Zebrafish as a model system for biomedical studies

Belyaeva, N. F.; Kashirtseva, V. N.; Medvedeva, N. V.; Khudoklinova, Yulia Yu.; Ipatova, O. M.; Archakov, Alexander I.

doi:10.1134/s1990750809040039

Cited by 14 publications

(9 citation statements)

References 41 publications

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“…Confirming data from the literature [25], even the lowest concentrations of adriamycin produced devastating effects if administered in the first 3 hours after fertilization, with death of all embryos by cardiac arrest, associated to head abnormalities and impaired eye formation.…”

Section: Discussionsupporting

confidence: 69%

“…Mechanistically, it has been hypothesized that cardiotoxicity is mediated by activation of free radicals-induced mitochondrial damage, which in turn imposes oxidative stress on the heart and triggers apoptotic cardiomyocyte death [22], [23]. In zebrafish embryos, cardiotoxicity has been reported with adriamycin concentrations higher than 40 µM [24] and manifests with loss of contractility and pericardial edema [25], [26].…”

Section: Resultsmentioning

confidence: 99%

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Podocyte Developmental Defects Caused by Adriamycin in Zebrafish Embryos and Larvae: A Novel Model of Glomerular Damage

et al. 2014

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The zebrafish pronephros is gaining popularity in the nephrology community, because embryos are easy to cultivate in multiwell plates, allowing large number of experiments to be conducted in an in vivo model. In a few days, glomeruli reach complete development, with a structure that is similar to that of the mammalian counterpart, showing a fenestrated endothelium and a basement membrane covered by the multiple ramifications of mature podocytes. As a further advantage, zebrafish embryos are permeable to low molecular compounds, and this explains their extensive use in drug efficacy and toxicity experiments. Here we show that low concentrations of adriamycin (i.e. 10 and 20 µM), when dissolved in the medium of zebrafish embryos at 9 hours post-fertilization and removed after 48 hours (57 hpf), alter the development of podocytes with subsequent functional impairment, demonstrated by onset of pericardial edema and reduction of expression of the podocyte proteins nephrin and wt1. Podocyte damage is morphologically confirmed by electron microscopy and functionally supported by increased clearance of microinjected 70 kDa fluorescent dextran. Importantly, besides pericardial edema and glomerular damage, which persist and worsen after adriamycin removal from the medium, larvae exposed to adriamycin 10 and 20 µM do not show any myocardiocyte alterations nor vascular changes. The only extra-renal effect is a transient delay of cartilage formation that rapidly recovers once adriamycin is removed. In summary, this low dose adriamycin model can be applied to analyze podocyte developmental defects, such as those observed in congenital nephrotic syndrome, and can be taken in consideration for pharmacological studies of severe early podocyte injury.

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Section: Discussionsupporting

confidence: 69%

Section: Resultsmentioning

confidence: 99%

Podocyte Developmental Defects Caused by Adriamycin in Zebrafish Embryos and Larvae: A Novel Model of Glomerular Damage

et al. 2014

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“…As a result, the variability of in vitro respiratory burst assay is usually high. The zebrafish is widely used as a model system in biomedical research because of its rapid rate of reproduction, the optical clarity of its embryos and the wealth of genetic information [33]. Recently, respiratory burst in vivo assay has been established in zebrafish using zebrafish embryos as the sources of phagocytic cells [19].…”

Section: Discussionmentioning

confidence: 99%

Xyloketal B Exhibits Its Antioxidant Activity through Induction of HO-1 in Vascular Endothelial Cells and Zebrafish

et al. 2013

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We previously reported that a novel marine compound, xyloketal B, has strong antioxidative actions in different models of cardiovascular diseases. Induction of heme oxygenase-1 (HO-1), an important endogenous antioxidant enzyme, has been considered as a potential therapeutic strategy for cardiovascular diseases. We here investigated whether xyloketal B exhibits its antioxidant activity through induction of HO-1. In human umbilical vein endothelial cells (HUVECs), xyloketal B significantly induced HO-1 gene expression and translocation of the nuclear factor-erythroid 2-related factor 2 (Nrf-2) in a concentration- and time-dependent manner. The protection of xyloketal B against angiotensin II-induced apoptosis and reactive oxygen species (ROS) production could be abrogated by the HO-1 specific inhibitor, tin protoporphyrin-IX (SnPP). Consistently, the suppressive effects of xyloketal B on NADPH oxidase activity could be reversed by SnPP in zebrafish embryos. In addition, xyloketal B induced Akt and Erk1/2 phosphorylation in a concentration- and time-dependent manner. Furthermore, PI3K inhibitor LY294002 and Erk1/2 inhibitor U0126 suppressed the induction of HO-1 and translocation of Nrf-2 by xyloketal B, whereas P38 inhibitor SB203580 did not. In conclusion, xyloketal B can induce HO-1 expression via PI3K/Akt/Nrf-2 pathways, and the induction of HO-1 is mainly responsible for the antioxidant and antiapoptotic actions of xyloketal B.

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“…Для оценки безопасности наночастиц нами была выбрана модель аквариумной рыбки Danio rerio (зебрафиш), которая щироко используется в биомедицинских исследованиях для оценки токсичности потенциальных лекарственных средств [6]. В последние годы эта модель все чаще используется для исследования токсичности различных НЧ [2,7,8].…”

Section: литературный обзорunclassified

Исследование Токсичности Наночастиц Золота И Алмазов

Беляева¹,

Золотарёв²,

Kashirtseva³

et al. 2014

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Проведено исследование токсичности наночастиц золота и алмазов на ранних стадиях развития зебрафиш (Danio rerio). Токсического действия нанозолота выявлено не было. В то же время, действие наноалмазов в течение 7 суток вызывало как летальные эффекты (LC 50 =104±18 мг/л), так и отклонения в развитии Ключевые слова: наночастицы, наноалмазы, нанозолото, токсические эффекты, модельные системы, зебрафиш, эмбрионы, личинки Toxicity of gold and diamond nanoparticles in zebrafish (Danio rerio) early life stages has been assessed. No toxic action of nanogold has been found. At the same time, nanodiamonds caused lethal effects (LC 50 is 104±18 mg/L) as well as developmental abnormalities during 7 days

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Zebrafish as a model system for biomedical studies

Cited by 14 publications

References 41 publications

Podocyte Developmental Defects Caused by Adriamycin in Zebrafish Embryos and Larvae: A Novel Model of Glomerular Damage

Podocyte Developmental Defects Caused by Adriamycin in Zebrafish Embryos and Larvae: A Novel Model of Glomerular Damage

Xyloketal B Exhibits Its Antioxidant Activity through Induction of HO-1 in Vascular Endothelial Cells and Zebrafish

Исследование Токсичности Наночастиц Золота И Алмазов

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