Abstract

Zinc (Zn) is necessary for the survival of aquatic organisms; nevertheless, the accumulation of Zn in excessive amounts may have toxic consequences. Few studies focusing on the biochemical, morphological, and transcriptional effects of aqueous Zn in Litopenaeus vannamei have been reported, and the underlying toxic mechanism remains largely unknown. The present study was performed to investigate the growth performance, morphological alterations, physiological changes, and transcriptional responses after Zn exposure at 0 (control), 0.01, 0.1, and 1 mg/L concentrations for 30 days in white shrimp L. vannamei hepatopancreas. The results found that survival rate (SR) and growth performance were significantly reduced in 1 mg/L Zn group. Significant structural damage and significant Zn accumulation in hepatopancreas were observed. The activities of trypsin and amylase (AMS), and the total antioxidant capacity (T-AOC) were attenuated, while the production of reactive oxygen species (ROS) and malondialdehyde (MDA) content were significantly increased after Zn exposure. Many differentially expressed genes (DEGs) were obtained after Zn exposure, and the majority of these DEGs were downregulated. Ten DEGs involved in oxidative stress, immunological response, apoptosis, and other processes were selected for qRT-PCR validation and the expression profiles of these DEGs kept well consistent with the transcriptome data, which confirmed the accuracy and reliability of the transcriptome results. Subsequently, we screened 12 genes to examine the changes of expression in different concentrations in more detail. All the results implying that Zn exposure caused severe histopathological changes and increased Zn accumulation in hepatopancreas, altered immune, antioxidant and detoxifying response by regulating the gene expressions of related genes, and eventually might trigger apoptosis. These findings provide valuable information and a new perspective on the molecular toxicity of crustaceans in response to environmental heavy metal exposure.

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