Effects of n-3 fatty acids on growth and survival of J774 macrophages

• Published in: Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 2000-03, Vol.62 (3), p.201-207
• Main Authors: Fyfe, D.J., Abbey, M.
• Format: Article
• Language: English
• Subjects: Animals; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cell Death - drug effects; Cell Division - drug effects; Cell Line; Cell Survival - drug effects; Chromatography, Gas; Chromatography, High Pressure Liquid; Fatty Acids - analysis; Fatty Acids, Omega-3 - pharmacology; Macrophages - cytology; Macrophages - drug effects; Macrophages - metabolism; Malondialdehyde - metabolism; Medical sciences; Mice
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1054/plef.2000.0142

To further understand potential mechanisms underlying the protective effects of eicosapentanoic acid (EPA) against atherosclerosis, J774 macrophages were used to explore cellular responses to growth in the presence of PUFA in vitro. Clonogenic assays indicated that 15μ,g/ml of EPA killed over 90% of J774 populations. Docosapentaenoic acid (DPA) was more cytotoxic than either EPA or docosahexaenoic acid (DHA). EPA was shown to be elongated to DPA. Cytotoxicity induced by EPA was not inhibited by the presence of alpha-tocopherol (a-toc) in the medium. Immunological screening for caspase enzymes and microscopic examination indicated that apoptosis was not the major cause of cell death. Proliferation assays demonstrated that total cell numbers of EPA-treated cells were not significantly different to control cells. Increasing does of EPA were correlated with increasing levels of intracellular malondialdehyde (MDA). These observations suggest that EPA may influence the growth parameters of macrophages whilst inducing moderately elevated levels of oxidative stress.