Ethanol-dependent toxicity in zebrafish is partially attenuated by antioxidants

Reimers, Mark J.; Du, Jane La; Periera, Cliff B.; Giovanini, Jack; Tanguay, Robert L.

doi:10.1016/j.ntt.2006.05.007

Cited by 107 publications

(81 citation statements)

References 41 publications

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“…24 Embryos were staged according to Kimmel et al and at *4 h postfertilization, the chorion was enzymatically digested using pronase (63.6 mg/mL, >3.5 U/mg, P5147; Sigma-Aldrich, St. Louis, MO) assisted by a customautomated instrument. 25,26 Embryos were maintained in 1· strength E2 embryo medium sans methylene blue (ZIRC protocols, http://zebrafish.org/documents/protocols/pdf/Fish _Nursery/E2_solution.pdf) under a 14-h light-10-h dark photoperiod at 28°C -1°C.…”

Section: Zebrafish Husbandrymentioning

confidence: 99%

Developing a Novel Embryo–Larval Zebrafish Xenograft Assay to Prioritize Human Glioblastoma Therapeutics

et al. 2016

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Glioblastoma is an aggressive brain cancer requiring improved treatments. Existing methods of drug discovery and development require years before new therapeutics become available to patients. Zebrafish xenograft models hold promise for prioritizing drug development. We have developed an embryo-larval zebrafish xenograft assay in which cancer cells are implanted in a brain microenvironment to discover and prioritize compounds that impact glioblastoma proliferation, migration, and invasion. We illustrate the utility of our assay by evaluating the well-studied, phosphatidylinositide 3-kinase inhibitor LY294002 and zinc oxide nanoparticles (ZnO NPs), which demonstrate selective cancer cytotoxicity in cell culture, but the in vivo effectiveness has not been established. Exposures of 3.125-6.25 lM LY294002 significantly decreased proliferation up to 34% with concentration-dependent trends. Exposure to 6.25 lM LY294002 significantly inhibited migration/invasion by *27% within the glioblastoma cell mass (0-80 lm) and by *32% in the next distance region (81-160 lm). Unexpectedly, ZnO enhanced glioblastoma proliferation by *19% and migration/invasion by *35% at the periphery of the cell mass (161+ lm); however, dissolution of these NPs make it difficult to discern whether this was a nano or ionic effect. These results demonstrate that we have a short, relevant, and sensitive zebrafishbased assay to aid glioblastoma therapeutic development.

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Section: Zebrafish Husbandrymentioning

confidence: 99%

Developing a Novel Embryo–Larval Zebrafish Xenograft Assay to Prioritize Human Glioblastoma Therapeutics

et al. 2016

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“…Water consisted of reverse osmosis (RO) water supplemented with a commercially available salt solution (0.6% Instant Ocean®). Zebrafish were spawned and embryos were collected and staged (Reimers et al, 2006). The chorion, an acellular envelope surrounding the embryo, was removed via enzymatic reaction with pronase at 24 hours post fertilization (hpf) as described previously (Usenko et al, 2007).…”

Section: General Exposure Protocolmentioning

confidence: 99%

“…This endpoint serves as an early indicator of perturbation based on previous evaluations that showed significant cell death could be detected after only 12 hours of exposure to C 60 (Reimers et al, 2006). Since cellular death was evaluated in whole embryos, potential targets of toxi city could be identified.…”

Section: Cellular Death Assaysmentioning

confidence: 99%

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Fullerene C60 exposure elicits an oxidative stress response in embryonic zebrafish

