کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4528843 1625930 2016 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Mediated effect of ultrasound treated Diclofenac on mussel hemocytes: First evidence for the involvement of respiratory burst enzymes in the induction of DCF-mediated unspecific mode of action
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم آبزیان
پیش نمایش صفحه اول مقاله
Mediated effect of ultrasound treated Diclofenac on mussel hemocytes: First evidence for the involvement of respiratory burst enzymes in the induction of DCF-mediated unspecific mode of action
چکیده انگلیسی


• DCF-mediated non specific mode of action on mussel hemocytes was investigated.
• DCF induces cytotoxic, oxidative and genotoxic effects.
• Respiratory burst activation could be responsible for DCF-mediated effects.
• Ultrasound (US) treatment of DCF eliminates its toxicity.
• US optimization could eliminate the toxic potential of DCF and its byproducts.

The present study investigates the toxic behavior of diclofenac (DCF) before and after its ultrasound (US) treatment, as well as the involvement of intracellular target molecules, such as NADPH oxidase and NO synthase, in the DCF-induced adverse effects on hemocytes of mussel Mytilus galloprovincialis. In this context, appropriate volumes (350 and 500 mL) of DCF solutions (at concentrations of 2, 2.5, 5 and 10 mg L−1) were treated under different ultrasound operating conditions (frequency at 582 and 862 kHz, electric power density at 133 and 167 W) for assessing US method efficiency. In parallel, DCF and US DCF-mediated cytotoxic (in terms of cell viability measured with the use of neutral red uptake/NRU method), oxidative (in terms of superoxide anions/.O2−, nitric oxides such as NO2− and lipid peroxidation products, such as malondialdehyde/MDA content) and genotoxic (DNA damage measured by the use of Comet assay method) effects were investigated in hemocytes exposed for 1 h to 5, 10 and 100 ng L−1 and 1, 10 and 20 μg L−1 of DCF. The involvement of NADPH oxidase and NO synthase to the DCF-induced toxicity was further investigated by the use of 10 μΜ L-NAME, a NO synthase inhibitor and 10 μΜ DPI, a NADPH oxidase inhibitor. According to the results, 350 mL of 2 mg L−1 DCF showed higher degradation ( > 50%) under 167 W electric power density and frequency at 862 kHz for 120 min, compared to degradation in all other cases, followed by a significant elimination of its toxicity. Specifically, US DCF-treated hemocytes showed a significant attenuation of DCF-mediated cytotoxic, oxidative and genotoxic effects, which appeared to be caused by NADPH oxidase and NO synthase activation, since their inhibition was followed by a significant elimination of .O2− and NO2− generation and the concomitant oxidative damage within cells. The results of the present study showed for the first time that unspecific mode of action of DCF, associated with the induction of NADPH oxidase and NO synthase in mussel hemocytes, could be significantly diminished after partial US degradation of DCF, at least under optimized operating conditions currently tested.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Aquatic Toxicology - Volume 175, June 2016, Pages 144–153
نویسندگان
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