Environmental concentrations of benz[a]anthracene induce developmental defects and DNA damage and impair photomotor response in Japanese medaka larvae

Mature male medaka were continuously exposed to 0.005, 0.0–5 or 1.0 ppb of estradiol-17β (E2 or 0.1, 10 or 100 ppb of p-nonylphenol (NP) or bis-phenol-A (BPA). Female-specific proteins (Fsp) were induced in medaka exposed to 0.005 ppb of E2, 0.1 ppb of NP, or 10 ppb of BPA. Concentrations of 0.005 pbb of E2 and 0.1 ppb of NP corresponded to concentrations of these chemicals detected in river water in Japan. The abilities of the 3 chemicals to induce Fsp were E2> NP> BPA. Embryonic medaka were exposed to E2, NP and BPA under conditions of static-renewal for 200–230 days until pre-maturity. Survival ratios of medaka exposed to E2 and NP declined in concentrations more than 25 ppb and 50 ppb, respectively. The groups of medaka exposed to E2 had individuals with testis-ova or abnormal gonad. There was no male in exposure to 1.0 ppb E2. When exposed to 100 ppb of NP or BPA, abnormal gonad was also detected. Abnormal anal fin (female-like) was observed in male exposed to 100 ppb of NP. The LC50 values for each of the 3 chemicals were much higher than the concentrations detected in water in the environment—the 3 chemicals were considered to have no lethal effect on medaka in aquatic environments. However, exposures to E2 or NP at environmental concentrations induced Fsp. BPA also had the ability to affect medaka as an environmental estrogen, although its extrogenic activity was weaker than that of E2 or NP.

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DNA damage, histologial changes and DNA repair in larval Japanese medaka (Oryzias latipes) exposed to ultraviolet-B radiation

Aquatic Toxicology ◽

10.1016/s0166-445x(01)00212-0 ◽

2002 ◽

Vol 58 (1-2) ◽

pp. 1-14 ◽

Cited By ~ 39

Author(s):

Tina N. Armstrong ◽

Renate Reimschuessel ◽

Brian P. Bradley

Keyword(s):

Dna Damage ◽

Dna Repair ◽

Oryzias Latipes ◽

Ultraviolet B ◽

Japanese Medaka ◽

Ultraviolet B Radiation

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Psychotropic drugs in mixture alter swimming behaviour of Japanese medaka (Oryzias latipes) larvae above environmental concentrations

Environmental Science and Pollution Research ◽

10.1007/s11356-014-3477-4 ◽

2014 ◽

Vol 23 (6) ◽

pp. 4964-4977 ◽

Cited By ~ 34

Author(s):

Axelle Chiffre ◽

Christelle Clérandeau ◽

Charline Dwoinikoff ◽

Florane Le Bihanic ◽

Hélène Budzinski ◽

...

Keyword(s):

Psychotropic Drugs ◽

Oryzias Latipes ◽

Japanese Medaka ◽

Swimming Behaviour ◽

Environmental Concentrations

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Replication fork dynamics and the DNA damage response

Biochemical Journal ◽

10.1042/bj20112100 ◽

2012 ◽

Vol 443 (1) ◽

pp. 13-26 ◽

Cited By ~ 77

Author(s):

Rebecca M. Jones ◽

Eva Petermann

Keyword(s):

Dna Damage ◽

Dna Replication ◽

Dna Damage Response ◽

Replication Fork ◽

Molecular Mechanisms ◽

S Phase ◽

Replication Initiation ◽

Developmental Defects ◽

Replication Fork Progression ◽

Damage Response

Prevention and repair of DNA damage is essential for maintenance of genomic stability and cell survival. DNA replication during S-phase can be a source of DNA damage if endogenous or exogenous stresses impair the progression of replication forks. It has become increasingly clear that DNA-damage-response pathways do not only respond to the presence of damaged DNA, but also modulate DNA replication dynamics to prevent DNA damage formation during S-phase. Such observations may help explain the developmental defects or cancer predisposition caused by mutations in DNA-damage-response genes. The present review focuses on molecular mechanisms by which DNA-damage-response pathways control and promote replication dynamics in vertebrate cells. In particular, DNA damage pathways contribute to proper replication by regulating replication initiation, stabilizing transiently stalled forks, promoting replication restart and facilitating fork movement on difficult-to-replicate templates. If replication fork progression fails to be rescued, this may lead to DNA damage and genomic instability via nuclease processing of aberrant fork structures or incomplete sister chromatid separation during mitosis.

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p53 drives premature neuronal differentiation in response to radiation-induced DNA damage during early neurogenesis

10.1101/2020.06.26.171132 ◽

2020 ◽

Author(s):

André-Claude Mbouombouo Mfossa ◽

Mieke Verslegers ◽

Tine Verreet ◽

Haris bin Fida ◽

Mohamed Mysara ◽

...

