Dopaminergic dysregulation and impaired associative learning behavior in zebrafish during chronic dietary exposure to selenium

Naderi, Mohammad; Salahinejad, Arash; Ferrari, Maud C. O.; Niyogi, Som; Chivers, Douglas P.

doi:10.1016/j.envpol.2018.02.033

Cited by 45 publications

(25 citation statements)

References 63 publications

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“…The DA signaling pathway is sensitive to neurotoxins in zebrafish . In accordance with the present study, chronic dietary Se-Met exposure leads to the dysfunction of the DA signaling pathway in zebrafish, possibly because of oxidative stress. , It is believed that mediation of the synthesis and metabolism of neurotransmitters in brain is complicated . For the DA signaling pathway, tyrosine and 3,4-dihydroxyphenylalanine (DOPA) are the two precursors for the biosynthesis of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) are the two major metabolites of DA. , In the present study, the decreased concentrations of DA, its precursors and metabolites (Figure A) suggest the DA pathway is markedly affected by dietary Se-Met in zebrafish.…”

Section: Resultssupporting

confidence: 82%

“…59 In accordance with the present study, chronic dietary Se-Met exposure leads to the dysfunction of the DA signaling pathway in zebrafish, possibly because of oxidative stress. 34,35 It is believed that mediation of the synthesis and metabolism of neurotransmitters in brain is complicated. 59 For the DA signaling pathway, tyrosine and 3,4dihydroxyphenylalanine (DOPA) are the two precursors for the biosynthesis of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) are the two major metabolites of DA.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

“…The experiment had four treatments, i.e., control (C), 3 (low: L), 10 (medium: M), and 30 (high: H) μg Se/g dry weight (dw). These concentrations were chosen according to previous studies (also see these references regarding the environmental relevance of these concentrations). ,, For diet preparation, an appropriate amount of seleno- l -methionine (Se-Met, purity >98%, Ryon Biological Technology Co., Ltd., Shanghai, China) was dissolved in 300 mL of deionized distilled water in a 1 L beaker to make a stock solution for each treatment (no Se-Met addition for C). This stock solution was mixed with the calculated amount of fish diet with a diameter of 0.36 mm (Otohime, Nissin Feed Products Co., Ltd., Japan) for each treatment.…”

Section: Methodsmentioning

confidence: 99%

“…Fish behaviors are important for their survival and population stability in the wild. , Swimming performance, locomotion, aggression, courting, feeding, and predator avoidance can all be impacted by exposure to toxicants, thereby affecting many aspects of fish physiological functions and impair growth and reproduction, leading ultimately to diminished fish populations. , Several groups have recommended that behavioral endpoints be incorporated into the risk assessment of chemical pollution. , Fish behaviors are often controlled by neurotransmitters secreted from areas of the central and peripheral nervous systems . As for Se, recent data have shown that Se-Met could affect the dopamine (DA) and serotonin (5-HT) in adult zebrafish. − However, mechanisms and key events associated with the effects of Se-Met on neurotransmitters and the associated behaviors in fish are unclear.…”

Section: Introductionmentioning

confidence: 99%

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Dietary Seleno-l-Methionine Causes Alterations in Neurotransmitters, Ultrastructure of the Brain, and Behaviors in Zebrafish (Danio rerio)

Xiao

Liu

et al. 2021

Environ. Sci. Technol.

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Elevated concentrations of dietary selenium (Se) cause abnormalities and extirpation of fish inhabiting in Se-contaminated environments. However, its effect on fish behavior and the underlying mechanisms remain largely unknown. In this study, two-month-old zebrafish (Danio rerio) was fed seleno-l-methionine (Se-Met) at environmentally relevant concentrations (i.e., control (2.61), low (5.43), medium (12.16), and high (34.61) μg Se/g dry weight (dw), respectively, corresponding to the C, L, M, and H treatments) for 60 days. Targeted metabolomics, histopathological, and targeted transcriptional endpoints were compared to behavioral metrics to evaluate the effects of dietary exposure to Se-Met . The results showed that the levels of total Se and malondialdehyde in fish brains were increased in a dose-dependent pattern. Meanwhile, mitochondrial damages and decreased activities of the mitochondria respiratory chain complexes were observed in the neurons at the M and H treatments. In addition, dietary Se-Met affected neurotransmitters, metabolites, and transcripts of the genes associated with the dopamine, serotonin, gamma-aminobutyric acid, acetylcholine, and histamine signaling pathways in zebrafish brains at the H treatments. The total swimming distance and duration in the Novel Arm were lowered in fish from the H treatment. This study has demonstrated that dietary Se-Met affects the ultrastructure of the zebrafish brain, neurotransmitters, and associated fish behaviors and may help enhance adverse outcome pathways for neurotransmitter-behavior key events in zebrafish.

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Section: Resultssupporting

confidence: 82%

Section: ■ Results and Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dietary Seleno-l-Methionine Causes Alterations in Neurotransmitters, Ultrastructure of the Brain, and Behaviors in Zebrafish (Danio rerio)

Xiao

Liu

et al. 2021

Environ. Sci. Technol.

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“…Conversely, increased levels of selenium in cerebrospinal fluid and plasma have been reported in PD patients [ 192 , 193 ]. Chronic exposure to selenium enhances oxidative stress in the brain and leads to cognitive impairment in animal models [ 194 , 195 ]. The underlying mechanism for these findings is unclear; however, evidence suggests that either a deficiency or excess of selenium may contribute to neurodegeneration or conversely PD pathology may impair mobilization of selenium in neurons.…”

Section: Neuroprotective Dietary Antioxidantsmentioning

confidence: 99%

Dietary Antioxidants and Parkinson’s Disease

Park

Ellis

2020

Antioxidants

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by the depletion of dopaminergic neurons in the basal ganglia, the movement center of the brain. Approximately 60,000 people are diagnosed with PD in the United States each year. Although the direct cause of PD can vary, accumulation of oxidative stress-induced neuronal damage due to increased production of reactive oxygen species (ROS) or impaired intracellular antioxidant defenses invariably occurs at the cellular levels. Pharmaceuticals such as dopaminergic prodrugs and agonists can alleviate some of the symptoms of PD. Currently, however, there is no treatment to halt the progression of PD pathology. Due to the nature of PD, a long and progressive neurodegenerative process, strategies to prevent or delay PD pathology may be well suited to lifestyle changes like dietary modification with antioxidant-rich foods to improve intracellular redox homeostasis. In this review, we discuss cellular and genetic factors that increase oxidative stress in PD. We also discuss neuroprotective roles of dietary antioxidants including vitamin C, vitamin E, carotenoids, selenium, and polyphenols along with their potential mechanisms to alleviate PD pathology.

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