TY - JOUR
T1 - Transcriptomics reveal triphenyltin-induced molecular toxicity in the marine mussel Perna viridis
AU - Ip, Jack Chi Ho
AU - Leung, Priscilla T.Y.
AU - Qiu, Jian Wen
AU - Lam, Paul K.S.
AU - Wong, Chris K.C.
AU - Chan, Leo L.
AU - Leung, Kenneth M.Y.
N1 - Funding Information:
This work was substantially supported by the Seed Collaborative Research Fund (2011) from the State Key Laboratory of Marine Pollution (City University of Hong Kong) which received funding support from the Innovation and Technology Commission of the Hong Kong SAR Government. The writing was partially supported by Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou) ( GML2019ZD0404 , GML2019ZD0409 ). The authors thank the Centre for Genomic Sciences of the University of Hong Kong for the service support in Illumina sequencing and bioinformatics analysis.
Publisher Copyright:
© 2021 The Authors
PY - 2021/10/10
Y1 - 2021/10/10
N2 - Triphenyltin (TPT) is widely used as an active ingredient in antifouling paints and fungicides, and continuous release of this highly toxic endocrine disruptor has caused serious pollution to coastal marine ecosystems and organisms worldwide. Using bioassays and transcriptome sequencing, this study comprehensively investigated the molecular toxicity of TPT chloride (TPTCl) to the marine mussel Perna viridis which is a commercially important species and a common biomonitor for marine pollution in Southeast Asia. Our results indicated that TPTCl was highly toxic to adult P. viridis, with a 96-h LC10 and a 96-h EC10 at 18.7 μg/L and 2.7 μg/L, respectively. A 21-day chronic exposure to 2.7 μg/L TPTCl revealed a strong bioaccumulation of TPT in gills (up to 36.48 μg/g dry weight) and hepatopancreas (71.19 μg/g dry weight) of P. viridis. Transcriptome analysis indicated a time course dependent gene expression pattern in both gills and hepatopancreas. Higher numbers of differentially expressed genes were detected at Day 21 (gills: 1686 genes; hepatopancreas: 1450 genes) and at Day 28 (gills: 628 genes; hepatopancreas: 238 genes) when compared with that at Day 7 (gills: 104 genes, hepatopancreas: 112 genes). Exposure to TPT strongly impaired the endocrine system through targeting on nuclear receptors and putative steroid metabolic genes. Moreover, TPT widely disrupted cellular functions, including lipid metabolism, xenobiotic detoxification, immune response and endoplasmic-reticulum-associated degradation expression, which might have caused the bioaccumulation of TPT in the tissues and aggregation of peptides and proteins in cells that further activated the apoptosis process in P. viridis. Overall, this study has advanced our understanding on both ecotoxicity and molecular toxic mechanisms of TPT to marine mussels, and contributed empirical toxicity data for risk assessment and management of TPT contamination.
AB - Triphenyltin (TPT) is widely used as an active ingredient in antifouling paints and fungicides, and continuous release of this highly toxic endocrine disruptor has caused serious pollution to coastal marine ecosystems and organisms worldwide. Using bioassays and transcriptome sequencing, this study comprehensively investigated the molecular toxicity of TPT chloride (TPTCl) to the marine mussel Perna viridis which is a commercially important species and a common biomonitor for marine pollution in Southeast Asia. Our results indicated that TPTCl was highly toxic to adult P. viridis, with a 96-h LC10 and a 96-h EC10 at 18.7 μg/L and 2.7 μg/L, respectively. A 21-day chronic exposure to 2.7 μg/L TPTCl revealed a strong bioaccumulation of TPT in gills (up to 36.48 μg/g dry weight) and hepatopancreas (71.19 μg/g dry weight) of P. viridis. Transcriptome analysis indicated a time course dependent gene expression pattern in both gills and hepatopancreas. Higher numbers of differentially expressed genes were detected at Day 21 (gills: 1686 genes; hepatopancreas: 1450 genes) and at Day 28 (gills: 628 genes; hepatopancreas: 238 genes) when compared with that at Day 7 (gills: 104 genes, hepatopancreas: 112 genes). Exposure to TPT strongly impaired the endocrine system through targeting on nuclear receptors and putative steroid metabolic genes. Moreover, TPT widely disrupted cellular functions, including lipid metabolism, xenobiotic detoxification, immune response and endoplasmic-reticulum-associated degradation expression, which might have caused the bioaccumulation of TPT in the tissues and aggregation of peptides and proteins in cells that further activated the apoptosis process in P. viridis. Overall, this study has advanced our understanding on both ecotoxicity and molecular toxic mechanisms of TPT to marine mussels, and contributed empirical toxicity data for risk assessment and management of TPT contamination.
KW - Detoxification
KW - Endocrine disruption
KW - Marine mussel
KW - Nuclear receptors
KW - Transcriptome
KW - Triphenyltin
UR - http://www.scopus.com/inward/record.url?scp=85107301110&partnerID=8YFLogxK
U2 - 10.1016/j.scitotenv.2021.148040
DO - 10.1016/j.scitotenv.2021.148040
M3 - Journal article
C2 - 34091345
AN - SCOPUS:85107301110
SN - 0048-9697
VL - 790
JO - Science of the Total Environment
JF - Science of the Total Environment
M1 - 148040
ER -
