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首页> 外文期刊>Trace Elements and Electrolytes >Protective effect of zinc ions against lead and nickel induced inhibition of delta-aminolevulinic acid dehydratase activity in mice liver
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Protective effect of zinc ions against lead and nickel induced inhibition of delta-aminolevulinic acid dehydratase activity in mice liver

机译:锌离子对铅和镍诱导的小鼠肝脏δ-氨基乙酰丙酸脱水酶活性的抑制作用

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摘要

The present study was devoted to assess the ability of zinc (Zn) to protect heme synthesis system from Pb and Ni toxicity and to compare toxic effects of lead (Pb) and nickel (Ni) to the activity of one of heme synthesis enzymes delta-aminolevulinic acid dehydratase (delta-ALAD), after single and 2-week exposure. Material and methods: For the single metal exposure, mice were injected once i.p. with a solution of Pb(CH3COO)(2) (242 mu mol Pb/l kg b.w.); NiCl2 (96 mu mol Ni/l kg b.w.) or ZnSO4 (24 mu mol Zn/l kg b.w.). For the repeated exposure, mice were i.p. injected for 14 days (once a day) with Pb(CH3COO)(2) (48 mu mol Pb/l kg b.w.); NiCl2 (19 mu mol Ni/l kg b.w.) or ZnSO4 (24 mu mol Zn/l kg b.w.) solution. The control mice received i.p. injections of saline. The activity of delta-ALAD was examined according to the method of Sassa [1]. For the determination of reaction product porphobilinogen the modified Ehrlichs reagent was used. Absorbance was measured at the wavelength 555 nm. Statistical analysis was performed using a statistical software package (Statistica 6.0). p-value less than 0.05 was considered statistically significant. Results: Single exposure to Pb2+ decreased delta-ALAD activity in mice liver and blood by 74% and 99%, respectively,, exposure to NiCl2 did so, however, not so drastically by 38% (in liver) and 53% (in blood). Though single exposure to ZnSO4 did not have any effect on the delta-ALAD activity neither in the liver, nor in the blood, Zn pre-treatment diminished the suppressing effect of Pb, increasing the liver and blood enzyme activity by 87% and 580%, respectively, as compared to the Pb treated mice group (p < 0.05). Single Zn2+ pre-treatment, 20 minutes before NiCl2 injections, completely restored enzyme activity to the control level in liver and blood of mice (Figure 1). Repeated administration of Pb(CH3COO)(2) inhibited liver and blood delta-ALAD activity by 73% and 92% respectively, while repeated NiCl2 administration suppressed enzyme activity only in the liver (by 32%). Repeated ZnSO4 administration did not affect the delta-ALAD activity neither in the liver nor in the blood, while Zn2+ pretreatment recovered Pb's suppressed enzyme activity in mice liver, as well as blood, respectively by 40% and 20%. After 14 days Zn2+ did not provide protection against Ni2+ induced delta-ALAD inhibition neither in the liver nor in the blood of mice.
机译:本研究致力于评估锌(Zn)保护血红素合成系统免受Pb和Ni毒性的能力,并比较铅(Pb)和镍(Ni)对一种血红素合成酶δ-的活性的毒性作用。暴露一周和两周后,氨基乙酰丙酸脱水酶(delta-ALAD)。材料和方法:对于单次金属暴露,小鼠腹腔注射一次。用Pb(CH3COO)(2)溶液(242μmol Pb / l kg b.w.); NiCl 2(96μmol Ni / l kg b.w.)或ZnSO4(24μmol Zn / l kg b.w.)。为了重复暴露,将小鼠腹膜内注射。用Pb(CH3COO)(2)(48μmol Pb / l kg b.w.)注入14天(每天一次); NiCl2(19μmol Ni / l kg b.w.)或ZnSO4(24μmol Zn / l kg b.w.)溶液。对照小鼠接受腹膜内注射。注射盐水。根据Sassa [1]的方法检查了delta-ALAD的活性。为了确定反应产物胆色素原,使用了改良的Ehrlichs试剂。在波长555nm处测量吸光度。使用统计软件包(Statistica 6.0)进行统计分析。 p值小于0.05被认为具有统计学意义。结果:单次暴露于Pb2 +可使小鼠肝脏和血液中的delta-ALAD活性分别降低74%和99%,而暴露于NiCl2则降低了38%(肝脏)和53%(血液) )。尽管单次暴露于ZnSO4对肝脏和血液中的delta-ALAD活性都没有影响,但是Zn预处理减弱了Pb的抑制作用,使肝脏和血液酶的活性分别增加了87%和580%分别与Pb治疗的小鼠组相比(p <0.05)。在注射NiCl2之前20分钟,单次Zn2 +预处理将酶的活性完全恢复到小鼠肝脏和血液中的对照水平(图1)。重复施用Pb(CH3COO)(2)分别抑制肝脏和血液δ-ALAD活性73%和92%,而重复施用NiCl2仅抑制肝脏中的酶活性(降低32%)。重复使用ZnSO4不会影响肝脏和血液中的delta-ALAD活性,而Zn2 +预处理可使Pb在小鼠肝脏和血液中抑制的酶活性分别恢复40%和20%。 14天后,Zn2 +在小鼠肝脏和血液中均未提供针对Ni2 +诱导的delta-ALAD抑制的保护作用。

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