The protective role of selenium against cadmium-induced hepatotoxicity in laying hens: Expression of Hsps and inflammation-related genes and modulation of elements homeostasis

Ecotoxicol Environ Saf. 2018 Sep 15:159:205-212. doi: 10.1016/j.ecoenv.2018.05.016. Epub 2018 May 21.

Abstract

The purpose of this study was to examine the potential role of high selenium (Se) diets in alleviating chronic cadmium (Cd) hepatic toxicity in laying hens. In the present study, 128 healthy 31-week-old laying hens were fed a diet supplemented with Se (Na2SeO3, 2 mg/kg), Cd (CdCl2, 150 mg/kg), or both Se and Cd (150 mg/kg of CdCl2 and 2 mg/kg of Na2SeO3) for 90 days. The expression levels of heat shock proteins (Hsps, including Hsp60, Hsp70 and Hsp90) and inflammation-related factors, including nuclear factor-kappa B p50 (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E synthases (PTGES), interleukin 1-beta (IL-1β), and tumor necrosis factor-α (TNF-α) were investigated. The concentrations of 28 elements were also determined. The results indicated that Cd treatment significantly increased the mRNA and protein expression levels of Hsps and significantly improved the expression of inflammation-related genes. Moreover, Cd addition to the diets resulted in disturbances in the systemic balance of 13 elements, leading to decrease in the concentrations of Cr, Mn, Sr, Ba, and Hg and increase in Li, B, Ca, Ti, Fe, Cu, Mo, and Cd concentrations. Treatment with Se significantly alleviated Cd-induced hepatic toxicity, as evidenced by a reduction in Hsp60, Hsp70, Hsp90, NF-κB, COX-2, PTGES, TNF-α, and IL-1β expression. Additionally, Se and Cd co-treatment alleviated the changes in Li, B, Ca, Fe, Ti, Cu, Mo, Cd, Cr, Se, Sr, Ba, and Hg concentrations, which was in contrast to that upon Cd induction. The study indicated that Se could help against the negative effects of Cd and may be related to the alleviation of Cd-induced Hsps stress and the inflammatory responses along with modulating the element homeostasis.

Keywords: Cadmium; Element homeostasis; Hsps; Inflammatory factor; Liver; Selenium.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Cadmium / toxicity*
  • Cadmium Chloride / toxicity
  • Chemical and Drug Induced Liver Injury / genetics
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Chickens / genetics
  • Chickens / metabolism
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Dietary Supplements
  • Female
  • Gene Expression Regulation / drug effects
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism
  • Homeostasis / drug effects
  • Interleukin-1beta / blood
  • Interleukin-1beta / genetics
  • NF-kappa B p50 Subunit / genetics
  • NF-kappa B p50 Subunit / metabolism
  • Prostaglandin-E Synthases / genetics
  • Prostaglandin-E Synthases / metabolism
  • Protective Agents / pharmacology*
  • RNA, Messenger / metabolism
  • Selenium / pharmacology*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Anti-Inflammatory Agents
  • Heat-Shock Proteins
  • Interleukin-1beta
  • NF-kappa B p50 Subunit
  • Protective Agents
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Cadmium
  • Cyclooxygenase 2
  • Prostaglandin-E Synthases
  • Selenium
  • Cadmium Chloride