Analysis of hematologic alterations, immune responses and metallothionein gene expression in Nile tilapia (Oreochromis niloticus) exposed to silver nanoparticles

Abstract

© 2016 Informa UK Limited, trading as Taylor & Francis Group. In this study, Nile tilapia (Oreochromis niloticus) fingerlings were used as a model to examine acute and chronic toxicity of silver nanoparticles (AgNP). Expression levels of metallothionein (MT) transcripts in fish exposed to 0, 1 or 100 mg AgNP/kg fish were investigated by quantitative real-time RT-PCR. The results showed MT expression levels were significantly decreased 0.3–0.7-fold in the liver and spleen of fish exposed to 1 or 100 mg AgNP/kg after 6–48 h. In contrast, during this period, MT mRNA expression levels were increased 2–3-fold in the head kidney of the fish exposed to either level of AgNP. Investigations of effects of AgNP on the fish immune responses and hematological parameters revealed that phagocytic activity, the amount of red blood cells (RBC) and the percent hematocrit (%Hct) in fish exposed to AgNP were decreased significantly 1 week after exposure, especially those exposed to 100 mg AgNP/kg. Fish immunized with Streptococcus agalactiae vaccine and simultaneously exposed to 100 mg AgNP/kg presented decreased antibody titers during the early phase. Lastly, a challenge test showed that vaccinated fish exposed to AgNP, regardless of concentration, remained protected against S. agalactiae infection, with a lower mortality (10–20%) compared to 70% in control fish. These findings indicated that expression patterns of the MT gene in the liver, spleen and head kidney at different timepoints could be used to assess acute and chronic exposure of Nile tilapia to AgNP. Additionally, changes in innate immune responses and hematological parameters in fish may prove useful for evaluation of AgNP toxicity. Data obtained in this study strongly support the use of Nile tilapia as an animal model to potentially serve as a bio-indicator of environment contamination caused by AgNP.