THE EFFECT OF 2-METHOXYETHANOL AND METHOXYACETIC ACID ON SERTOLI-CELL LACTATE PRODUCTION AND PROTEIN-SYNTHESIS INVITRO
THE EFFECT OF 2-METHOXYETHANOL AND METHOXYACETIC ACID ON SERTOLI-CELL LACTATE PRODUCTION AND PROTEIN-SYNTHESIS INVITRO
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DOI：
10.1016/0041-008x(84)90028-0
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发表时间：
1984-01-01
影响因子：
3.8
通讯作者：
BRABEC, MJ
中科院分区：
文献类型：
--
作者：
BEATTIE, PJ;WELSH, MJ;BRABEC, MJ
2-甲氧基乙醇（ME）是一种乙二醇醚，由于其独特的溶剂特性，已在表面涂料、油墨、染料、液压制动液和水基清洁剂中作为一种组分得到广泛应用。暴露于ME或其主要代谢产物甲氧基乙酸（MA），导致大鼠精母细胞耗竭和睾丸萎缩。精子发生的部位在曲细精管内。支持细胞支持精子发生，合成和分泌蛋白质和代谢底物，通过在曲细精管内分化生殖细胞来利用。一个底物乳酸，优先代谢精母细胞。由于生殖细胞依赖于支持细胞的代谢产物，因此在培养的大鼠支持细胞中测定ME和MA对乳酸产生和蛋白质合成的影响。将细胞培养物与0、3或10 mM ME或MA一起孵育长达12小时。[3H] L掺入法测定总蛋白合成无显著差异。ME和MA对细胞活力无明显影响。乳酸浓度和乳酸积累率显着降低MA，但不是ME，在3和10 mM孵育后6，9和12小时。ME或MA暴露导致的支持细胞乳酸产生的抑制可能是这些化合物对精子发生的抑制作用的原因。
2-Methoxyethanol (ME) is a glycol ether, which, because of its unique solvent characteristics, has found numerous applications as a component in surface coatings, inks, dyes, hydraulic brake fluids and water-based cleaners. Exposure to ME or its major metabolite, methoxyacetic acid (MA), resulted in spermatocyte depletion and testicular atrophy in rats. The site of spermatogenesis was within the seminiferous tubule. Sertoli cells supported spermatogenesis, synthesizing and secreting proteins and metabolic substrates for utilization by differentiating germ cells in the seminiferous tubule lumen. One substrate lactate, was preferentially metabolized by spermatocytes. Because germ cells were dependent upon the metabolic products of Sertoli cells, the effect of ME and MA on production of lactate and protein synthesis was measured in cultured rat Sertoli cells. Cell cultures were incubated with ME or MA at 0, 3 or 10 mM for up to 12 h. No significant difference was seen in total protein synthesis as measured by [3H]L incorporation. ME and MA had no apparent effect on cell viability. Lactate concentrations and rates of lactate accumulation were significantly decreased by MA, but not ME, at 3 and 10 mM following incubation for 6, 9 and 12 h. Inhibition of Sertoli cell lactate production resulting from ME or MA exposure could have accounted for the inhibitory action of these compounds on spermatogenesis.