Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA306030 | ENA |
REPOSITORIES: ENA
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Project description:Multigenerational effects of arsenic in aquatic organisms remain poorly understood, particularly under environmentally realistic dietary exposure conditions. This study investigated neurobehavioural toxicity in larval offspring of parental Zebrafish treated with arsenic-contaminated natural diet. Adult Zebrafish (F0) were fed with oligochaete blackworms (Lumbriculus variegatus) with arsenic body burdens of <0.05 (Control), 32.42 (Low), and 72.47 (High) µg/g dry weight, respectively, for 60 days. Fish were then bred to generate F1 embryos, which were reared in clean water and diet until 30 days post-fertilization (dpf). In F1 larvae, reactive oxygen species (ROS), apoptosis and lipid peroxidation were evaluated at 5-dpf by fluorescence imaging, and immunostaining was performed at 24 hours post-fertilization (hpf) and 5-dpf to assess neurogenesis and neural signalling pathways. Behavioral assessments included photomotor response (5-dpf), thigmotaxis (15-dpf), social preference (21-dpf), and novel object recognition (30-dpf). Whole-transcriptome analysis in 5-dpf larvae was performed to identify molecular pathways associated with neurobehavioral alterations. Parental dietary arsenic exposure resulted in a dose-dependent increase in ROS production, apoptotic cells, and lipid peroxidation in offspring. Neurodevelopmental impairments were also evident in arsenic lineages, including reduced hypothalamic neurogenesis and impaired development of dopaminergic and motor neurons. Larvae exhibited behavioral abnormalities such as reduced locomotor activity, heightened anxiety, reduced social interaction, and cognitive impairments. Transcriptomic analysis revealed significant dysregulation in pathways related to early neurodevelopment and synaptic functions. These findings demonstrate that environmentally realistic parental arsenic exposure can induce neurobehavioral deficits in offspring by inducing oxidative stress and disrupting neurogenesis and neural signaling pathways.
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Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5µg/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide
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Project description:Genome-wide identification of molecular pathways and biomarkers in response to arsenic exposure in zebrafish liver
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