Renal and hepatic ALA-D activity and selected oxidative stress parameters of rats exposed to inorganic mercury and organoselenium compounds.
Renal and hepatic ALA-D activity and selected oxidative stress parameters of rats exposed to inorganic mercury and organoselenium compounds.
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DOI：
10.1016/j.fct.2003.08.002
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发表时间：
2004
期刊：
影响因子：
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通讯作者：
J. Perottoni;O. Rodrigues;M. Paixão;G. Zeni;L. P. Lobato;A. Braga;J. Rocha;T. Emanuelli
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文献类型：
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作者：
J. Perottoni;O. Rodrigues;M. Paixão;G. Zeni;L. P. Lobato;A. Braga;J. Rocha;T. Emanuelli
本文评价了有机硒化合物[依布硒啉、硒代胱氨酸N-乙基氨基甲酸酯（SeCis）、双-4-异丙基-2-恶唑啉基苯基二硒醚（AASe）]对HgCl_2毒性的防护能力。大鼠皮下注射有机硒化合物（0或50 μmol/kg）后6 h，再皮下注射氯化汞（0或17 μmol/kg）。HgCl_2抑制肾脏ALA-D活性（约48%），增加肾脏TBARS含量（约52%），降低肝脏非蛋白巯基含量（约40%），但有机硒化合物不能阻止这种作用。SeCis本身增加肾脏TBARS水平（约42%），而AASe增加肝脏抗坏血酸含量（约38%）。在体外实验中，HgCl_2（125 μm）、ebselen（122 μm）和SeCl_3（144 μm）对肾和肝ALA-D活性均有抑制作用。HgCl 2（400 μm）可显著增加体外肾和肝组织制备物中TBARS的产生，有机硒化合物可完全或部分阻止这种作用。Ebselen在我们的测定条件下表现出巯基过氧化物酶活性，而SeCis表现出巯基氧化性质，无论过氧化物的存在。AASe对巯基氧化没有影响。结果表明，有机硒化合物不能防止汞在体内的毒性。这些化合物对汞诱导的TBARS体外生产增加的保护作用可能与抗氧化作用有关，而不是与汞结合。
This paper evaluates the ability of organoselenium compounds [ebselen, selenocystine N-ethyl-carbamate (SeCis), bis-4-isopropyl-2-oxazolinyl phenyl diselenide (AASe)] to prevent HgCl2toxicity. Rats were injected with HgCl2(0 or 17 μmol/kg, sc) 6 h after organoselenium compounds had been injected (0 or 50 μmol/kg, sc). In vivo, HgCl2inhibited renal ALA-D activity (∼48%), increased TBARS level in kidney (∼52%) and reduced the hepatic content of non-protein thiol groups (∼40%), but organoselenium compounds did not prevent such effects. SeCis, per se, increased renal TBARS level (∼42%), while AASe increased hepatic content of ascorbic acid (∼38%). In vitro, renal and hepatic ALA-D activity was inhibited by HgCl2(⩾25 μm), ebselen (⩾12 μm) and SeCis (⩾4 μm). HgCl2(400 μm) significantly increased TBARS production in renal and hepatic tissue preparations in vitro, and this effect was completely or partially prevented by organoselenium compounds. Ebselen exhibited thiol peroxidase activity in our assay conditions, while SeCis exhibited thiol-oxidizing properties regardless of the presence of peroxide. AASe had no effect on thiol oxidation. Results suggest that organoselenium compounds could not prevent mercury toxicity in vivo. The protective effect of these compounds against mercury-induced increase of TBARS production in vitro is probably related to an antioxidant action rather than to mercury binding.