n-6及n-3多元不飽和脂肪酸(尤其是DHA(docosahexaenoic acid, C22:6 n-3)及ARA(arachidonic acid, C20:4 n-6))對出生前後胎兒的發展很重要。因為脂肪酸與戴奧辛有相似的化學特性及食物來源,所以可能這些n-6及n-3 長鏈多元不飽和脂肪酸運送至胎兒時也可能被胎兒暴露於親脂性有機氯所影響。本研究分析來自台中34位懷孕婦女胎盤中n-3 及 n-6多元不飽和脂肪酸(wt%)與胎盤中戴奧辛及多氯聯苯(TEQ)濃度的相關性。本研究發現,胎盤的單元不飽和脂肪酸(C16:1 n-7、C18:1 n-9及C20:1 n-9)與胎盤的PCDFs的低、中、高三組濃度呈線性正相關 (p trend < 0.05)。相反地,胎盤中PCDFs由低到高濃度的增加會使胎盤的n-6多元不飽和脂肪酸有減少的傾向,而這些n-6多元不飽和脂肪酸包含C20:3 n-6 (p trend=0.011)、C20:4 n-6 (p trend=0.020)、C22:4 n-6 (p trend=0.036)及C22:5 n-6 (p trend=0.003)。然而類似的結果也發現在PCDDs方面,但只有C20:3 n-6 (p trend=0.054)及C22:5 n-6 (p trend=0.067)與PCDDs有相關,而C20:4 n-6與PCDDs只有邊緣性相關(p=0.123)。針對n-3長鏈多元不飽和脂肪酸,我們發現當胎盤PCDFs增加時,胎盤DHA會顯著的降低(p trend=0.025)。而胎盤的單元不飽和脂肪酸(C16:1 n-7及C18:1 n-9)與胎盤的PCBs的低、中、高三組濃度呈線性正相關 (p trend < 0.05),胎盤中類戴奧辛的多氯聯苯由低到高濃度的增加會使胎盤的多元不飽和脂肪酸有增加的傾向,而這些多元不飽和脂肪酸包含C18:2 n-6 (p trend=0.035)、C18:3 n-3 (p trend=0.020)。使用多變量線性迴歸分析校正一些可能的干擾因子(包含年齡、教育程度、家庭年收入及身體質量指數)後,PCDFs與胎盤中DHA (beta=-0.403, p=0.196)及戴奧辛與ARA (beta=-2.114, p=0.057)呈邊緣性負相關。故孕婦體內戴奧辛及多氯聯苯的暴露增加,可能與胎盤中某些n-3及n-6長鏈多元不飽和脂肪酸(包含DHA及ARA)的減少有趨勢相關。在未來之研究將需要進一步探討戴奧辛的暴露可能會干擾胎盤中DHA及ARA的運輸機轉。
N-6 and n-3 polyunsaturated fatty acids (PUFA), especially DHA (docosahexaenoic acid, C22:6 n-3) and ARA (arachidonic acid, C20:4 n-6) are important in perinatal development. Because of the similar chemical properties and origins of food sources, it is possible that critical delivery of these n-6 and n-3 LCPUFA to the fetus may also serve to increase the fetal exposures to lipophilic organo-chlorines. This study was aimed to examine relationships between placental n-3 and n-6 PUFA and placental PCDD/Fs and PCBs toxic equivalent (TEQ) levels in 34 pregnant women from central Taiwan. Linear and positive associations were observed between monounsaturates (C16:1 n-7, C18:1 n-9, C20:1 n-9) and low, mid and high TEQ levels of PCDFs (p trend < 0.05). On the other hand, trends of decreases in n-6 PUFA including C20:3 n-6 (p trend=0.011), C20:4 n-6 (p trend=0.020), C22:4 n-6 (p trend=0.036) and C22:5 n-6 (p trend=0.003) were observed as PCDF increased from low to high TEQ levels. Similarly, trends of decreases in these n-6 PUFA were also found against increased PCDDs levels; however, only C20:3 n-6 (p trend=0.054) and C22:5 n-6 (p trend=0.067) were correlated and C20:4 n-6 were marginally correlated with PCDDs levels. For n-3 PUFA, only DHA was significantly decreased as PCDFs levels increased (p trend=0.025). Linear and positive associations were observed between monounsaturates (C16:1 n-7, C18:1 n-9) and low, mid and high TEQ levels of total PCBs (p trend < 0.05). Trends of increases in PUFA including C18:2 n-6 (p trend=0.035), C18:3 n-3 (p trend=0.020) were observed as dioxin-like PCBs increased from low to high TEQ levels. After adjusting for potential confounders (age, education, income, BMI) only PCDFs was marginally and negatively correlated with placental DHA (beta=-0.403, p=0.196) and total dioxin (PCDD/Fs and dioxin-like PCBs) was marginally and negatively correlated with placental ARA (beta=-2.114, p=0.057). Increases in dioxin exposures appeared to correlate with trends of decreases in some n-3 and n-6 PUFA including DHA and ARA. Mechanisms regarding placental DHA and ARA transfer which may be interfered by dioxin exposure warrant further investigations.