Neurodegeneration in zebrafish embryos and adults after cadmium exposure

Antonio, Miguel; Capriello, Teresa; Grimaldi, Maria Consiglio; Schiano, Valentina; Ferrandino, Ida

doi:10.4081/ejh.2017.2833

Cited by 45 publications

(17 citation statements)

References 29 publications

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“…In this study, 24 h exposure of Cd exhibited alteration of oxidative stress markers (Cu/Zn-SOD, CAT, and iNOS) and brain inflammatory markers (COX-2, NF-κB, Keep1, COX-2) at all transcription, translation, and post-translation levels [175]. In line with similar results, Cd had also reported altering brain (glial and neuronal cells) and mitochondrial morphology in zebrafish on incubation at a lower dose [176,177]. Cadmium induced oxidative stress may damage brain lipids and protein, but it's interesting to observe that a well-known toxicant like chlorpyrifos has acted like an antagonistic to Cd [178].…”

Section: Cadmium (Cd)supporting

confidence: 87%

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Patwa

Flora

2020

IJMS

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Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic disorders, cancer, etc. Small blood vessels are highly vulnerable to heavy metals as they are directly exposed to the blood circulatory system, which has comparatively higher concentration of heavy metals than other organs. Cerebral small vessel disease (CSVD) is an umbrella term used to describe various pathological processes that affect the cerebral small blood vessels and is accepted as a primary contributor in associated disorders, such as dementia, cognitive disabilities, mood disorder, and ischemic, as well as a hemorrhagic stroke. In this review, we discuss the possible implication of heavy metals/metalloid exposure in CSVD and its associated disorders based on in-vitro, preclinical, and clinical evidences. We briefly discuss the CSVD, prevalence, epidemiology, and risk factors for development such as genetic, traditional, and environmental factors. Toxic effects of specific heavy metal/metalloid intoxication (As, Cd, Pb, Hg, and Cu) in the small vessel associated endothelium and vascular dysfunction too have been reviewed. An attempt has been made to highlight the possible molecular mechanism involved in the pathophysiology, such as oxidative stress, inflammatory pathway, matrix metalloproteinases (MMPs) expression, and amyloid angiopathy in the CSVD and related disorders. Finally, we discussed the role of cellular antioxidant defense enzymes to neutralize the toxic effect, and also highlighted the potential reversal strategies to combat heavy metal-induced vascular changes. In conclusion, heavy metals in small vessels are strongly associated with the development as well as the progression of CSVD. Chelation therapy may be an effective strategy to reduce the toxic metal load and the associated complications.

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Section: Cadmium (Cd)supporting

confidence: 87%

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Patwa

Flora

2020

IJMS

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“…It is reported that long‐term exposure (from days to weeks) to certain metals, including Cd, affects several processes and behaviors (LeFauve & Connaughton, 2017; Monaco et al., 2017) including swimming abilities in developing larvae (Capriello et al., 2019). On another hand, brief Cd exposure (up to 3 hr) during embryonic development can inhibit specifically the olfactory system, leading to the activation of cell death pathways in the larval olfactory epithelium (Blechinger et al., 2007).…”

Section: Discussionmentioning

confidence: 99%

Short‐term exposure to the simple polyphenolic compound gallic acid induces neuronal hyperactivity in zebrafish larvae

Annona

Tarallo

Nittoli

et al. 2020

Eur J of Neuroscience

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A growing body of evidence suggests that the biological effects of polyphenols are not restricted to antioxidant activity, but they exert a wide range of modulatory effects on metabolic pathways, cellular signaling and gene expression. In this study, we tested the minimum safe concentration of gallic acid (GA) in 72 hpf zebrafish larvae in order to evaluate the effects on the central nervous system and the behavioral response. We showed that a short exposure (30 min) induces the depletion of the two main excitatory and inhibitory neurotransmitters, Glu and GABA, respectively, in the larval nervous system. The acute impairment of GABAergic‐glutamatergic balance was paralleled by an increase of the fosab neuronal activity marker in specific brain areas, such as the forebrain, olfactory bulbs, pallial area, ventral midbrain, tegmentum, and the medulla oblongata ventral area. The neuronal excitation was mirrored by the increased cumulative motor response. The inhibition of the olfactory epithelium with brief cadmium exposition suggests a direct involvement of olfaction in the larvae response to GA. Our results demonstrate that a brief exposure to GA induces motoneuronal hyperexcitability in zebrafish. The behavioral response was probably elicited through the activation of an odorous, or chemical, stimulus. The specificity of the activated neuronal territories suggests the involvement of additional signaling pathways. Although the underlying molecular mechanisms remain to be elucidated, our data support the hypothesis that GA acts as an excitatory molecule, capable of inducing a specific nerve response. These results offer a new vision on potential effects of GA.

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“…Cadmium (Cd) exposure produces significant olfactory epithelium alterations, including reduction in OSNs and disruption in olfactory epithelium neurogenesis, through an increase in the generation of reactive oxygen species. These olfactory alterations correlate with a long-term decrease in alarm and avoidance responses [88,114,115,116,117,118,119]. Exposure to Copper (Cu) causes marked OSN death, with a preferential loss of ciliated in comparison to microvillous OSNs; impairs the transcription of a wide variety of genes involved in olfactory processing, such as ORs and ionic channels; and reduces the recognition of bile salts while impairing odor-mediated alarm responses [120,121,122,123,124].…”

Section: The Olfactory System Of Zebrafish As a Model Of Neuroplasmentioning

confidence: 99%

The Olfactory System of Zebrafish as a Model for the Study of Neurotoxicity and Injury: Implications for Neuroplasticity and Disease

Calvo-Ochoa

Byrd-Jacobs

2019

IJMS

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The olfactory system, composed of the olfactory organs and the olfactory bulb, allows organisms to interact with their environment and through the detection of odor signals. Olfaction mediates behaviors pivotal for survival, such as feeding, mating, social behavior, and danger assessment. The olfactory organs are directly exposed to the milieu, and thus are particularly vulnerable to damage by environmental pollutants and toxicants, such as heavy metals, pesticides, and surfactants, among others. Given the widespread occurrence of olfactory toxicants, there is a pressing need to understand the effects of these harmful compounds on olfactory function. Zebrafish (Danio rerio) is a valuable model for studying human physiology, disease, and toxicity. Additionally, the anatomical components of the zebrafish olfactory system are similar to those of other vertebrates, and they present a remarkable degree of regeneration and neuroplasticity, making it an ideal model for the study of regeneration, reorganization and repair mechanisms following olfactory toxicant exposure. In this review, we focus on (1) the anatomical, morphological, and functional organization of the olfactory system of zebrafish; (2) the adverse effects of olfactory toxicants and injury to the olfactory organ; and (3) remodeling and repair neuroplasticity mechanisms following injury and degeneration by olfactory toxicant exposure.

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Neurodegeneration in zebrafish embryos and adults after cadmium exposure

Cited by 45 publications

References 29 publications

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

Short‐term exposure to the simple polyphenolic compound gallic acid induces neuronal hyperactivity in zebrafish larvae

The Olfactory System of Zebrafish as a Model for the Study of Neurotoxicity and Injury: Implications for Neuroplasticity and Disease

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