Keyword(s):

Dna Damage ◽

Neuronal Differentiation ◽

Cell Fate ◽

Epithelial To Mesenchymal Transition ◽

Brain Size ◽

Critical Role ◽

Neural Progenitor Cell ◽

Developmental Defects ◽

Mesenchymal Transition ◽

Radiation Induced

Abstractp53 regulates the cellular DNA damage response (DDR). Hyperactivation of p53 during embryonic development, however, can lead to a range of developmental defects including microcephaly. Here, we induce microcephaly by acute irradiation of mouse fetuses at the onset of neurogenesis. Besides a classical DDR culminating in massive apoptosis, we observe ectopic neurons in the subventricular zone in the brains of irradiated mice, indicative of premature neuronal differentiation. A transcriptomic study indicates that p53 activates both DDR genes and differentiation-associated genes. In line with this, mice with a targeted inactivation of Trp53 in the dorsal forebrain, do not show this ectopic phenotype and partially restore brain size after irradiation. Irradiation furthermore induces an epithelial-to-mesenchymal transition-like process resembling the radiation-induced proneural-mesenchymal transition in glioma and glioma stem-like cells. Our results demonstrate a critical role for p53 beyond the DDR as a regulator of neural progenitor cell fate in response to DNA damage.

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Developmental toxicity and DNA damage from exposure to parking lot runoff retention pond samples in the Japanese medaka (Oryzias latipes)

Marine Environmental Research ◽

10.1016/j.marenvres.2014.04.007 ◽

2014 ◽

Vol 99 ◽

pp. 117-124 ◽

Cited By ~ 8

Author(s):

Meryl D. Colton ◽

Kevin W.H. Kwok ◽

Jennifer A. Brandon ◽

Isaac H. Warren ◽

Ian T. Ryde ◽

...

Keyword(s):

Dna Damage ◽

Developmental Toxicity ◽

Oryzias Latipes ◽

Japanese Medaka ◽

Retention Pond ◽

Parking Lot

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Cytotoxic and genotoxic effects of perfluorododecanoic acid (PFDoA) in Japanese medaka

Knowledge and Management of Aquatic Ecosystems ◽

10.1051/kmae/2017058 ◽

2018 ◽

pp. 9

Author(s):

Isaac O Ayanda ◽

Min Yang ◽

Zhang Yu ◽

Jinmiao Zha

Keyword(s):

Dna Damage ◽

Comet Assay ◽

Chronic Exposure ◽

Tail Length ◽

Toxicity Study ◽

Japanese Medaka ◽

Genotoxic Effects ◽

Gradual Decline ◽

Nuclear Abnormalities ◽

Fish Blood

This study investigated the cytotoxic and genotoxic potential of perfluorododecanoic acid (PFDoA), a perfluorinated carboxylic chemical (PFC) that has broad applications and distribution in the environment in Japanese medaka, Oryzias latipes. Micronucleus (MN) test and Comet assay were used for the toxicity study. Three groups of fish were exposed to 0.1 mg/L, 0.5 mg/L and 2.5 mg/L concentration of the chemical for 28 days. Another group served as control. Sampling of the fish blood and liver were done after days 1, 4, 7, 14, 21 and 28 for analysis of different erythrocyte abnormalities and damage to DNA using the MN test and Comet assay respectively. Results showed that there was a significant time and concentration dependent increase (p < 0.05) in percent tail length of DNA and frequency of erythrocyte abnormalities. Nuclear abnormalities observed include micronucleus, fragmented apoptotic cells, lobed nuclei, and bean-shaped cells. Increase in induction of erythrocyte abnormalities and percent tail length of DNA peaked at days 14 and 7, respectively, after which there was a gradual decline. The results indicate that sub-chronic exposure of PFDoA to Japanese medaka caused DNA damage with a simultaneous induction of different erythrocyte abnormalities.

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Haemodynamic dependence of mechano-genetic evolution of the cardiovascular system in Japanese medaka

Journal of The Royal Society Interface ◽

10.1098/rsif.2021.0752 ◽

2021 ◽

Vol 18 (183) ◽

Author(s):

Sreyashi Chakraborty ◽

Elizabeth Allmon ◽

Maria S. Sepúlveda ◽

Pavlos P. Vlachos

Keyword(s):

Ventricular Outflow Tract ◽

Japanese Medaka ◽

Atrioventricular Canal ◽

Flow Measurements ◽

Developmental Defects ◽

Monotonic Trend ◽

Micro Particle Image Velocimetry ◽

Cardiac Wall ◽

Cardiac Gene

The progression of cardiac gene expression–wall shear stress (WSS) interplay is critical to identifying developmental defects during cardiovascular morphogenesis. However, mechano-genetics from the embryonic to larval stages are poorly understood in vertebrates. We quantified peak WSS in the heart and tail vessels of Japanese medaka from 3 days post fertilization (dpf) to 14 dpf using in vivo micro-particle image velocimetry flow measurements, and in parallel analysed the expression of five cardiac genes ( fgf8 , hoxb6b , bmp4 , nkx2.5 , smyd1 ). Here, we report that WSS in the atrioventricular canal (AVC), ventricular outflow tract (OFT), and the caudal vessels in medaka peak with inflection points at 6 dpf and 10–11 dpf instead of a monotonic trend. Retrograde flows are captured at the AVC and OFT of the medaka heart for the first time. In addition, all genes were upregulated at 3 dpf and 7 dpf, indicating a possible correlation between the two, with the cardiac gene upregulation preceding WSS increase in order to facilitate cardiac wall remodelling.

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