機車廢氣對大鼠系統毒性之影響

Abstract

在盛行以機車為交通運輸工具的地區，機車排放廢氣乃空氣污染的主要來源。機車廢氣組成當中包含許多致毒物質與致癌物質，能對囓齒類動物或哺乳類細胞造成氧化壓力、DNA 損傷、發炎反應、酵素誘導以及其他毒性反應。本研究主要目的為探討以呼吸曝露或經雄性或雌性親代曝露方式，曝露十倍稀釋的機車廢氣，對雄性與雌性大鼠造成心臟、生殖發育與神經行為毒性之可能性。親代雄性或雌性大鼠在經每天兩小時，每週五天，為期八週的機車廢氣呼吸曝露後，分別與未經處理的雌性或雄性大鼠交配。結果顯示，呼吸曝露機車廢氣引發雄性大鼠的心臟毒性，且該毒性機轉與心房排鈉素 (atrial natriuretic peptide)、纖維母細胞生成因子第二亞型 (fibroblast growth factor-2 ) 與白間素1β 亞型 (interleukin-1β) 之 mRNA 表現量上升有正相關性。經雄性或雌性親代曝露機車廢氣，雄性子代陰莖包皮分離與雌性子代陰道開口天數無提早或延遲現象。呼吸曝露機車廢氣後，僅有雌性而非雄性大鼠，會在明暗穿箱測詴中發現焦慮行為，在閃尾測詴中展現疼痛耐受度增加表現，以及在血清中有乙醯膽鹼酶活性降低現象；但於強迫游泳測詴中卻發現，無論是呼吸曝露或經雌性親代曝露機車廢氣，雄性大鼠與雌性大鼠皆產生憂鬱行為。曝露機車廢氣雌性大鼠在大腦皮質和小腦的5羥色胺（2A）受體之 mRNA 表現量並有下降趨勢。結果指出，機車廢氣會造成大鼠心臟及神經行為毒性，但未出現下一代以陰莖包皮分離與陰道開口年齡為指標的生殖發育毒性。機車廢氣對大鼠系統毒性作用機轉仍有待進一步研究。

The emission of motorcycle exhaust (ME) are a major source of air pollution in areas where motorcycles are a popular means of transportation. ME contains many toxicants and carcinogens which can cause oxidative stress, DNA damage, inflammation, enzyme induction, and other toxicological responses in rodents or mammalian cell lines. The major objectives of the present study were to explore the possible effects on cardiac, reproductive development, and neurobehavior toxicities of male and female rats exposed to 1:10 diluted ME by inhalation 2 hours daily and five days a week for 8 weeks. ME-exposed female or male rats were then mated with untreated males or females, respectively. ME exposure of male rats caused cardiotoxicity which was associated with increased mRNA expression of atrial natriuretic peptide, fibroblast growth factor-2, and interleukin-1β. Paternal and maternal exposures had no effects on the dates of preputial separation of male offspring and vaginal opening of female offspring. ME exposure induced changes in anxiety-like behavior in light-dark transition test and analgesia-like behavior in tail-flick test and reduced serum acetylcholinesterase activity of female rats but not of males. ME and maternal ME exposures changed depression-like behavior in forced-swimming test in males and females. ME exposure decreased 5-hydroxytryptamine 2A receptor mRNA expression in female rat brain cortex and cerebellum. These present findings demonstrate that ME causes cardiotoxicity and neurobehavior toxicity. The mechanisms underlying these ME systemic effects require further investigations.