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Background Hypertriglyceridemia increases risk for atherosclerotic cardiovascular disease and may contribute to atherosclerosis by changing circulating monocyte phenotypes. High-dose n-3 polyunsaturated fatty acids (PUFAs) reduce blood triglyceride levels. Effects of triglyceride-lowering therapy on monocyte phenotypes are not well known. Objective We examined effects of n-3 PUFA treatments (eicosapentaenoic acid [EPA] plus docosapentaenoic acid [DPA] [MAT9001] versus EPA ethyl esters [EPA-EE]) on monocyte phenotypes in individuals with hypertriglyceridemia. Methods Individuals with triglycerides 200–400 mg/dL were recruited. Subjects received two treatments in randomized order for 14 days each: MAT9001 and EPA-EE, at 4 g/day. At 2 days before the start of, and on the last day of, each treatment, nile red staining for lipids and phenotypes of each monocyte subset were examined by flow cytometry after an overnight fast and postprandially after a high-fat meal. Results Treatment with MAT9001 or EPA-EE reduced fasting triglyceride levels and decreased proportions of intermediate monocytes. Only MAT9001 decreased postprandial blood triglyceride levels, lowered fasting nile red levels, indicating less lipid in classical and intermediate monocytes, and reduced postprandial CD11c levels on nonclassical monocytes. MAT9001 and EPA-EE each reduced fasting and postprandial CD11c and CD36 levels on classical and intermediate monocytes and postprandial CCR5 levels on intermediate and nonclassical monocytes, with no significant differences between the two treatments. Conclusions Treatment with MAT9001 in individuals with hypertriglyceridemia reduced fasting nile red staining for lipids in classical and intermediate monocytes. MAT9001 and EPA-EE each improved fasting and postprandial monocyte phenotypes, which could potentially help to protect against atherosclerosis.

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Azomethane (AM) gas was identified as a major metabolite of 1,2-dimethylhydrazine (1,2-DMH) in the expired air of F344 rats. The compound was characterized by high-pressure liquid chromatography, gas chromatography, and mass spectrometry, in comparison to a synthetic standard. At a dose of 21 mg 1,2-DMH/kg sc, approximately 14 and 11% of the dose were exhaled as AM and CO2, respectively, in 24 hours. At 200 mg 1,2-DMH/kg, 23 and 4% of the dose appeared as AM and CO2, respectively, in the respired air within the same period. Most AM was seen in the first 6 hours, but the CO2 evolution was more progressive, especially after the higher dose of 1,2-DMH.

1. The effects of disulfiram on the metabolism of 1,2-dimethylhydrazine were studied in CDF rats. 2. Treatment with disulfiram causes enhanced elimination of azomethane in the expired air, inhibition of CO2 production, and decreased levels of 1,2-dimethylhydrazine metabolites in the urine. 3. These results suggest that disulfiram inhibits the N-oxidation of azomethane to azoxymethane, thus preventing further metabolism to the ultimate carcinogenic species, and provide an explanation for the observations that disulfiram inhibits 1,2-dimethylhydrazine-induced neoplasia of the large intestine.