No abstract

Selenium (Se) can play a protective role against heavy metal toxicity. This experiment aims to evaluate the effect of Se supplementation at different doses on the chicken brains. Oxidative stress was induced in the chicken brains by chromium(VI). A total of 105 Hyland brown male chickens were randomly divided into seven groups, including the control group, poisoned group [6%LD KCrO body weight (B.W.)], and detoxification groups KCrO (6%LD) + Se (0.31, 0.63, 1.25, 2.50, and 5.00 NaSeO mg/kg B.W.) orally in water for 42 days. The chickens were detected by the activities of mitochondrial membrane potential, 2'-benzoyloxycinnamaldehyde, superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and Ca-ATPase. Cr(VI) administration caused histopathological damage. In addition, changes in oxidative stress indicators were observed in the chicken's brains. Se supplement increased the levels of GSH, mitochondrial membrane potential (MMP), and Ca-ATPase and reduced MDA activity in the detoxification groups. However, the high-dose Se supplementation groups of 2.50 and 5.00 mg/kg reduced the activities of GSH, MMP, and Ca-ATPase; increased the brain-body ratio; and increased SOD activity. In conclusion, Cr(VI) exposure caused oxidative stress. Se exerted a remission effect on toxic responses in the chicken brains. However, a high Se concentration was synergistic to the toxic effect of Cr(VI).

This study aims to investigate the contents of trace elements in the brain and serum of male chickens and the effect of selenium-chromium(VI) interaction. A chronic experimental model was established by supplementing 22.14 mg/kg KCrO with 0.00, 0.31, 0.63, 1.25, 2.50, and 5.00 mg/kg NaSeO mg/kg B.W. to water for chicken daily. After 14, 28, and 42 days of exposure to the solution, the brain and serum of chickens from each group were collected to detect the levels of Ca, Cu, Mn, Fe, Zn, and Mg by inductively coupled plasma mass spectrometer (ICP-MS). Cr(VI) time-dependently accumulated in the brain and serum. The contents of Cr increased both in the brain and serum with prolonged exposure. Cr contents in the brain and serum decreased in all Se groups compared with those in only Cr-treated groups. Ca contents decreased with prolonged exposure and increasing Se dosage. The contents of Cu and Mn increased on the 28th day but decreased on the 42nd day in the brain and serum. Fe and Zn contents decreased in the serum under prolonged exposure and increased on the 28th day but decreased on the 42nd day in the brain. Cr exposure did not significantly affect Mg contents in the brain but slightly decreased those in the serum. Therefore, appropriate doses of Se affected Cr accumulation, leading to adjustments in the contents and correlations of trace elements.

No abstract

This study aimed to clarify the effect of selenium (Se) on chromium (VI) [Cr(VI)]-induced damage in chicken liver. A total of 105 chickens were randomly divided into seven groups of 15. Group I received deionized water; group II received Cr(VI) (7.83 mg/kg/d) alone; and other groups orally received both Cr(VI) (7.83 mg/kg/d) and Se of different doses (0.14, 0.29, 0.57, 1.14, and 2.28 mg/kg/d). The levels of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), Ca -ATPase, and mitochondrial membrane potential (MMP) were measured. Results showed that Cr(VI) increased MDA content and decreased GSH content, T-SOD activity, Ca -ATPase activity, and MMP level. Meanwhile, Se co-treatment (0.14, 0.29, and 0.57 mg/kg/d) increased the viability of the above indicators compared with Cr(VI)-treatment alone. In addition, histopathologic examination revealed that Cr(VI) can cause liver damage, whereas Se supplementation of moderate dose inhibited this damage. This study confirmed that Se exerted protective effect against Cr(VI)-induced liver damage.