镉对体外培养肾组织中Ca^(2+)-ATPase的影响及尼莫地平的干预作用

Effects of cadmium on Ca^(2+)-ATPase activity in rat kidney slices and the intervention of Nimodipine

目的 探讨镉对肾组织中Ca2 + ATPase的影响及尼莫地平 (Nimo)对其的干预作用。方法 在体外条件下 ,测定CdCl2 对肾组织Ca2 + ATPase及乳酸脱氢酶 (LDH)、碱性磷酸酶 (ALP)、尿N 乙酰 D 氨基葡萄苷酶 (NAG)等多种肾损伤标志酶活力的作用及Nimo干预处理后的影响。结果 在低浓度CdCl2 组 ,Ca2 + ATPase的活力明显升高 ,10 0mg/LCdCl2 组Ca2 + ATPase的活力为(4 2 .12± 3.35 ) μmolPi·g-1·h-1,与对照组 [(31.2 3± 2 .5 9) μmolPi·g-1·h-1]的差异有显著性 (P <0 .0 5 ) ;而随CdCl2 浓度升高 ,Ca2 + ATPase活力受到明显抑制 ,2 0 0mg/LCdCl2 组的Ca2 + ATPase活力为 (2 0 .6 7± 2 .46 ) μmolPi·g-1·h-1,明显低于对照组 ,差异有显著性 (P <0 .0 5 )。而染镉前经Nimo预处理后 ,2 0 0mg/LCdCl2 +Nimo组的NAG活力 ,10 0、15 0、2 0 0mg/LCdCl2 +Nimo组的LDH活力及 15 0、2 0 0mg/LCdCl2 +Nimo组的ALP活力均低于单纯染CdCl2 组 ,差异有显著性 (P <0 .0 5 ) ;10 0mg/LCdCl2 +Nimo组的Ca2 + ATPase活力低于、而 2 0 0mg/LCdCl2 +Nimo组则高于单纯CdCl2 组 ,差异均有显著性 (P <0 .0 5 )。结论 CdCl2 对Ca2 + ATPase活力的影响是双相的 ,Nimo可部分解除CdCl2 对Ca2 + ATPase活力的抑制 ,并具有减轻镉?

Objective To study the effects of cadmium on Ca 2+ ATPase activity in rat kidney slices and the intervention of nimodipine(Nimo).Methods The incubation of kidney slice was used to measure the effects of cadmium on mark enzymes of renal injury and the intervention of Nimo.Results In lower dose of cadmium group,the Ca 2+ ATPase activity was significantly increased [(42.12±3.35)μmol Pi·g -1 ·h -1 vs (31.23±2.59)μmol Pi·g -1 ·h -1 at 100 mg/L of CdCl 2 ( P < 0.05) ],but as the dose of cadmium increased,it was decreased [(20.67±2.46)μmol Pi·g -1 ·h -1 ],significantly lower than the control at 200 mg/L of CdCl 2( P < 0.05) .When the kidney slices were incubated with Nimo prior to incubation with cadmium,the activity of NAG,LDH,ALP in medium at certain doses of CdCl 2 were significantly lower than in cadmium alone group,whereas the Ca 2+ ATPase activity was lower at 100 mg/L of CdCl 2 and higher at 200 mg/L of CdCl 2 than corresponding CdCl 2 alone group( P <0.05). Conclusion Cadmium has biphasic effect on Ca 2+ ATPase activity.Nimo could partly relieve the inhibition on Ca 2+ ATPase activity induced by cadmium and may protect against cadmium induced nephrotoxicity.