No abstract

Heavy metal pollution threatens the health and life of animals and humans through the food chain. This study was performed to survey the heavy metal contamination in feedstuffs and feeds in Hubei Province, People's Republic of China, from 2012 to 2016. Samples were analyzed for cadmium (306 samples), mercury (117 samples), chromium (149 samples), and arsenic (4,358 samples) using atomic absorption spectrometry or atomic fluorescence spectrometry. The incidence rates of cadmium, mercury, chromium, and arsenic contamination of feedstuffs and feeds were high, and feeds were most often contaminated with chromium, followed by arsenic, cadmium, and mercury. The concentrations of heavy metals in samples positive for cadmium, mercury, chromium, and arsenic ranged from 0.001 to 1.200, 0.002 to 6.540, 0.060 to 8737.000, and 0.070 to 33.000 mg/kg, respectively. The mineral and additive samples had higher concentrations of heavy metals. The present study findings highlight the importance of monitoring heavy metals in feedstuffs and feeds and implementing feed management and bioremediation strategies to reduce heavy metal exposure. HIGHLIGHTS

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 41 weeks 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 60 mg Cd /kg of feed. After 6 weeks of exposure the results show that administration of 60 mg/kg Cd significantly reduced (P < 0.05) eggshell thickness. With an increase in the Cd concentration in feed, the concentrations of renal Zn, 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 GPX and CAT was significantly reduced (P＜0.05), while the activity of T-AOC was decreased (P＜0.05) only in the 60 mg/kg Cd group. RNA-seq analysis revealed that 410 genes displayed differential expression (≥ 1.5-fold) in the 60 mg/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.

Cadmium (Cd) is an environmental pollutant with destructive impact on many organ systems, such as chronic kidney diseases, liver diseases, osteoporosis, cardiovascular diseases and so on. The liver is the target organ of cadmium exposure. This study was performed to evaluate the adverse effects of prolonged high intake of dietary cadmium on production performance, serum biochemistry, liver antioxidant status, histopathology and the residue in liver and eggs in laying hens. 72 Hy-Line Brown laying hens aged 40 weeks were randomly allocated to four groups, with three replicates of six birds. Each group was fed a corn-soy basal diet (BD) and an oral dose of Cd at 0, 15, 30, 60 mg/kg per day for 6 weeks, respectively. Results revealed that the administration of 60 mg/kg Cd had no significant influences (P &gt; 0.05) on production performance. Compared with the control, dietary Cd significantly increased (P &lt; 0.05) the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, compared with the control, hepatic glutathione peroxide (GPX) activities were significantly decreased (P &lt; 0.05), while malondialdehyde (MDA) was significantly increased (P &lt; 0.05) when supplemented Cd over 15 mg/kg, and glutathione (GSH) was only decreased significantly (P &lt; 0.05) in 30 mg/kg Cd group. Hepatic histopathology also showed hepatic injury, mild vasculitis and a small amount of lymphocyte infiltration occurred in the liver tissue in 15 mg/kg Cd group and the symptoms were exacerbated with the increased dose. In the 60 mg/kg group, hepatic sinusoidal dilatation and mild congestion were also observed. The residue of Cd in the liver and yolk were increased (P &lt; 0.05) with the increasing concentration of dietary Cd. In conclusion, hepatic injuries in laying hens were induced when diets supplemented with Cd up to 15 mg/kg. Cd levels also managed to accumulated in liver and yolk of laying hens.

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 41 weeks 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 60 mg Cd /kg of feed. After 6 weeks of exposure the results show that administration of 60 mg/kg Cd signi cantly reduced (P < 0.05) eggshell thickness. With an increase in the Cd concentration in feed, the concentrations of renal Zn, 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 GPX and CAT was signi cantly reduced (P 0.05), while the activity of T-AOC was decreased (P 0.05) only in the 60 mg/kg Cd group. RNA-seq analysis revealed that 410 genes displayed differential expression (≥ 1.5-fold) in the 60 mg/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.