Methylmercury-induced changes in target organs of suckling rat pups

被引:2
作者
Abdalla, Faida Husein [1 ]
Belle, Luziane Potrich [2 ]
Rodrigues Bitencourt, Paula Eliete [1 ]
da Silva, Jose Edson [1 ]
Roman, Silvana [4 ]
da Rosa, Cintia [3 ]
Schetinger, Maria Rosa [3 ]
Moretto, Maria Beatriz [1 ,2 ]
机构
[1] Hlth Sci Ctr, Postgrad Program Pharmaceut Sci, BR-97105900 Santa Maria, RS, Brazil
[2] Postgrad Program Pharmacol, BR-97105900 Santa Maria, RS, Brazil
[3] Univ Fed Santa Maria, Dept Chem, BR-97105900 Santa Maria, RS, Brazil
[4] Integrated Reg Univ, Erechim, RS, Brazil
关键词
Methylmercury; n-Acetyl-beta-D-glucosaminidase; Lipid peroxidation; Adenosine deaminase; Rat; BETA-D-GLUCOSAMINIDASE; ADENOSINE-DEAMINASE ACTIVITY; OXYGEN SPECIES FORMATION; METHYL MERCURY; PRIMARY CULTURES; METAL EXPOSURE; TOXICITY; EXCRETION; BRAIN; CELLS;
D O I
10.1016/j.etp.2010.12.002
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Methylmercury (MeHg) is an organic form of mercury with toxic effects in multiple organs. The aim of the present investigation was to evaluate the in vivo effects of MeHg (1 and 4 mg/kg) given orally for seven consecutive days on adenosine deaminase (ADA), n-acetyl-beta-D-glucosaminidase (NAG) and ecto-nucleoside triphosphate phosphohydrolase (NTPDase) activities, and on lipid peroxidation in hippocampus, cerebral cortex, kidney and liver of suckling rat pups. The results showed that NAG activity and lipid peroxidation levels increased in the kidney in both treatments, whereas urinary NAG activity increased only in the 1 mg/kg treatment. Despite the fact that the lipid peroxidation increased in both cerebral cortex and hippocampus, the latter appeared to be more vulnerable to MeHg exposure as it also had an increase in ADA activity. Thus, although dietary MeHg modified renal cell function, it did not alter histological features in suckling rat pups. The results of our investigation are of significant importance because they demonstrated responses to exposition to low doses of MeHg in target organs during the development of the rat. Especially the kidney was affected by the oral exposure to MeHg, suggesting the vulnerability of this organ at this stage of development. Moreover, the urinary NAG may provide important data that could serve as basis for risk assessment purposes following MeHg exposure. (C) 2010 Elsevier GmbH. All rights reserved.
引用
收藏
页码:605 / 609
页数:5
相关论文
共 44 条
[21]  
GIBLETT ER, 1972, LANCET, V2, P1067
[22]  
Giusti G., 1974, Methods of Enzymatic Analysis, P1092, DOI DOI 10.1016/B978-0-12-091302-2.50108-0
[23]   Technical report: Mercury in the environment: Implications for pediatricians [J].
Goldman, LR ;
Shannon, MW .
PEDIATRICS, 2001, 108 (01) :197-205
[24]  
HORAK E, 1981, CLIN CHEM, V27, P1180
[25]   The in vitro effects of selenomethionine on methylmercury-induced neurotoxicity [J].
Kaur, Parvinder ;
Evje, Lars ;
Aschner, Michael ;
Syversen, Tore .
TOXICOLOGY IN VITRO, 2009, 23 (03) :378-385
[26]   RENAL FUNCTIONAL TERATOGENESIS RESULTING FROM ADRIAMYCIN EXPOSURE [J].
KAVLOCK, RJ ;
ROGERS, EH ;
REHNBERG, BF .
TERATOLOGY, 1986, 33 (02) :213-220
[27]   Lipid peroxidation in liver of rats administrated with methyl mercuric chloride [J].
Lin, TH ;
Huang, YL ;
Huang, SF .
BIOLOGICAL TRACE ELEMENT RESEARCH, 1996, 54 (01) :33-41
[28]   Effects of postnatal exposure to methylmercury on spatial learning and memory and brain NMDA receptor mRNA expression in rats [J].
Liu, Wenjun ;
Wang, Xinmei ;
Zhang, Rong ;
Zhou, Yikai .
TOXICOLOGY LETTERS, 2009, 188 (03) :230-235
[29]   Enzymes that hydrolyze adenine nucleotides in diabetes and associated pathologies [J].
Lunkes, GI ;
Lunkes, D ;
Stefanello, F ;
Morsch, A ;
Morsch, VM ;
Mazzanti, CM ;
Schetinger, MRC .
THROMBOSIS RESEARCH, 2003, 109 (04) :189-194
[30]   The possibility of determining N-acetyl-β-D-glucosaminidase isoenzymes under alkaline conditions [J].
Mandic, LM ;
Acimovic, JM ;
Jovanovic, VB .
CLINICAL BIOCHEMISTRY, 2005, 38 (04) :384-389