Effect of dietary flaxseed on fatty acid composition, superoxide, nitric oxide generation and antilisterial, activity of peritoneal, macrophages from female Sprague-Dawley rats

The impact of ground flaxseed (FS) or flaxseed meal (FSM) diets on the fatty acid composition and functions of rat peritoneal exudate cells (PEG) was determined. Female weanling Sprague-Dawley rats (10/group) were fed isocaloric AIN-76 diets supplemented with 0.0, 10.0% (w/w) FS or 6.2% (w/w) FSM. A the end of 56-days, rat serum and thiogrycollate-elicited PEC were analyzed for total lipid fatty acids. Production of nitric oxide (NO) and superoxide (O-2(-)), Listeria monocytonenes (LM) phagocytic index and antilisterial activity of resident PEC were also assessed. A significant increase in a-linolenic (C18:3), eicosapentanoic (C20:5) and docosahexanoic (C22:6) acids, as well as a significant reduction in arachidonic acid (C20:4) was observed in the serum of rats fed 10% FS. Dietary FS caused a significant reduction in palmitic acid (C16:0) and an increase in stearic acid (C18:0) of PEC. Defatted FSM produced a significant increase in long chain fatty acids, which included eicosadienoic acid (C20:2) in PEC and C22:6 in serum. PEC from rats fed 10.0% FS produced significantly less (about 50%) O-2(-) in response to phorbol myristate acetate (PMA), than did PEC from control animals; dietary treatment had no effect on O-2(-) in response to LM. FSM had no impact on the O-2(-) production by PEC in response to PMA or LM. Antilisterial activity of PEC was determined by comparing bacterial uptake after 1 hr with recovery 24 hrs later. Despite comparably equivalent bacterial uptake, few viable intracellular LM were recovered at T=24 for all test samples, indicating that, regardless of the dietary treatment, PEC were able to handle the in vitro LM infection. This bacterial clearance was accompanied by equivalent NO generation by PEC from each dietary group in response to LM. Summarily, dietary FS produced significant changes in fatty acid composition of serum and PEG, inhibited O-2(-) generation by PEG, and was ineffectual to both NO production by and antilisterial activity of PEC.