Usenko

Harper

Tanguay

2008

Toxicology and Applied Pharmacology

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Due to its unique physicochemical and optical properties, C 60 has raised interest in commercialization for a variety of products. While several reports have determined this nanomaterial to act as a powerful antioxidant, many other studies have demonstrated a strong oxidative potential through photoactivation. To directly address the oxidative potential of C 60 , the effects of light and chemical supplementation and depletion of glutathione (GSH) on C 60 -induced toxicity were evaluated. Embryonic zebrafish were used as a model organism to examine the potential of C 60 to elicit oxidative stress responses. Reduced light during C 60 exposure significantly decreased mortality and the incidence of fin malformations and pericardial edema at 200 and 300 ppb C 60 . Embryos co-exposed to the glutathione precursor, N-acetylcysteine (NAC), also showed reduced mortality and pericardial edema; however, fin malformations were not reduced. Conversely, co-exposure to the GSH synthesis inhibitors, butathionine sulfoximine (BSO) and diethyl maleate (DEM), increased the sensitivity of zebrafish to C 60 exposure. Co-exposure of C 60 or its hydroxylated derivative, C 60 (OH) 24 , with H 2 O 2 resulted in increased mortality along the concentration gradient of H 2 O 2 for both materials. Microarrays were used to examine the effects of C 60 on the global gene expression at two time points, 36 and 48 hours post fertilization (hpf). At both life stages there were alterations in the expression of several key stress response genes including glutathione-S-transferase, glutamate cysteine ligase, ferritin, α-tocopherol transport protein and heat shock protein 70. These results support the hypothesis that C 60 induces oxidative stress in this model system.

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“…A study in mice (Tenkova et al, 2003) has shown the apoptogenic potential of acute ethanol intoxication in the visual system during synaptogenesis. In zebrafish, cell death within the CNS and the eye takes place following early embryonic ethanol exposure Reimers et al, 2006), suggesting that ethanol may cause its deleterious effects by a similar mechanism across vertebrate species. However, apoptosis specifically within the retina has not been studied following ethanol exposure during retinal neurogenesis, and the remaining mechanisms (decreased proliferation, decreased cell differentiation) have not been pursued.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms for persistent microphthalmia following ethanol exposure during retinal neurogenesis in zebrafish embryos

2007

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The exposure of the developing human embryo to ethanol results in a spectrum of disorders involving multiple organ systems, including the visual system. One common phenotype seen in humans exposed to ethanol in utero is microphthalmia. The objective of this study was to describe the effects of ethanol during retinal neurogenesis in a model organism, the zebrafish, and to pursue the potential mechanisms by which ethanol causes microphthalmia. Zebrafish embryos were exposed to 1% or 1.5% ethanol from 24 to 48 h after fertilization, a period during which the retinal neuroepithelium undergoes rapid proliferation and differentiation to form a laminated structure composed of different retinal cell types. Ethanol exposure resulted in significantly reduced eye size immediately following the treatment, and this microphthalmia persisted through larval development. This reduced eye size could not entirely be accounted for by the accompanying general delay in embryonic development. Retinal cell death was only slightly higher in ethanol-exposed embryos, although cell death in the lens was extensive in some of these embryos, and lenses were significantly reduced in size as compared to those of control embryos. The initiation of retinal neurogenesis was not affected, but the subsequent waves of cell differentiation were markedly reduced. Even cells that were likely generated after ethanol exposure-rod and cone photoreceptors and Müller glia-were delayed in their expression of cell-specific markers by at least 24 h. We conclude that ethanol exposure over the time of retinal neurogenesis resulted in persistent microphthalmia due to a combination of an overall developmental delay, lens abnormalities, and reduced retinal cell differentiation.

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Ethanol-dependent toxicity in zebrafish is partially attenuated by antioxidants

Cited by 107 publications

References 41 publications

Developing a Novel Embryo–Larval Zebrafish Xenograft Assay to Prioritize Human Glioblastoma Therapeutics

Developing a Novel Embryo–Larval Zebrafish Xenograft Assay to Prioritize Human Glioblastoma Therapeutics

Fullerene C60 exposure elicits an oxidative stress response in embryonic zebrafish

Mechanisms for persistent microphthalmia following ethanol exposure during retinal neurogenesis in zebrafish embryos

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