Environmental Risk Assessment of Oxaliplatin Exposure on Early Life Stages of Zebrafish ( Danio rerio ).
Davide Di PaolaFabiano CapparucciJessica Maria AbbateMarika CordaroRosalia CrupiRosalba SiracusaRamona D'amicoRoberta FuscoTiziana GenoveseDaniela ImpellizzeriSalvatore CuzzocreaNunziacarla SpanòEnrico GugliandoloAlessio Filippo PeritorePublished in: Toxics (2022)
Pharmaceuticals are actually identified as a threat to the ecosystem. Nowadays, the growing consumption of antineoplastic agents has been related to their continuous input in natural environments. These substances can interfere with physiological and biochemical processes of aquatic species over their entire life cycle. Oxaliplatin (OXA) is a widely used chemotherapeutic agent to treat colon or rectal cancer. This study was aimed to evaluate the developmental toxicity of the OXA exposure. To this end, zebrafish embryos were incubated with 0.001, 0.1, 0.5 mg/L OXA. At different timepoints mortality rate, hatching rate, developmental abnormalities, histological analysis, oxidative stress and mRNA expression of gene related to oxidative stress were evaluated. Our results showed that OXA exposure can induce increased mortality and developmental abnormalities reducing the hatching rate. Histological analysis demonstrated that OXA induced liver, intestine, muscle and heart injury. Superoxide dismutase and catalase activities were significantly increased after OXA exposure demonstrating its oxidative effects. The mRNA expression levels of apoptosis-related genes (caspase-3, bax and bcl-2) were significantly upregulated by OXA exposure. In conclusion, we highlighted that OXA exposure led to a dose-related developmental toxicity, oxidative stress and apoptosis.
Keyphrases
- oxidative stress
- acinetobacter baumannii
- klebsiella pneumoniae
- diabetic rats
- multidrug resistant
- induced apoptosis
- risk assessment
- drug resistant
- pseudomonas aeruginosa
- dna damage
- escherichia coli
- rectal cancer
- life cycle
- endoplasmic reticulum stress
- human health
- risk factors
- climate change
- cardiovascular events
- nitric oxide
- heart failure
- cardiovascular disease
- atrial fibrillation
- genome wide
- dna methylation
- coronary artery disease
- heavy metals
- drug induced
- gene expression
- skeletal muscle
- hydrogen peroxide
- heat stress