4.6 Article

Transcriptomic analysis of lead-induced hepatoxicology in female Japanese quails (Coturnix japonica): Implications of triglyceride synthesis, degradation and transport disruption

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpc.2021.109024

Keywords

Histopathology; Japanese quail; Lead; Liver; Transcriptome; Triglyceride

Funding

  1. National Natural Science Foundation of China [33372201]

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The study found that lead exposure caused tissue damage and ultrastructural damage in the liver of Japanese quails, disrupted molecular signaling and gene expression, and perturbed triglyceride metabolism pathways.
Lead (Pb) pollution poses great threats to mammals including human and it is also hazardous to bird life. In this study, RNA sequencing analysis was employed to examine the molecular responses to lead exposure in the liver of a toxicological model species Japanese quails (Coturnix japonica). Female birds were exposed to 0, 50, 500 and 1000 ppm waterborne Pb for 49 days. The results showed that hepatic microstructure was damaged under lead exposure featured by sinusoids dilation and irregularity as well as cell necrosis. Moreover, ultrastructural injury in the liver including mitochondrial swelling and vacuolization as well as nuclear deformation was induced by lead exposure. Lead exposure also caused the decrease of lipid droplets in the liver by oil red O staining. In addition, liver transcriptomic analysis revealed that molecular signaling and functional pathways were disrupted by lead exposure. Meanwhile, the expression of genes involved with hepatic glycerophospholipids metabolism of triglyceride synthesis and lipid transport of triglyceride transfer was significantly down-regulated by lead exposure. Moreover, the up-regulation of genes associated with fatty acid oxidation and the down-regulation of genes related with fatty acid synthesis were caused by lead exposure. The present study implied that lead induced liver malfunction and bird health risks through histopathological damages, molecular signaling disruption, genetic expression alteration and triglyceride metabolism disturbance.

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