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Neurotoxicol Teratol. 2012 Nov-Dec;34(6):581-6. doi: 10.1016/j.ntt.2012.09.001. Epub 2012 Sep 10.

Developmental lead acetate exposure induces embryonic toxicity and memory deficit in adult zebrafish.

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  • 1Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, Wenzhou Medical College, Wenzhou 325035, PR China.

Abstract

Lead is a persistent metal and commonly present in our living environment. The present study was aimed to investigate lead-induced embryonic toxicity, behavioral responses, and adult learning/memory deficit in zebrafish. Lead acetate (PbAc) induced malformations such as uninflated swim bladder, bent spine and yolk-sac edema with an EC₅₀ of 0.29 mg/L at 120 h post fertilization (hpf). Spontaneous movement as characterized by tail bend frequency was significantly altered in zebrafish embryos following exposure to PbAc. Behavior assessment demonstrated that lead exposure changed behavioral responses in zebrafish larvae, as hyperactivity was detected within the first minute of light-to-dark transition in the fish exposed to PbAc from 6 to 96 hpf, and a different dose-dependent change was found in swimming speeds in the dark and in the light at 120 hpf following lead exposure. Learning/memory task assay showed that embryos exposed to PbAc from 6 to 120 hpf developed learning/memory deficit at adulthood as exhibited by a significant decrease in accuracy rate to find the food and a significant increase in finding time. Overall, our results suggested that low dose of developmental lead exposure resulted in embryonic toxicity, behavioral alteration, and adult learning/memory deficit in zebrafish.

Copyright © 2012 Elsevier Inc. All rights reserved.

[PubMed - indexed for MEDLINE]
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