Effect of chromium (VI) exposure on antioxidant defense status and trace element homeostasis in acute experiment in rat
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
23625905
DOI
10.1177/0748233713487244
PII: 0748233713487244
Knihovny.cz E-resources
- Keywords
- Hexavalent chromium, antioxidant defense, oxidative stress, selenoenzymes, trace elements,
- MeSH
- Antioxidants metabolism MeSH
- Chromium toxicity MeSH
- Potassium Dichromate toxicity MeSH
- Glutathione metabolism MeSH
- Glutathione Reductase genetics metabolism MeSH
- Homeostasis drug effects MeSH
- Liver drug effects metabolism MeSH
- Hydrogen-Ion Concentration MeSH
- Rats MeSH
- Thiobarbituric Acid Reactive Substances metabolism MeSH
- Kidney drug effects metabolism MeSH
- Copper metabolism MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- Rats, Wistar MeSH
- Trace Elements pharmacology MeSH
- Thioredoxin-Disulfide Reductase antagonists & inhibitors metabolism MeSH
- Iron metabolism MeSH
- Zinc metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- Chromium MeSH
- Potassium Dichromate MeSH
- Glutathione MeSH
- Glutathione Reductase MeSH
- Thiobarbituric Acid Reactive Substances MeSH
- Copper MeSH
- Trace Elements MeSH
- Thioredoxin-Disulfide Reductase MeSH
- Iron MeSH
- Zinc 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.
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