Arsenic and selenium toxicity and their interactive effects in humans.
Arsenic (As) and selenium (Se) are unusual metalloids as they both induce and cure cancer. They both cause carcinogenesis, pathology, cytotoxicity, and genotoxicity in humans, with reactive oxygen species playing an important role. While As induces adverse effects by decreasing DNA methylation and affecting protein 53 expression, Se induces adverse effects by modifying thioredoxin reductase. However, they can react with glutathione and S-adenosylmethionine by forming an As-Se complex, which can be secreted extracellularly. We hypothesize that there are two types of interactions between As and Se. At low concentration, Se can decrease As toxicity via excretion of As-Se compound [(GS3)2AsSe](-), but at high concentration, excessive Se can enhance As toxicity by reacting with S-adenosylmethionine and glutathione, and modifying the structure and activity of arsenite methyltransferase. This review is to summarize their toxicity mechanisms and the interaction between As and Se toxicity, and to provide suggestions for future investigations.
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, Jiangsu 210046, China.
Hong-Jie
HJ
Sun
Horticultural Sciences Department, University of Florida, Gainesville, FL 32611, United States.
Bala
B
Rathinasabapathi
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, Jiangsu 210046, China.
Bing
B
Wu
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, Jiangsu 210046, China.
Jun
J
Luo
Suzhou Health College, Suzhou, Jiangsu 215000, China.
Li-Ping
LP
Pu
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, Jiangsu 210046, China; Soil and Water Science Department, University of Florida, Gainesville, FL 32611, USA. Electronic address: lqma@ufl.edu.
Lena Q
LQ
Ma
D000818:Animals; D001151:Arsenic / Q000493:pharmacokinetics / Q000633:toxicity*; D003603:Cytotoxins / Q000493:pharmacokinetics / Q000633:toxicity; D004347:Drug Interactions; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D046911:Macromolecular Substances / Q000378:metabolism* / Q000633:toxicity; D053858:Metabolic Networks and Pathways / Q000502:physiology; D008780:Methyltransferases / Q000378:metabolism; D008956:Models, Chemical; D009153:Mutagens / Q000493:pharmacokinetics / Q000633:toxicity; D051381:Rats; D012643:Selenium / Q000493:pharmacokinetics / Q000633:toxicity*
D003603:Cytotoxins; D046911:Macromolecular Substances; D009153:Mutagens; D008780:Methyltransferases; C116338:arsenite methyltransferase; D005978:Glutathione; D012643:Selenium; D001151:Arsenic
Antagonistic; Arsenic; Arsenite methyltransferase; Glutathione; Selenium; Synergistic