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首页> 外文期刊>Life sciences >Comparative toxicity of oleic and linoleic acid on human lymphocytes.
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Comparative toxicity of oleic and linoleic acid on human lymphocytes.

机译：油酸和亚油酸对人淋巴细胞的比较毒性。

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摘要

Commercially available lipid emulsions for parenteral nutrition are mainly composed by long chain triacylglycerol containing a high proportion of linoleic acid (LA) or oleic acid (OA). The immunological impact of such therapy is particularly important because parenteral diets are often administered to critically ill patients as a mechanism to supply adequate nutrition during catabolic stress conditions. The comparative toxicity of OA and LA on human lymphocytes and the type of cell death induced by these fatty acids were determined in vitro. Parameters of cell death were investigated by flow cytometry-cell viability, DNA fragmentation, phosphatidylserine externalization, mitochondrial depolarization, neutral lipid accumulation and production of reactive oxygen species-and by fluorescence microscopy-chromatin condensation. Additionally a spectrofluorometric assay was employed to determine the activities of caspase--3, 6 and 8. Evidence is presented herein that OA is less toxic to human lymphocytes than LA. However, both fatty acids promoted apoptosis and necrosis of these cells. The mechanism of cell death induced by OA involved activation of caspase 3 while the mechanism of death induced by LA involved mitochondrial depolarization and ROS production. Importantly, neutral lipid accumulation may be a mechanism to protect lymphocytes against the toxicity induced by OA. OA may offer an immunological less problematic alternative to LA with respect to fatty acid composition of parenteral nutritional emulsions.
机译：用于肠胃外营养的可商购的脂质乳剂主要由含有高比例的亚油酸（LA）或油酸（OA）的长链三酰基甘油组成。这种疗法的免疫学影响尤其重要，因为肠胃外饮食通常是给重症患者服用的，这是在分解代谢应激条件下提供足够营养的一种机制。在体外测定了OA和LA对人淋巴细胞的相对毒性以及这些脂肪酸诱导的细胞死亡类型。细胞死亡的参数通过流式细胞仪-细胞活力，DNA片段化，磷脂酰丝氨酸外在化，线粒体去极化，中性脂质蓄积和活性氧的产生以及荧光显微镜-染色质浓缩进行了研究。另外，采用荧光分光光度测定法测定胱天蛋白酶-3、6和8的活性。本文提供了证据：OA对人淋巴细胞的毒性小于LA。然而，两种脂肪酸都促进这些细胞的凋亡和坏死。 OA诱导的细胞死亡机制涉及caspase 3的激活，而LA诱导的死亡机制涉及线粒体去极化和ROS的产生。重要的是，中性脂质蓄积可能是保护淋巴细胞免受OA诱导的毒性的机制。就肠胃外营养乳液的脂肪酸组成而言，OA可以为LA提供一种免疫学上没有问题的替代方案。

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