The role of selenium in cadmium toxicity: interactions with essential and toxic elements

Abstract

1. The study was part of a project designed to investigate if organic selenium (Se) can ameliorate the toxic effects of cadmium (Cd). The main objective of the present study was to investigate, in the chicken, the interactions between Se, Cd and the following elements: Sb, Ca, Cr, Co, Cu, Fe, Pb, Mg, Mn, Mo, Ni, V and Zn. 2. A total of 300 1-d-old chickens (broilers) were randomly distributed among 4 dietary treatments with 5 replicate pens per treatment. In T1, chickens were fed on a diet with 0·3 mg/kg added Se, without added Cd. In T2, chickens were fed on a diet with 0·3 mg/kg Se and 10 mg/kg Cd. In T3, chickens were fed on a diet with 0·3 mg/kg Se and 100 mg/kg of Cd added and in T4 treatment, chickens were fed on a diet with 3 mg/kg Se and 100 mg/kg Cd added. Se was added as Se-yeast. Cd was added as cadmium chloride (CdCl₂). On d 28 and 42, two chickens per replicate pen were killed for collection of whole blood, liver, kidney and breast muscle samples. Samples were analysed by ICP-MS. The data were analysed using a multivariate linear model. 3. While low Cd concentrations in the diet led only to an increase of Cd concentration in the examined tissues, addition of high concentrations of Cd increased the concentration of Cd, Cu, Sb and V and decreased that of Se, Mn and Fe. Addition of high Se concentrations did not significantly reduce Cd concentration. 4. Prior to model application, correlations of 78 elements were noted, while after model application 39 correlations were noted. Most notably, Cd was correlated with Ca, Co, Cu and Mg, while Se was correlated with Mn. 5. The present study revealed several correlations between essential, probably essential and toxic elements illustrating the importance of the balance between pro-oxidants and antioxidants.

Effects of selenium and zinc supplementation on cadmium toxicity in broilers

“…The present study revealed that the concentrations of Cd, As, and V in breast muscle were significantly affected by the dietary treatments while the concentration of all other examined elements remained unaffected. The extend of increase of Cd level in breast muscle is in line with previous studies [16,17] indicating that breast muscle is a tissue that accumulates relative lower amounts of Cd compared to other nonedible tissues. Regarding the Cd level in breast muscle between the 2 treatments that had 50 ppm of added Cd in the diet, no statistically significant differences were noted.…”

Methylmercury Induced Neurotoxicity and the Influence of Selenium in the Brains of Adult Zebrafish (Danio rerio)

“…Additionally, cadmium-induced cell death, while not inhibited, was also significantly reduced in RICTOR-silenced PC12 cells [31], highlighting the importance of this regulator in the context of heavy metal toxicity in the brain. In addition to rapamycin, selenium was also reported to antagonise cadmium induced toxicity; most likely also through effects on the important balance between pro-oxidant toxic metals and antioxidant essential elements [33,34,35]. …”

Effect of combined exposure to lead and decabromodiphenyl ether on neurodevelopment of zebrafish larvae

“…Several studies have demonstrated a role for iodothyronine deiodinase in catalyzing debromination of PBDEs in fish (Browne et al, 2009;Noyes et al, 2011); it may be that Pb can inhibit iodothyronine deiodinase activity via increasing oxidative damage (Chaurasia et al, 1996). Furthermore, iodothyronine deiodinase is a Se-containing enzyme with selenocysteine making up a critical component of the active site of deiodinase (St Germain and Galton, 1997;Köhrle, 2000) and studies indicate that competition between another heavy metal (Cd) and Se (Al-Waeli et al, 2012;El-Sharaky et al, 2007) is a possible mechanism involved in Cd-induced inhibition of iodothyronine deiodinase. Hence, it is plausible that increased Pb in fish might also inhibit iodothyronine deiodinase activity via competition between Pb and Se, which would lead to reduced BDE-209 metabolism, and fewer metabolic products of BDE-209.…”