Abstract
Acrylamide is a commonly used industrial chemical that is known to be neurotoxic to mammals. However, its developmental toxicity is rarely assessed in mammalian models because of the cost and complexity involved. We used zebrafish to assess the neurotoxicity, developmental and behavioral toxicity of acrylamide. At 6 h post fertilization, zebrafish embryos were exposed to four concentrations of acrylamide (10, 30, 100, or 300 mg/L) in a medium for 114 h. Acrylamide caused developmental toxicity characterized by yolk retention, scoliosis, swim bladder deficiency, and curvature of the body. Acrylamide also impaired locomotor activity, which was measured as swimming speed and distance traveled. In addition, treatment with 100 mg/L acrylamide shortened the width of the brain and spinal cord, indicating neuronal toxicity. In summary, acrylamide induces developmental toxicity and neurotoxicity in zebrafish. This can be used to study acrylamide neurotoxicity in a rapid and cost-efficient manner.
Highlights
Acrylamide is a water-soluble alkene primarily used to synthesize polyacrylamide for personal care products, and is used in various chemical industries, wastewater treatment processes, chemical grouting, and soil conditioning [1,2]
The developmental toxicity of acrylamide has been characterized in laboratory animals, but developmental neurotoxicity has not, highlighting the need for validated animal models of acrylamide-induced developmental neurotoxicity for the clinical management of patients affected by occupational exposure to acrylamide [14,15]
There is a lack of information on acrylamide-induced developmental toxicity in rodents because of the associated cost
Summary
Acrylamide is a water-soluble alkene primarily used to synthesize polyacrylamide for personal care products, and is used in various chemical industries, wastewater treatment processes, chemical grouting, and soil conditioning [1,2]. Acrylamide is a common ingredient in plant-based foods, such as potato and grain products and in roasted coffee [3,4]. Human exposure to acrylamide results in neurotoxicity that is characterized by lethargy, skeletal muscle weakness, gait abnormalities, weight loss, ataxia, numbness of the extremities, and polyneuropathy [6,10]. Acrylamide neurotoxicity has been associated with central–peripheral distal axonopathy [11,12]. Molecular initiating events of acrylamide neurotoxicity include formation of adducts with sulfhydryl thiolate sites involved in synaptic vesicle recycling in vesicle docking (synaptotagmin, synaptophysin, and syntaxin), vesicle priming (complexin 2), SNARE (SNAP Receptor) core dissolution (N-ethylmaleimide-sensitive factor), endocytosis (clathrin), neurotransmitter re-uptake (membrane dopamine transporter), and vesicular storage (vesicular monoamine transporter) at nerve terminals [13]. The developmental toxicity of acrylamide has been characterized in laboratory animals, but developmental neurotoxicity has not, highlighting the need for validated animal models of acrylamide-induced developmental neurotoxicity for the clinical management of patients affected by occupational exposure to acrylamide [14,15]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
