Relationship analysis between tributyltin exposure and human diseases based on “big data”
LIU Min, ZHANG Ji-liang, ZHANG Chun-nuan, QI Qian, CUI Wei, FENG Hai-yang
Laboratory of Aquatic Environment and Animal Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China
The potential influence information of tributyltin (TBT) was excavated to predict the relationship between TBT exposure and human-related diseases by using the "big data" of toxicology database. In comparative toxicogenomics database (CTD), 488 genes interacting with TBT were collected. Among the 488 genes, TP53 was the most associated genes, followed by ESR1 and FN1. Using CTD analysis, it was also found that cancer, nervous system diseases, cardiovascular diseases, urogenital disease (female), digestive system diseases, metabolic disease, urogenital disease (male), endocrine system diseases, immune system diseases and respiratory tract disease were the top 10diseases related to TBT exposure. Based KEGG pathway and DAVID gene function annotation analysis, metabolic diseases were more susceptible to be induced by TBT exposure; moreover, intensive genes interacting with TBT were annotated in the pathways of glucose metabolism. PASS prediction found that biological activities of many sugar-related enzymes could be affected by TBT exposure, which suggested that the impact of TBT on glucose metabolism should be of concern.
Antizar-Ladislao B. Environmental levels, toxicity and human exposure to tributyltin (TBT)-contaminated marine environment. a review[J]. Environment International, 2008,34:292-308.
[2]
Furdek M, Vah?i? M, S?an?ar J, et al. Organotin compounds in seawater and Mytilus galloprovincialis mussels along the Croatian Adriatic Coast[J]. Marine Pollution Bulletin, 2012,64(2):189-199.
[3]
Kucuksezgin F, Aydin-Onen S, Gonul L T, et al. Assessment of organotin (butyltin species) contamination in marine biota from the Eastern Aegean Sea, Turkey[J]. Marine Pollution Bulletin, 2011,62:1984-1988.
[4]
Kannan K, Takahashi S, Fujiwara N, et al. Organotin compounds, including butyltins and octyltins, in house dust from Albany, New York, USA[J]. Archives of Environmental Contamination and Toxicology, 2010,58:901-907.
[5]
Airaksinen R, Rantakokko P, Turunen A W, et al. Organotin intake through fish consumption in Finland[J]. Environmental Research, 2010,110:544-547.
[6]
Santos M M, Enes P, Reis-Henriques M A, et al. Organotin levels in seafood from Portuguese markets and the risk for consumers[J]. Chemosphere, 2009,75:661-666.
[7]
Guerin T, Sirot V, Volatier J L, et al. Organotin levels in seafood and its implications for health risk in high-seafood consumers[J]. Science of The Total Environment, 2007,388:66-77.
[8]
Lee C C, Wang T, Hsieh C Y, et al. Organotin contamination in fishes with different living patterns and its implications for human health risk in Taiwan[J]. Environmental Pollution, 2005,137:198-208.
[9]
Zhou Q F, Jiang G B, Liu J Y. Small-scale survey on the contamination status of butyltin compounds in seafoods collected from seven Chinese cities[J]. Journal of Agricultural and Food Chemistry, 2001,49:4287-4291.
Rantakokko P, Turunen A, Verkasalo P K, et al. Blood levels of organotin compounds and their relation to fish consumption in Finland[J]. Science of The Total Environment, 2008,399:90-95.
[13]
Nielsen J B., Strand J. Butyltin compounds in human liver[J]. Environmental Research, 2002,88(2):129-133.
Dudimah F D, Griffey D, Wang X, et al. Activation of p44/42MAPK plays a role in the TBT-induced loss of human natural killer (NK) cell function[J]. Cell Biology and Toxicology, 2010,26(5):435-444.
[16]
Ishihara Y, Kawami T, Ishida A, et al. Tributyltin induces oxidative stress and neuronal injury by inhibiting glutathione S-transferase in rat organotypic hippocampal slice cultures[J]. Neurochemistry International, 2012,60(8):782-790.
[17]
Nakatsu Y,Kotake Y,Takai N,et al. Involvement of autophagy via mammalian target of rapamycin (mTOR) inhibition in tributyltin-induced neuronal cell death[J]. The Journal of Toxicological Sciences, 2010,35(2):245-251.
[18]
Zuo Z, Chen S, Wu T, et al. Tributyltin causes obesity and hepatic steatosis in male mice[J]. Environmental Toxicology, 2011,26(1):79-85.
