Effect of chromium (VI) exposure on antioxidant defense status and trace element homeostasis in acute experiment in rat

Abstract

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.

Temporal Changes in Rat Liver Gene Expression after Acute Cadmium and Chromium Exposure

“…There was also a dose-dependent accumulation of Cr on day 1 ( Fig 1B ). The high dose Cr accumulation was consistent with a previous experiment that also utilized the same method of exposure [ 50 ]. In contrast to the pattern of Cd accumulation, Cr levels rapidly declined from their peak at day 1 and were substantially reduced on days 3 and 7, indicative of its rapid clearance from the body.…”

“…Toxicological endpoints of metal exposure and ROS induction were also investigated. Hydroxyl and other radical species can interact with the lipids composing cellular membranes, leading to cellular damage [ 59 ], and both Cd and Cr have been reported to induce hepatic lipid peroxidation in vivo [ 10 , 15 , 50 , 60 , 61 ]. Radical induced lipid damage was estimated using a colorimetric assay for the lipoxidation end-product malondialdehyde (MDA).…”

“…There is little information in the literature about the effects of metal-induced ROS, its’ associated cellular damage, and the inflammatory response in the liver after a single acute exposure. The few studies that we have identified do not examine beyond a few days [ 50 , 120 , 121 ]. This study has provided insight into the mechanism of Cd and Cr induced liver damage and has provided experimental evidence for the contribution of •OH in their toxicity.…”

Oral exposure of mice to cadmium (II), chromium (VI) and their mixture induce oxidative- and endoplasmic reticulum-stress mediated apoptosis in the livers

“…Shaikh et al () reported that chronic injection of 0.6 mg kg −1 Cd (5 days week −1 ) for 22 weeks to Sprague–Dawley rats increased hepatic and renal lipid peroxidation levels, along with increases in tissue glutathione levels. Kotyzová et al () reported that a single dose injection of 20 mg kg −1 of body weight K 2 Cr 2 O 7 caused the increase of lipid peroxidation, GSH content and GPX activities in the liver of rat. Taken together, according to previous data and our results, it is indicated that the heavy metals have the potential to induce oxidative in different organisms both by acute exposure or low level and long period exposure.…”

Effects of Hydrolyzed Oat Bran Proteins on Free Radicals, Toxic Metals and Lipid Oxidation

“…It attacks most cellular components and damage them. Haber Weiss postulated that superoxide anion (O 2 ─• ) reacts with hydrogen peroxide (H 2 O 2 ) to produce hydroxyl radical (HO • ) and the reaction is facilitated by metal catalysts (Kotyzova, Hodkova, Bludovska, & Eybl, 2013).…”