摘要:
邻苯二甲酸二乙基己酯(DEHP) 是一种持久性的有机污染物(POPs),具有潜在毒性、致癌性。选取马氏珠母贝(Pinctada martensi) 为研究对象,研究 DEHP 对其血淋巴细胞免疫功能和脂质过氧化水平的影响。将成年马氏珠母贝暴露于不同浓度(0.5、2.0、8.0、16.0 mg·L-1) 的 DEHP 中,暴露 14 d 后测定血细胞数目(THC)、吞噬能力(phagocytic activity)、细胞膜稳定性(cell membrane stability)、脂质过氧化程度(LPO) 和总谷胱甘肽含量(T-GSH) 的变化。结果显示,血细胞数目随 DEHP 浓度的升高而降低,呈明显的剂量-效应关系,最低可见效应浓度(LOEC) < 0.5 mg·L-1。细胞膜稳定性和吞噬活力均随 DEHP 浓度的升高,呈现先升高后降低的变化趋势,其 LOEC 值分别小于 2 和 8 mg·L-1。细胞中丙二醛(MDA) 含量随染毒浓度增加逐渐升高,在 8 mg·L-1 浓度组达到最高值,之后降低,与之相应的脂质过氧化水平也呈现先升高后降低的变化趋势,LOEC < 2 mg·L-1。8mg·L-1 浓度组的总谷胱甘肽含量与对照组相比存在显著差异性(P < 0.05),LOEC < 8 mg·L-1。研究结果表明:DEHP 染毒 14 d对马氏珠母贝血淋巴细胞免疫功能有明显的影响,同时还会诱导机体产生氧化应激效应,在所测试的指标中,血细胞计数对DEHP 的胁迫最敏感(LOEC < 0.5 mg·L-1),细胞膜稳定性和脂质过氧化水平的敏感性次之(LOEC < 2 mg·L-1)。
Abstract:
Diethylhexyl phthalate (DEHP) is one of persistent organic pollutants (POPs), and poses a significant risk for carcinogenicity, teratogenicity and mutagenicity. In this study, changes of total haemocyte counts (THC), cell membrane stability, phagocytic activity and oxidative stress parameters, including lipid peroxidation (LPO) and total glutathione (TGSH), of haemocytes of Pinctada martensi were measured in the haemolymph after exposure to different concentrations of DEHP (0.5, 2, 8 mg·L-1) for 14 days. The results showed that THC decreased while DEHP concentrations increased, showing an apparent negative dose-response curve. The lowest-observed-effect concentration (LOEC) for THC decrease was lower than 0.5 mg·L-1. Besides, cell membrane stability, phagocytic activity and lipid peroxidation level were reduced after a short-time rise with increasing DEHP concentration, showing an inverted U-shaped curve with LOEC value <2 mg·L-1, <8 mg·L-1 and <2 mg·L-1, respectively. The T-GSH content in 8 mg·L-1 group showed significant difference compared with the control group (P < 0.05), with LOEC value <8 mg·L-1. It is indicated that 14 d-exposure to DEHP had significantly negative effect on the immune functions of haemocytes, and could induce oxidative stress in Pinctada martensii. The THC was the most sensitive indicator to the exposure of DEHP, followed by cell membrane stability and lipid peroxidation level.
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