Mustafa Kemal University, Biology Department, Antakya/Hatay/Turkey.
Toxicol Mech Methods. 2004;14(4):241-5. doi: 10.1080/15376520490434485.
In previous studies, the transport of dinitrophenyl-glutathione from erythrocytes has been extensively investigated. However, the effect of treatment of erythrocytes with such xenobiotics on free-SH status of cells has not been well documented. Also, the effects of N-acetyl-L-cysteine or other-SH containing compounds on glutathione conjugate transport have not been investigated. The objectives of the present study were to investigate how the presence N-acetyl-L-cysteine and L-cysteine affect the free-SH status of 1-chloro-2,4-dinitrobenzene treated erythrocytes and how N-acetyl-L-cysteine or L-cysteine affects the rate of dinitrophenyl-glutathione conjugate transport form erythrocytes. Our results indicated that L-cysteine is more efficient than N-acetyl-L-cysteine in increasing the free-SH content of erythrocytes in the presence of 1-chloro-2,4-dinitrobenzene. At the end of 20 min of exposure, free-SH levels remained at 5.3 mumol/ml erythrocyte in the presence of L-cysteine. However, in the presence of N-acetyl-L-cysteine the free-SH level was 2 mumol/ml erythrocyte. In the absence of 1-chloro-2,4-dinitrobenze, L-cysteine uptake by erythrocytes was not efficient compared to N-acetyl-L-cysteine. The free-SH concentrations in the presence of N-acetyl-L-cysteine and L-cysteine, in this case were, 9 +/- 1 and 1.5 +/- 0.1 mumol/ml erythrocytes respectively. These results clearly suggest that 1-chloro-2,4-dinitrobenzene stimulates the L-cysteine uptake in eryhtrocytes by a mechanism not described before. Our results also indicated that 1-chloro-2,4-dinitrobenzene induced L-cysteine uptake is a Na(+) and ATP dependent process. Replacement of NaCl with LiCl decreased the L-cysteine uptake by about 5-fold and in the presence of NaF decrease in L-cysteine uptake was about 2 fold. Our results conclude the presence of an in vitro L-cysteine uptake mechanism in erythrocytes stimulated by 1-chloro-2,4-dinitrobenzene.
在以前的研究中，已经广泛研究了二硝基苯谷氨酸从红细胞中的转运。然而，用此类外源性化学物质处理红细胞对细胞游离-SH 状态的影响尚未得到很好的记录。此外，N-乙酰-L-半胱氨酸或其他含-SH 化合物对谷胱甘肽共轭物转运的影响也尚未得到研究。本研究的目的是研究 N-乙酰-L-半胱氨酸和 L-半胱氨酸的存在如何影响 1-氯-2,4-二硝基苯处理的红细胞的游离-SH 状态，以及 N-乙酰-L-半胱氨酸或 L-半胱氨酸如何影响二硝基苯-谷胱甘肽共轭物从红细胞中的转运速率。我们的结果表明，在 1-氯-2,4-二硝基苯存在下，L-半胱氨酸比 N-乙酰-L-半胱氨酸更有效地增加红细胞的游离-SH 含量。在 20 分钟的暴露结束时，L-半胱氨酸存在时红细胞中的游离-SH 水平保持在 5.3 μmol/ml 红细胞。然而，在 N-乙酰-L-半胱氨酸存在下，游离-SH 水平为 2 μmol/ml 红细胞。在没有 1-氯-2,4-二硝基苯的情况下，与 N-乙酰-L-半胱氨酸相比，红细胞对 L-半胱氨酸的摄取效率不高。在 N-乙酰-L-半胱氨酸和 L-半胱氨酸存在的情况下，游离-SH 浓度分别为 9±1 和 1.5±0.1 μmol/ml 红细胞。这些结果清楚地表明，1-氯-2,4-二硝基苯通过以前未描述的机制刺激红细胞中 L-半胱氨酸的摄取。我们的结果还表明，1-氯-2,4-二硝基苯诱导的 L-半胱氨酸摄取是一个需要 Na(+)和 ATP 的过程。用 LiCl 替代 NaCl 可使 L-半胱氨酸摄取减少约 5 倍，而在 NaF 存在下，L-半胱氨酸摄取减少约 2 倍。我们的结果得出结论，存在一种由 1-氯-2,4-二硝基苯刺激的红细胞中 L-半胱氨酸摄取机制。
