Mitochondria as targets for toxicity and metabolism research using zebrafish

Azevedo, Rafael David Souto de; Falcão, Kívia Vanessa Gomes; Amaral, Ian P.G.; Leite, Antônio Cesar Rios; Bezerra, Ranilson S.

doi:10.1016/j.bbagen.2020.129634

Cited by 24 publications

(4 citation statements)

References 53 publications

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“…It has been shown for more than a decade that zebrafish cells respond rapidly to production. Zebrafish can now be used to solve problems related to in vivo or real-time REDOX states, oxidative stress, ROS production, and apoptosis, especially because of the similarity of mitochondrial dynamics between zebrafish and other animal models …”

Section: Resultsmentioning

confidence: 99%

Selective Antitumor Effect and Lower Toxicity of Mitochondrion-Targeting Derivatization of Triptolide

Xing,

Liu,

Zhang

et al. 2024

J. Med. Chem.

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Triptolide has a significant antitumor activity, but its toxicity limits its clinical application. As the mitochondriontargeting strategy showed an advantage in selective antitumor effect based on the higher mitochondrial membrane potential (MMP) in tumor cells than normal cells, the lipophilic cations triphenylphosphonium and E-4-(1H-indol-3-yl vinyl)-N-methylpyridinium iodide (F16) were selected as targeting carriers for structural modification of triptolide. The derivatives bearing F16 generally retained most antitumor activities, overcame its inhibition plateau phenomena, and enhanced its selective antitumor effect in lung cancer. The representative derivative F9 could accumulate in the mitochondria of NCI-H1975 cells, inducing apoptosis and a dose-dependent increase in intracellular reactive oxygen species and reducing MMP. Moreover, no effects were observed in normal cells BEAS-2B. In vivo studies showed that the developmental, renal, and liver toxicities of F9 to zebrafish were significantly lower than those of triptolide. This study provides a promising idea to relieve the toxicity problem of triptolide.

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Section: Resultsmentioning

confidence: 99%

Selective Antitumor Effect and Lower Toxicity of Mitochondrion-Targeting Derivatization of Triptolide

Xing,

Liu,

Zhang

et al. 2024

J. Med. Chem.

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“…The zebrafish is a freshwater fish naturally found throughout Central Asia [8]. This fish has been adopted as a model by many because of its multiple scientific advantages, such as transparent embryos, external development, easy growth and manipulability, and possession of genes relevant to mammal and human work [9]. Specifically, the zebrafish is a vertebrate and has early developmental processes (e.g., gastrulation, neurulation, and organogenesis) similar to humans, making it a relevant developmental model [10].…”

Section: Of 12mentioning

confidence: 99%

High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish

Seli,

Prendergast,

Ergun

et al. 2024

IJMS

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Salt is frequently introduced in ecosystems, where it acts as a pollutant. This study examined how changes in salinity affect the survival and development of zebrafish from the two-cell to the blastocyst stage and from the blastocyst to the larval stage. Control zebrafish embryos were cultured in E3 medium containing 5 mM Sodium Chloride (NaCl), 0.17 mM Potassium Chloride (KCL), 0.33 mM Calcium Chloride (CaCl2), and 0.33 mM Magnesium Sulfade (MgSO4). Experiments were conducted using increasing concentrations of each individual salt at 5×, 10×, 50×, and 100× the concentration found in E3 medium. KCL, CaCl2, and MgSO4 did not result in lethal abnormalities and did not affect early embryo growth at any of the concentrations tested. Concentrations of 50× and 100× NaCl caused embryonic death in both stages of development. Concentrations of 5× and 10× NaCl resulted in uninflated swim bladders in 12% and 65% of larvae, compared to 4.2% of controls, and caused 1654 and 2628 genes to be differentially expressed in blastocysts, respectively. The ATM signaling pathway was affected, and the Sonic Hedgehog pathway genes Shh and Ptc1 implicated in swim bladder development were downregulated. Our findings suggest that increased NaCl concentrations may alter gene expression and cause developmental abnormalities in animals found in affected ecosystems.

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“…In physiological conditions, mitochondria buffer cytosolic Ca 2+ levels. MeHg was reported to cause mitochondrial dysfunction via interaction with mitochondrial proteins presented in the respiratory chain or via excessive mitochondrial Ca 2+ influx through Ca 2+ channels [205,206]. In human neuronal progenitor cells, MeHg overloads mitochondrial Ca 2+ leading to an impairment in ATP synthesis [207].…”

Section: Neuronsmentioning

confidence: 99%

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

Novo

Martins

Raposo

et al. 2021

IJMS

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Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine populations. There has been much interest in the neurotoxicity of MeHg due to recent environmental disasters. Studies have also addressed the implications of long-term MeHg exposure for humans. The central nervous system is particularly susceptible to the deleterious effects of MeHg, as evidenced by clinical symptoms and histopathological changes in poisoned humans. In vitro and in vivo studies have been crucial in deciphering the molecular mechanisms underlying MeHg-induced neurotoxicity. A collection of cellular and molecular alterations including cytokine release, oxidative stress, mitochondrial dysfunction, Ca2+ and glutamate dyshomeostasis, and cell death mechanisms are important consequences of brain cells exposure to MeHg. The purpose of this review is to organize an overview of the mercury cycle and MeHg poisoning events and to summarize data from cellular, animal, and human studies focusing on MeHg effects in neurons and glial cells. This review proposes an up-to-date compendium that will serve as a starting point for further studies and a consultation reference of published studies.

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Mitochondria as targets for toxicity and metabolism research using zebrafish

Cited by 24 publications

References 53 publications

Selective Antitumor Effect and Lower Toxicity of Mitochondrion-Targeting Derivatization of Triptolide

Selective Antitumor Effect and Lower Toxicity of Mitochondrion-Targeting Derivatization of Triptolide

High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

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