Natural Resources, School of


Date of this Version



Wang, Jiayi. 2015. Acute Toxicity of β-N-Methylamino-L-Alanine (BMAA) to Fathead Minnow (Pimephales promelas) and Zebrafish (Danio rerio). M.S. Thesis, University of Nebraska. 103 p.


A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science, Major: Natural Resource Sciences, Under the Supervision of Professors Kyle Hoagland and Daniel Snow. Lincoln, Nebraska: May, 2015

Copyright (c) 2015 Jiayi Wang


β-N-methylamino-L-alanine (BMAA) is a neurotoxic amino acid produced by most species of cyanobacteria. Exposure to BMAA has been hypothesized as a cause of ALS and possibly Parkinson’s and Alzheimer’s diseases for several decades. Both in vitro and in vivo experiments revealed that exposure to elevated concentrations of BMAA can damage motor neurons and cause motor dysfunctions. However, the exact mechanism of BMAA-induced neurotoxicity has not been well understood.

Based on the available literature and in spite of its water-soluble and non-protein nature, BMAA appears to be able to bioaccumulate in organisms. The ubiquity of cyanobacteria and the potential for bioaccumulation of BMAA, arouse wide human health concern. Previous investigations into toxicity of BMAA mainly focused on various mammalian test models, including rats, mice and primates. However, the toxic effect of BMAA on aquatic organisms has attracted limited attention. Due to the potential for widespread BMAA production in aquatic ecosystems, it is important to understand the toxicity of BMAA in aquatic organisms, such as fish, from an ecotoxicological perspective

Because limited information exists about how exposure to BMAA influences fish, we investigated the acute toxic effect of β-N-methylamino-L-alanine (BMAA) on two widely adopted model fish: fathead minnow (Pimephales promelas) and zebrafish (Danio rerio). The 96 h toxicity tests revealed that BMAA is not acutely lethal to fathead minnow (juveniles: 96 h LC50 > 10 mg/L; larvae: 96 h LC50 > 10 mg/L) or zebrafish (larvae: 96 h LC50 > 10 mg/L; embryos: 10-day LC50 > 100 mg/L) at concentrations well above those reported in the literature. However, exposure to BMAA at 100 mg/L significantly affected the heart rate of zebrafish embryos. Additionally, in the zebrafish embryo-larvae behavioral assay, a range of locomotor function anomalies in zebrafish embryo-larvae exposed to BMAA were observed. On one hand, BMAA was found to accelerate the onset of spontaneous contractions and enhanced touch-evoked contractions. On the other hand, BMAA reduced performance in touch-evoked escape, free swimming and startle response.

To our knowledge, we are the first to investigate the acute toxicity of BMAA in fathead minnow and its behavioral effects on fish. The finding that BMAA influenced locomotor behaviors of fish is of both neurotoxicological and ecological importance.

Advisors: Kyle Hoagland and Daniel Snow