N -acetylcysteine inhibits Mancozeb-induced impairments to the normal development of zebrafish embryos
Autor: | Andrés Delgado Cañedo, Pratícia de Brum Vieira, José Cláudio Fonseca Moreira, Illana Kemmerich Martins, Mauro Eugênio Medina Nunes, Renata Siqueira de Mello, D. G. Costa-Silva, Nelson Rodrigues de Carvalho, Luana Paganotto Leandro, Thaís Posser, Adriano Alves de Paula, Andressa Rubim Lopes, Jeferson Luis Franco, Lucia Emanueli Schimith |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Programmed cell death Embryo Nonmammalian Antioxidant DNA damage medicine.medical_treatment Embryonic Development 010501 environmental sciences Toxicology 01 natural sciences Acetylcysteine 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound Developmental Neuroscience medicine Animals Zebrafish 0105 earth and related environmental sciences Zineb chemistry.chemical_classification Reactive oxygen species Behavior Animal Cell Death biology Glutathione biology.organism_classification Fungicides Industrial Cell biology Comet assay 030104 developmental biology chemistry Maneb Comet Assay Reactive Oxygen Species DNA Damage medicine.drug |
Zdroj: | Neurotoxicology and Teratology. 68:1-12 |
ISSN: | 0892-0362 |
Popis: | Mancozeb (MZ), a manganese/zinc-containing ethylene-bis-dithiocarbamate (EBCD) fungicide has been claimed to present low acute toxicity and short environmental persistence, however, its effects on embryogenesis in non-target organisms is unclear. Here, we used zebrafish embryos (5 hpf) to assess the potential embryotoxic effects induced by MZ (up to 72 hpf) as well as the role of reactive oxygen species (ROS) in this process by pre-treatment with a classical antioxidant (N-acetylcysteine, NAC). Markers of reactive oxygen species production (ROS), glutathione (GSH) levels and glutathione S-transferase (GST) activity were measured along with genotoxicity (comet assay), cell death (Acridine Orange) and behavioral parameters (spontaneous movement, touch stimulation and swimming response), in order to determine potential mechanisms of embryotoxicity. According to results, MZ was able to induce morphological abnormalities such as body axis distortion, DNA damage, cell death, increased ROS generation and changes in behavioral endpoints during zebrafish development. All these toxic effects were inhibited by the pre-treatment with NAC indicating a key role of redox unbalance during MZ-induced embryotoxicity. At least in our knowledge, this is the first report on the deleterious effect of MZ to the normal embryogenesis of zebrafish. In addition, the importance of ROS generation during this pathophysiological condition was highlighted. |
Databáze: | OpenAIRE |
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