PUBLICATION
Effects of Ru(CO)3Cl-glycinate on the developmental toxicities induced by X-ray and carbon-ion irradiation in zebrafish embryos
- Authors
- Zhou, R., Song, J., Si, J., Zhang, H., Liu, B., Gan, L., Zhou, X., Wang, Y., Yan, J., Zhang, Q.
- ID
- ZDB-PUB-161113-1
- Date
- 2016
- Source
- Mutation research 793-794: 41-50 (Journal)
- Registered Authors
- Keywords
- Apoptosis, CORM-3, Carbon-ion irradiation, Oxidative stress, X-ray irradiation, Zebrafish embryos
- MeSH Terms
-
- Animals
- Carbon/adverse effects*
- DNA Damage/drug effects
- DNA Damage/radiation effects
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/radiation effects*
- Gene Expression Regulation, Developmental/drug effects
- Gene Expression Regulation, Developmental/radiation effects
- Heavy Ions/adverse effects*
- Organometallic Compounds/pharmacology*
- Radiation, Ionizing
- X-Rays/adverse effects*
- Zebrafish
- PubMed
- 27837686 Full text @ Mutat. Res.
Citation
Zhou, R., Song, J., Si, J., Zhang, H., Liu, B., Gan, L., Zhou, X., Wang, Y., Yan, J., Zhang, Q. (2016) Effects of Ru(CO)3Cl-glycinate on the developmental toxicities induced by X-ray and carbon-ion irradiation in zebrafish embryos. Mutation research. 793-794:41-50.
Abstract
The inhibitory effects of carbon monoxide (CO), generated by Ru(CO)3Cl-glycinate [CO-releasing molecule (CORM-3)], on developmental toxicity in zebrafish embryos induced by ionizing radiation with different linear energy transfer (LET) were studied. Zebrafish embryos at 5h post-fertilization were irradiated with X-ray (low-LET) and carbon-ion (high-LET) with or without pretreatment of CORM-3 1h before irradiation. CORM-3 pre-treatment showed a significant inhibitory effect on X-ray irradiation-induced developmental toxicity, but had little effect on carbon-ion irradiation-induced developmental toxicity. X-ray irradiation-induced significant increase in ROS levels and cell apoptosis could be modified by CORM-3 pretreatment. However, embryos exposed to carbon-ion irradiation showed significantly increase of cell apoptosis without obvious ROS generation, which could not be attenuated by CORM-3 pretreatment. CORM-3 could inhibit apoptosis induced by ionizing radiation with low-LET as an effective ROS scavenger. The expression of pro-apoptotic genes increased significantly after X-ray irradiation, but increased expression was reduced markedly when CORM-3 was applied before irradiation. Moreover, the protein levels of P53 and γ-H2AX increased markedly after X-ray irradiation, which could be modified by the presence of CORM-3. The protective effect of CORM-3 on X-ray irradiation occurred mainly by suppressing ROS generation and DNA damage, and thus inhibiting the activation of P53 and the mitochondrial apoptotic pathway, leading to the attenuation of cell apoptosis and consequently alleviating X-ray irradiation-induced developmental toxicity at lethal and sub-lethal levels.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping