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Effect of chromium (VI) exposure on antioxidant defense status and trace element homeostasis in acute experiment in rat
D. Kotyzová, A. Hodková, M. Bludovská, V. Eybl,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 1999-01-01 do 2015-11-30
SAGE Publications Journals
od 1999-01-01 do 2015-12-31
Health & Medicine (ProQuest)
od 1999-01-01 do 2015-11-30
Public Health Database (ProQuest)
od 1999-01-01 do 2015-11-30
PubMed
23625905
DOI
10.1177/0748233713487244
Knihovny.cz E-zdroje
- MeSH
- antioxidancia metabolismus MeSH
- chrom toxicita MeSH
- dvojchroman draselný toxicita MeSH
- glutathion metabolismus MeSH
- glutathionreduktasa genetika metabolismus MeSH
- homeostáza účinky léků MeSH
- játra účinky léků metabolismus MeSH
- koncentrace vodíkových iontů MeSH
- krysa rodu rattus MeSH
- látky reagující s kyselinou thiobarbiturovou metabolismus MeSH
- ledviny účinky léků metabolismus MeSH
- měď metabolismus MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Wistar MeSH
- stopové prvky farmakologie MeSH
- thioredoxin-disulfidreduktasa antagonisté a inhibitory metabolismus MeSH
- železo metabolismus MeSH
- zinek metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Occupational exposure to hexavalent chromium (Cr(VI)) compounds is of concern in many Cr-related industries and their surrounding environment. Cr(VI) is a proven toxin and carcinogen. The Cr(VI) compounds are easily absorbed, can diffuse across cell membranes, and have strong oxidative potential. Despite intensive studies of Cr(VI) pro-oxidative effects, limited data exist on the influence of Cr(VI) on selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (GPx)-important components of antioxidant defense system. This study investigates the effect of Cr(VI) exposure on antioxidant defense status, with focus on these selenoenzymes, and on trace element homeostasis in an acute experiment in rat. Male Wistar rats (130-140g) were assigned to two groups of 8 animals: I. control; and II. Cr(VI) treated. The animals in Cr(VI) group were administered a single dose of K2Cr2O7 (20 mg /kg, intraperitoneally (ip)). The control group received saline solution. After 24 h, the animals were sacrificed and the liver and kidneys were examined for lipid peroxidation (LP; thiobarbituric acid reactive substances (TBARS) concentration), the level of reduced glutathione (GSH) and the activities of GPx-1, TrxR-1, and glutathione reductase (GR). Samples of tissues were also used to estimate Cr accumulation and alterations in zinc, copper, and iron levels. The acute Cr(VI) exposure caused an increase in both hepatic and renal LP (by 70%, p < 0.01 and by 15%, p < 0.05, respectively), increased hepatic GSH level and GPx-1 activity, and decreased renal GPx-1 activity. The activity of GR was not changed. A significant inhibitory effect of Cr(VI) was found on TrxR-1 activity in both the liver and the kidneys. The ability of Cr(VI) to cause TrxR inhibition could contribute to its cytotoxic effects. Further investigation of oxidative responses in different in vivo models may enable the development of strategies to protect against Cr(VI) oxidative damage.
Citace poskytuje Crossref.org
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