[19]
Grondin M, Marion M, Denizeau F, et al. Tributyltin induces apoptotic signaling in hepatocytes through pathways involving the endoplasmic reticulum and mitochondria[J]. Toxicology and Applied Pharmacology, 2007,222(1):57-68.
[20]
Ye H, Ng H W, Sakkiah S, et al. Pathway Analysis Revealed Potential Diverse Health Impacts of Flavonoids that Bind Estrogen Receptors[J]. International Journal of Environmental Research and Public Health, 2016,13(4):373.
[21]
Davis A P, Wiegers T C, King B L, et al. Generating Gene Ontology-Disease Inferences to Explore Mechanisms of Human Disease at the Comparative Toxicogenomics Database[J]. PLOS ONE, 2016,11(5):e0155530.
[22]
Hu B, Gifford E, Wang H, et al. Analysis of the ToxCast Chemical-Assay Space Using the Comparative Toxicogenomics Database[J]. Chemical Research in Toxicology, 2015,28(11):2210-2223.
[23]
Cheng L, Jiang Y, Wang Z, et al. DisSim:an online system for exploring significant similar diseases and exhibiting potential therapeutic drugs[J]. Scientific Reports, 2016,6:30024.
[24]
Davis A P, Grondin C J, Johnson R J, et al. The Comparative Toxicogenomics Database:update 2017[J]. Nucleic Acids Research, 2017,45(D1):D972-D978.
[25]
Boyle E I, Weng S, Gollub J, et al. GO::TermFinder-open source software for accessing Gene Ontology information and finding significantly enriched Gene Ontology terms associated with a list of genes[J]. Bioinformatics, 2004,20(18):3710-3715.
[26]
Kanehisa M, Furumichi M, Tanabe M, et al. KEGG:new perspectives on genomes, pathways, diseases and drugs[J]. Nucleic Acids Research, 2017,45(D1):D353-D361.
[27]
Huang D W, Sherman B T, Lempicki R A. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources[J]. Nature Protocols, 2009,4(1):44-57.
[28]
Huang D W, Sherman B T, Lempicki R A. Bioinformatics enrichment tools:paths toward the comprehensive functional analysis of large gene lists[J]. Nucleic Acids Research, 2009,37(1):1-13.
[29]
Filimonov D A, Lagunin A A, Gloriozova T A, et al. Prediction of the biological activity spectra of organic compounds using the PASS online web resource[J]. Chemistry of Heterocyclic Compounds, 2014,50(3):444-457.
[30]
Shao X, Wang M, Wei X, et al. Peroxisome proliferator-activated receptor-γ:master regulator of adipogenesis and obesity[J]. Current Stem Cell Research & Therapy, 2016,11(3):282-289.
[31]
Grün F, Blumberg B. Environmental obesogens:organotins and endocrinedisruption via nuclear receptor signaling[J]. Endocrinology, 2006,147:S50-S55.
[32]
Zhang J, Zuo Z, He C, et al. Effect of tributyltin on testicular development in Sebastiscus marmoratus and the mechanism involved[J]. Environmental Toxicology and Chemistry, 2009,28:1528-1535.
[33]
Zenz T, Eichhorst B R, Denzel T, et al. TP53 mutation and survival in chronic lymphocytic leukemia[J]. Journal of Clinical Oncology, 2010, 28(29):4473-4479.
Sang H P, Yun I D, Sang U L, et al. Color image segmentation based on 3-D clustering:morphological approach fn1[J]. Pattern Recognition, 1998,31(8):1061-1076.
[36]
Lawrence S, Pellom S T Jr, Shanker A, et al. Tributyltin exposure alters cytokine levels in mouse serum[J]. Journal of Immunotoxicology, 2016,13(6):870-878.
[37]
Zhang J, Sun P, Kong T, et al. Tributyltin promoted hepatic steatosis in zebrafish (Danio rerio) and the molecular pathogenesis involved[J]. Aquatic Toxicology, 2016,170:208-215.
[38]
Papenfort K, Sun Y, Miyakoshi M, et al. Small RNA-mediated activation of sugar phosphatase mRNA regulates glucose homeostasis[J]. Cell, 2013,153(2):426-437.
[39]
Nagy C, Einwallner E. Study of in vivo glucose metabolism in high-fat diet-fed mice using oral glucose tolerance test (OGTT) and insulin tolerance test (ITT)[J]. Journal of Visualized Experiments, 2018,131:e56672
