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.

Iron is an essential element which, under certain conditions, can have prooxidant and cancerogenic effects. The effect of iron and iron chelators on the activity of selenoenzymes has been studied. Acute experiments in male Wistar rats demonstrated the prooxidant effect of iron on the selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (GPx). These enzymes represent an important part of the antioxidant defense system. Deferiprone (L1) has been shown to abolish the stimulating effect of iron on lipid peroxidation and reduced glutathione (GSH) levels, and also to inhibit the influence of iron on the activity of TrxR and GPx. Similarly, the flavonoid quercetin abolished the influence of iron on the activity of TrxR. The activity of both selenoenzymes has also been shown to be stimulated using L1, naringin (NAR), quercetin (QUE) and myricetin (MYR) in the absence of iron. Further studies including the combination of synthetic and natural compounds (e.g., flavonoids) are being considered for their possible development and clinical use in antioxidant therapies.

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