Baggett J M, Berndt W O
Toxicol Appl Pharmacol. 1986 May;83(3):556-62. doi: 10.1016/0041-008x(86)90238-3.
Rats pretreated with diethyl maleate (DEM, 3.37 mmol/kg, ip) and buthionine sulfoximine (BSO, 0.45 mmol/kg, ip) and subsequently given mercuric chloride (HgCl2, 0.014 mmol/kg, sc) had a significantly greater mortality rate over the 24 hr after injection than rats given only HgCl2 or HgCl2 following either DEM or BSO alone. Depletion of nonprotein sulfhydryls (NPSH) in the kidney significantly decreased mercury uptake in that organ. A similar effect was not seen in the liver despite marked depletion of NPSH. Similarly, there was a tendency for less in vitro mercury accumulation in renal cortical slices from rats made glutathione deficient by DEM + BSO compared to control, or rats made glutathione deficient by DEM or BSO alone. Depletion of nonprotein sulfhydryls by the combination of the depleting agents diethyl maleate plus buthionine sulfoximine (DEM + BSO) had a greater effect to alter organic ion accumulation in renal cortical slices than the agents alone. The higher mortality produced by mercuric chloride after DEM + BSO pretreatment may have been due to an increased availability of mercury in lethal concentrations at other organ sites. These data suggest the possible importance of NPSH in renal mercuric ion accumulation, but not in the liver.
用马来酸二乙酯（DEM，3.37 mmol/kg，腹腔注射）和丁硫氨酸亚砜胺（BSO，0.45 mmol/kg，腹腔注射）预处理的大鼠，随后给予氯化汞（HgCl2，0.014 mmol/kg，皮下注射），在注射后的24小时内，其死亡率显著高于仅给予HgCl2或仅给予DEM或BSO后再给予HgCl2的大鼠。肾脏中非蛋白巯基（NPSH）的耗竭显著降低了该器官对汞的摄取。尽管NPSH明显耗竭，但在肝脏中未观察到类似的效应。同样，与对照组相比，或与仅用DEM或BSO使谷胱甘肽缺乏的大鼠相比，用DEM + BSO使谷胱甘肽缺乏的大鼠肾皮质切片中体外汞积累有减少的趋势。马来酸二乙酯加丁硫氨酸亚砜胺（DEM + BSO）联合使用使非蛋白巯基耗竭，比单独使用这些试剂对改变肾皮质切片中有机离子积累的影响更大。DEM + BSO预处理后氯化汞产生的较高死亡率可能是由于其他器官部位有更多致死浓度的汞可利用。这些数据表明NPSH在肾脏汞离子积累中可能具有重要作用，但在肝脏中并非如此。
