Intake of n-3 Polyunsaturated Fatty Acids Increases Omega-3 Index in Aged Male and Female Spontaneously Hypertensive Rats

The purpose of this study was to examine whether n-3 PUFA intake affects n-3 and n-6 FA levels in plasma and red blood cells as well as omega-3 index in old male and female spontaneously hypertensive (SHR) and healthy rats. Plasma linoleic acid and eicosapentaenoic acid increased due to n-3 PUFA intake in SHR and healthy rats. Comparing to healthy rats the levels of PUFA in red blood cells of SHR were lower in males and higher in females with exception of arachidonic acid, which was high in males and low in females. Feeding of rats with n-3 PUFA resulted in increase of red blood cells levels of eicosapentaenoic acid and/or docosahexaenoic acid in a sex- and strain-dependent manner. Moreover, n-3 PUFA intake decreased arachidonic acid in healthy female rats but increased it in SHR and did not affect it in males. Omega-3 index was lower in SHR comparing to healthy rats and it increased due to the consumption of n-3 PUFA. Results point out sex- and strain-related differences in red blood cells levels of n-3 and n-6 PUFA in basal conditions as well as in response to n-3 PUFA intake. 1. Background Polyunsaturated n-3 fatty acids (n-3 PUFA) are important components of cell membranes affecting their function, as they are incorporated into the phospholipids. Dietary deprivation of the essential fatty acids is deleterious to health. Mammals do not produce Δ12 and Δ15 desaturase enzymes and therefore cannot produce either linoleic acid (LA; 18:2n-6) or α-linolenic acid (ALA; 18:3n-3), precursors of the n-6 and n-3 fatty acids de novo [1]. ALA is metabolized to produce long-chain n-3 (omega) PUFA, the most prevalent of which are eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3). LA is metabolized to produce longchain n-6 PUFA, such as arachidonic acid (AA; 20:4n-6) and gamma-linolenic acid (GLA; 18:3n-6). EPA is further metabolized by the cyclooxygenase and lipoxygenase pathways to produce the n-3 series of eicosanoids (prostaglandins, thromboxanes, and leukotrienes) that are potent, short-acting, local hormones, or second messengers exhibiting anti-inflammatory properties, while the n-2 series of eicosanoids derived from AA are rather proinflammatory [1]. A reduced ratio AA/EPA shifts the spectrum of ecosanoids production toward an increase in thromboxane A3 and PGI3 at the expense of TXA2 and PGI2. This shift was found to reduce the risk of fatal arrhythmias [2]. Data from clinical [3, 4] and experimental studies [5, 6] support the hypothesis that consumption of n-3 PUFA lowers the risk of cardiovascular diseases and sudden cardiac