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[PMID]: | 28222982 |
[Au] Autor: | Zeeshan M; Murugadas A; Ghaskadbi S; Ramaswamy BR; Akbarsha MA |
[Ad] Endereço: | Mahatma Gandhi-Doerenkamp Center, Bharathidasan University, Tiruchirappalli 620024, India; Dept. of Environmental Biotechnology, Bharathidasan University, Tiruchirappalli 620024, India. |
[Ti] Título: | Ecotoxicological assessment of cobalt using Hydra model: ROS, oxidative stress, DNA damage, cell cycle arrest, and apoptosis as mechanisms of toxicity. |
[So] Source: | Environ Pollut;224:54-69, 2017 May. | [Is] ISSN: | 1873-6424 |
[Cp] País de publicação: | England |
[La] Idioma: | eng |
[Ab] Resumo: | The mechanisms underlying cobalt toxicity in aquatic species in general and cnidarians in particular remain poorly understood. Herein we investigated cobalt toxicity in a Hydra model from morphological, histological, developmental, and molecular biological perspectives. Hydra, exposed to cobalt (0-60 mg/L), were altered in morphology, histology, and regeneration. Exposure to standardized sublethal doses of cobalt impaired feeding by affecting nematocytes, which in turn affected reproduction. At the cellular level, excessive ROS generation, as the principal mechanism of action, primarily occurred in the lysosomes, which was accompanied by the upregulation of expression of the antioxidant genes SOD, GST, GPx, and G6PD. The number of Hsp70 and FoxO transcripts also increased. Interestingly, the upregulations were higher in the 24-h than in the 48-h time-point group, indicating that ROS overwhelmed the cellular defense mechanisms at the latter time-point. Comet assay revealed DNA damage. Cell cycle analysis indicated the induction of apoptosis accompanied or not by cell cycle arrest. Immunoblot analyses revealed that cobalt treatment triggered mitochondria-mediated apoptosis as inferred from the modulation of the key proteins Bax, Bcl-2, and caspase-3. From this data, we suggest the use of Hydra as a model organism for the risk assessment of heavy metal pollution in aquatic ecosystems. |
[Mh] Termos MeSH primário: |
Apoptose/efeitos dos fármacos Pontos de Checagem do Ciclo Celular/efeitos dos fármacos Cobalto/toxicidade Dano ao DNA/efeitos dos fármacos Hydra/efeitos dos fármacos Espécies Reativas de Oxigênio/metabolismo
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[Mh] Termos MeSH secundário: |
Animais Antioxidantes/metabolismo Caspase 3/metabolismo Ensaio Cometa Proteínas de Choque Térmico HSP70/metabolismo Lisossomos/efeitos dos fármacos Lisossomos/metabolismo Metais Pesados/toxicidade Mitocôndrias Estresse Oxidativo
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[Pt] Tipo de publicação: | JOURNAL ARTICLE |
[Nm] Nome de substância:
| 0 (Antioxidants); 0 (HSP70 Heat-Shock Proteins); 0 (Metals, Heavy); 0 (Reactive Oxygen Species); 3G0H8C9362 (Cobalt); EC 3.4.22.- (Caspase 3) |
[Em] Mês de entrada: | 1705 |
[Cu] Atualização por classe: | 170517 |
[Lr] Data última revisão:
| 170517 |
[Sb] Subgrupo de revista: | IM |
[Da] Data de entrada para processamento: | 170223 |
[St] Status: | MEDLINE |
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