Paper
Trimethyltin chloride induces reactive oxygen species-mediated apoptosis in retinal cells during zebrafish eye development.
Published Feb 25, 2019 · Jin Kim, C‐Yoon Kim, H. Oh
The Science of the total environment
Q1 SJR score
39
Citations
2
Influential Citations
Abstract
Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.
Study Snapshot
Trimethyltin chloride (TMT) is toxic during eye development in zebrafish, causing reactive oxygen species-mediated apoptosis in retinal cells.
PopulationOlder adults (50-71 years)
Sample size24
MethodsObservational
OutcomesBody Mass Index projections
ResultsSocial networks mitigate obesity in older groups.
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References
Cypermethrin: Oxidative stress and genotoxicity in retinal cells of the adult zebrafish.
Cypermethrin exposure in zebrafish retinal cells causes DNA damage, oxidative stress, and can induce apoptosis, with a dose-dependent response.
2018·45citations·E. Paravani et al.·Mutation research. Genetic toxicology and environmental mutagenesis
Mutation research. Genetic toxicology and environmental mutagenesis
Correlation between photoreceptor injury-regeneration and behavior in a zebrafish model
Zebrafish retinas can regenerate after high-intensity light stimulation, but visual impairment and stress responses contribute to altered behaviors during the injury-regeneration process.
2017·10citations·Ya-Jie Wang et al.·Neural Regeneration Research
Neural Regeneration Research
Confirmation of TENM3 involvement in autosomal recessive colobomatous microphthalmia
TENM3 mutations are associated with colobomatous microphthalmia, expanding the phenotypic spectrum associated with these gene variants.
2016·35citations·N. Chassaing et al.·American Journal of Medical Genetics Part A
American Journal of Medical Genetics Part A
Coenzyme Q10 Ameliorates Trimethyltin Chloride Neurotoxicity in Experimental Model of Injury in Dentate Gyrus of Hippocampus: A Histopathological and Behavioral Study
Coenzyme Q10 reduces neuronal necrosis and improves learning memory in mice with trimethyltin chloride-induced hippocampal damage, partly due to its antioxidative effects.
2016·10citations·M. Sakhaie et al.·Iranian Red Crescent Medical Journal
Iranian Red Crescent Medical Journal
Citations
Mechanisms by which Ganglioside GM1, a specific type of glycosphingolipid, ameliorates BMAA-induced neurotoxicity in early-life stage of zebrafish embryos.
Ganglioside GM1 alleviates BMAA-induced neurotoxicity in early-life zebrafish embryos, potentially through the MAPK pathway, offering new insights into lipid signaling for neuroprotective effects.
2024·0citations·Yanjun Liu et al.·Food research international
Food research international
Exposure to Trimethyltin Chloride Induces Pyroptosis and Immune Dysfunction in Grass Carp CIK Cells by Activating the NF-κB Pathway Through Oxidative Stress.
Exposure to trimethyltin chloride (TMT) induces dose-dependent oxidative stress, activates the NF-B pathway, and leads to pyroptosis and immune dysfunction in grass carp kidney cells.
2024·0citations·Xiaotong Ni et al.·Environmental toxicology
Environmental toxicology
Caspase-8 promotes NLRP3 inflammasome activation mediates eye development defects in zebrafish larvae exposed to perfulorooctane sulfonate (PFOS).
Caspase-8 activation plays a crucial role in PFOS-induced eye development defects, as it promotes NLRP3 inflammasome activation, leading to retinal inflammatory injury.
2024·2citations·Luyin Wu et al.·Environmental pollution
Environmental pollution
Retinal toxicity of heavy metals and its involvement into retinal pathology.
Toxic metal exposure is associated with retinal pathology, including age-related macular degeneration, and may cause retinal damage through oxidative stress, apoptosis, DNA damage, mitochondrial dysfunction, and inflammation.
2024·2citations·Michael Aschner et al.·Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
Aspartame Causes Developmental Defects and Teratogenicity in Zebra Fish Embryo: Role of Impaired SIRT1/FOXO3a Axis in Neuron Cells
Aspartame can cause developmental defects and teratogenicity in zebrafish embryos by impairing the SIRT1/FOXO3a axis in neuron cells, reducing autophagy.
2024·4citations·Athiram Pandaram et al.·Biomedicines
Biomedicines
Chlorinated Polyfluoroalkyl Ether Sulfonic Acids (Cl-PFESAs) Are Associated with Eye Diseases in Humans and Eye Toxicity in Zebrafish
Exposure to PFASs increases the odds of developing eye toxicity in humans and zebrafish, with 8:2 Cl-PFESA being the dominant risk factor.
2024·5citations·Luyin Wu et al.·Environment & Health
Environment & Health
Effect of tributyltin exposure on the eye of zebrafish
Tributyltin exposure at 250 and 500 ng/L significantly decreases CAT activity and total antioxidant capacity in adult zebrafish eyes, increasing lipid peroxidation and mild depigmentation of the retinal pigmented epithelium layer.
2024·0citations·Rajkumar S Delvadiya et al.·International Journal of Advanced Biochemistry Research
International Journal of Advanced Biochemistry Research
Effects of chronic diazepam exposure on the behaviors and oxidative stress homeostasis in the eyes and brains of female Japanese medaka.
Chronic diazepam exposure reduces swimming activity and anxiety in female Japanese medaka, while increasing social interaction, and may impact ocular and brain oxidative stress homeostasis.
2023·3citations·Sijing Wang et al.·Comparative biochemistry and physiology. Toxicology & pharmacology : CBP
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP