In vitro cell culture experiments have lead to the consensus in the literature that certain PUFAs have a selective cytotoxic or anti-proliferative effect on tumour cells and a minimal, or no effect on normal cells. Re-examination of key publications showed that when normal cells were used for comparison, they were generally not from the same cell, tissue, or species type as the tumour cells. Recently, investigations have included more appropriate normal control cells, and though tumour specific cytotoxic/anti-proliferative PUFA effects are found in some cell types, in others the normal cells are more sensitive. Cell type differences were found in the relative ability of individual PUFAs to act. However, within a cell type differences in susceptibility were influenced by grade and stage of tumour, immortalisation and tumourigenic status, cell culture media and cell plating density. Together these results suggest that the consensus is not valid, and that susceptibility to PUFA is cell type specific, and alters during neoplastic progression. Furthermore, the cytotoxic/anti-proliferative effect induced by both n-3 and n-6 PUFAs on a wide variety of cell types, associated with an increase in lipid peroxidation in vitro, cannot account for the in vivo data on the relationship between dietary fat and certain cancers. However, the effects of PUFAs and their metabolites on cell signalling pathways may explain the in vivo data.

中文翻译：

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多不饱和脂肪酸与癌症之间关系的体外研究：肿瘤或组织特异性作用？

体外细胞培养实验已在文献中达成共识，即某些PUFA对肿瘤细胞具有选择性的细胞毒性或抗增殖作用，而对正常细胞的作用则微乎其微或无作用。对主要出版物的重新检查显示，当使用正常细胞进行比较时，它们通常不是与肿瘤细胞相同的细胞，组织或物种类型。最近，研究包括更合适的正常对照细胞，尽管在某些细胞类型中发现了肿瘤特异性的细胞毒性/抗增殖PUFA作用，但在另一些细胞中，正常细胞更加敏感。在个体PUFA的相对能力中发现细胞类型差异。但是，在细胞类型内，易感性的差异受肿瘤的级别和阶段，永生化和致瘤性状态的影响，细胞培养基和细胞平板密度。这些结果加在一起表明，该共识是无效的，并且对PUFA的敏感性是特定于细胞类型的，并在肿瘤进展过程中发生改变。此外，n-3和n-6 PUFA诱导的多种细胞类型的细胞毒性/抗增殖作用，与体外脂质过氧化作用的增加有关，不能解释关于饮食之间关系的体内数据。脂肪和某些癌症。但是，PUFA及其代谢物对细胞信号通路的影响可能解释了体内数据。n-3和n-6 PUFA诱导的多种细胞类型的细胞毒性/抗增殖作用与体外脂质过氧化作用的增加有关，不能解释体内饮食脂肪与脂肪之间关系的数据。某些癌症。但是，PUFA及其代谢物对细胞信号通路的影响可能解释了体内数据。n-3和n-6 PUFA诱导的多种细胞类型的细胞毒性/抗增殖作用与体外脂质过氧化作用的增加有关，不能解释体内饮食脂肪与脂肪之间关系的数据。某些癌症。但是，PUFA及其代谢物对细胞信号通路的影响可能解释了体内数据。