Subject(s) - eicosapentaenoic acid , chromatography , capillary gas chromatography , chemistry , mass spectrometry , gas chromatography–mass spectrometry , thromboxane b2 , gas chromatography , electron ionization , prostaglandin , thromboxane , medicine , fatty acid , biochemistry , polyunsaturated fatty acid , organic chemistry , platelet , ion , ionization
The low incidence of myocardial infarction in Greenland Eskimos has been related to their traditional marine diet rich in eicosapentaenoic acid. However, whether dietary eicosapentaenoic acid is indeed transformed in man to antiaggregatory PGI 3 and weakly proaggregatory TXA 3 has not been clarified. In our studies we ingested either cod liver oil or mackerel both rich in eicosapentaenoic acid. Formation of TXB 3 , the hydrolysis product of TXA 3 , in platelet‐rich plasma stimulated ex vivo with collagen was traced by capillary GC/EIMS. Via external standard, TXB 3 formation in platelets was estimated to be 5–15% of TXB 2 formation. From urine we extracted dinor metabolites of PGI according to a selective method. We utilized Δ17‐2,3‐dinor‐6‐keto‐PGF 1α (PGI 3 ‐M) as an index of total body production of PGI 3 in analogy to 2,3‐dinor‐6‐keto‐PGF 1α (PGI 2 ‐M), the major urinary metabolite of PGI 2 . We separated PGI 2 ‐M and PGI 3 ‐M as the Me, MO, Me 3 Si derivatives by capillary gas chromatography and identified PGI 3 ‐M by EI mass spectrometry. Excretion of PGI 3 ‐M, which was not detectable under control conditions, was 83±25 ng/24 h (SD) after ingestion of cod liver oil and 134±38 ng/24 h, respectively. Our findings with diets rich in EPA show that it is possible in man to change in vivo the spectrum of biologically active prostanoids by nutritional means and alter it in a favourable direction.