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首页> 外文期刊>Human and Experimental Toxicology >Stimulation of C32 and G361 melanoma cells using oleoyl acetyl glycerol and its effect on sulphur mustard cytotoxicity.
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Stimulation of C32 and G361 melanoma cells using oleoyl acetyl glycerol and its effect on sulphur mustard cytotoxicity.

机译：使用油酰乙酰甘油刺激C32和G361黑色素瘤细胞及其对硫芥菜细胞毒性的影响。

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摘要

Epidermal melanocytes have a higher sensitivity to sulphur mustard (HD) compared with other skin cell types. This may be due to the enzymatic production of melanin precursors exerting an additional cytotoxic effect following HD depletion of the cellular protectant, GSH. Stimulation of the protein kinase C pathway in melanocytes is known to increase melanin production in melanocytes and melanoma cell lines. In order to investigate the role of pigment synthesis in HD toxicology, cultures of an unpigmented melanoma cell line (C32) and of a pigmented melanoma line (G361) were treated with the potent diacyl glycerol analogue, oleoyl acetyl glycerol (OAG), in order to determine if protein kinase C-mediated increases in pigment production could increase sensitivity to subsequent HD exposure. Stimulation of C32 cells with OAG exerted a significant protective effect against the cytotoxic effects of HD. However, this was not due to increased melanin synthesis because this cell line cannot synthesize melanin pigments. The protective action observed is postulated to be due to modulation of protein kinase C activity. In contrast, stimulation of G361 melanoma cells with OAG resulted in an increased level of cytotoxicity upon subsequent exposure to HD. Protein kinase C controls several cellular pathways including checkpoints in the cell cycle, stalling the cell in G and promoting transition through the G2/M boundary. Given the genotoxic properties of HD, these two points in the cell cycle are important in determining the overall cytotoxic effect of HD. Control of the cell cycle by protein kinase C modulation and manipulation of melanin synthetic pathways may have therapeutic benefits.
机译：与其他皮肤细胞类型相比，表皮黑素细胞对硫芥子（HD）的敏感性更高。这可能是由于黑色素前体的酶促产生，在细胞保护剂GSH的HD耗尽后，其产生了额外的细胞毒性作用。已知刺激黑素细胞中的蛋白激酶C途径会增加黑素细胞和黑素瘤细胞系中黑色素的产生。为了研究色素合成在HD毒理学中的作用，依次用强力的二酰基甘油类似物油酰乙酰基甘油（OAG）处理未色素沉着的黑色素瘤细胞系（C32）和色素沉着的黑色素瘤系（G361）的培养。以确定蛋白激酶C介导的色素生成增加是否可以增加对随后HD暴露的敏感性。 OAG刺激C32细胞对HD的细胞毒性作用具有显着的保护作用。但是，这不是由于黑色素合成增加所致，因为该细胞系无法合成黑色素色素。据推测观察到的保护作用是由于蛋白激酶C活性的调节。相反，用OAG刺激G361黑色素瘤细胞会导致随后暴露于HD的细胞毒性水平升高。蛋白激酶C控制几种细胞途径，包括细胞周期中的检查点，使细胞停滞在G中并促进通过G2 / M边界的过渡。考虑到HD的遗传毒性，细胞周期中的这两点对于确定HD的总体细胞毒性作用很重要。通过蛋白激酶C调节和黑色素合成途径的操纵来控制细胞周期可能具有治疗益处。

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