Transcriptomics and transmission ultrastructural examination reveals the nephrotoxicity of cadmium in laying hens.

Man Zhao,Zhifeng Xiong,Can Tao,Beiyu Zhang,Wenbo He,Shuai Wang,Zhangjian Sun,Niya Zhang

doi:10.1007/s11356-021-18405-2

Abstract

The objective of this study was to reveal the effects of cadmium (Cd) on ultrastructural changes, oxidative stress, and transcriptome expression in the kidneys of laying hens. Seventy-two healthy Hy-Line brown laying hens at 41weeks old were randomly allocated to four treatment groups with six replicates. The control group received a basal diet without additional Cd incorporation, and the other three treatment groups received diets supplemented with 15, 30, or 60mg Cd /kg of feed. After 6weeks of exposure, the results show that administration of 60mg/kg Cd significantly reduced (P < 0.05) eggshell thickness. With an increase in the Cd concentration in feed, the concentrations of renal Zn and Fe also had changed. Renal histopathology and ultrastructure also showed aggravated damage to glomeruli and renal tubules and the deformation of nuclei and mitochondria in all Cd treatment groups. With an increase in Cd in feed, the activity of glutathione peroxide (GPX) and catalase (CAT) was significantly reduced (P < 0.05), while the activity of total antioxidant capacity (T -AOC) was decreased (P < 0.05) only in the 60mg/kg Cd group. RNA-seq analysis revealed that 410 genes displayed differential expression (≥ 1.5-fold) in the 60mg/kg supplementation group, compared to the control group. GO and KEGG pathway analysis results showed that Cd affected many genes involved in mitochondria and ion transport. In conclusion, this study elaborates the mechanisms underlying renal toxicity caused by Cd, which might provide target candidate genes for alleviating Cd poisoning in laying hens.

Highlights

Cadmium (Cd) is a toxic heavy metal pollutant that poses great health risks for human, animals and plants
The results of residual Cd in kidneys of laying hens show that dietary exposure of Cd at 15 mg/kg, 30 mg/kg and 60 mg/kg significantly increased the residue of Cd in kidney (P < 0.01) in a dose-dependent manner (Fig. 2A), with a significant positive association between dietary Cd concentration and residual Cd in the kidneys of laying hens (y=1.9638x+4.584, R2=0.9812)
Our study indicates that the marked fluctuations in mRNA expression of inflammation-related and growth/apoptosis-related genes may be the result of renal damage induced by Cd exposure

Summary

Introduction

Cadmium (Cd) is a toxic heavy metal pollutant that poses great health risks for human, animals and plants. Once the Cd content exceeds the binding capacity of MT, unconjugated Cd accumulates in the proximal tubules of the kidney and thereby lead to renal damage (Liu et al 2015). Cd exposure may increase the production of reactive oxygen species (ROS) and induce damage and death in kidney cells (Shi et al 2017; Abdeen et al 2019). Following accumulation of ROS in proximal tubular cells, Cd may further induce apoptosis by the loss of mitochondrial membrane potential (Wang et al 2009). The proximal tubule of the kidney is the main site of calcium reabsorption, so exposure with Cd may lead to disturbances in Ca balance in the body

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