Toxicogenomics of Five Cytostatics in Fathead Minnow (Pimephales promelas) Larvae
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View abstract on PubMed
Summary
This summary is machine-generated.Five cytostatics impacted gene expression in fathead minnow larvae, altering toxicity biomarkers and thyroid hormone pathways. This reveals subtle molecular effects, even without visible changes.
Area Of Science
- Environmental Toxicology
- Molecular Biology
- Ecotoxicogenomics
Background
- Cytostatics are widely used in cancer treatment.
- Pharmaceuticals in aquatic environments pose risks to wildlife.
- Fathead minnow (Pimephales promelas) is a standard model organism for ecotoxicology.
Purpose Of The Study
- To investigate the toxicogenomic effects of five common cytostatics on fathead minnow larvae.
- To assess the impact of these drugs on toxicity biomarker genes and thyroid hormone pathways.
- To evaluate subtle molecular responses in fish exposed to cytostatics.
Main Methods
- Fathead minnow eggs were exposed to varying concentrations of tamoxifen, methotrexate, capecitabine, cyclophosphamide, and ifosfamide for six days.
- Gene expression levels of two toxicity biomarkers were quantified.
- Expression of four thyroid hormone-related gene pathways was measured using quantitative PCR.
Main Results
- All tested cytostatics significantly affected the transcription levels of both toxicity biomarker genes.
- Thyroid hormone-related gene expression differed from control groups across all cytostatic treatments.
- Cyclophosphamide and ifosfamide induced the most significant alterations in thyroid hormone pathway genes.
Conclusions
- The five cytostatics induce subtle molecular changes in Pimephales promelas, affecting gene expression.
- Assessing molecular endpoints is crucial for understanding the full impact of cytostatics on aquatic organisms.
- This study underscores the need for multi-level biological assessments to evaluate contaminant effects.
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