Antioxidative Potential and Activity of Potassium Polyacrylate and Coenzyme Q۱۰ on Rat Hepatic Mitochondrial Permeability Transition Pores
محل انتشار: مجله آرشیو رازی، دوره: 79، شماره: 4
سال انتشار: 1403
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 72
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شناسه ملی سند علمی:
JR_ARCHRAZI-79-4_016
تاریخ نمایه سازی: 15 شهریور 1403
چکیده مقاله:
Multiple biological activities of coenzyme Q۱۰ have been demonstrated, opening up opportunities for research and development. The biological action of potassium polyacrylate and its impact on the mitochondrial permeability transition (mPT) pores, however, are both poorly understood. Therefore, this study investigated the in vitro antioxidative potential of potassium polyacrylate (PCK) and coenzyme Q۱۰ (CoQ۱۰) and their effects on mitochondrial permeability transition pores. In vitro antioxidant and angiotensin-converting enzyme inhibitory activities were determined using standard procedures, and lipid peroxidation was also determined. Mitochondrial swelling was assessed as the change in absorbance under succinate-energized conditions. Cytochrome c release and mitochondrial ATPase activity were assessed as previously reported. The results showed that PCK and CoQ۱۰ significantly scavenged DPPH and nitric oxide radicals in a concentration-dependent manner and exhibited a greater ferric-reducing antioxidant potential. PCK showed a high DPPH radical scavenging ability with the lowest IC۵۰ value of ۵۴.۰۵ µg/mL while CoQ۱۰ exhibited higher reducing power with the IC۵۰ value of ۸۲.۱۴ µg/mL. It was also observed that they both inhibited angiotensin-converting enzyme activity. Moreover, PCK and CoQ۱۰ significantly (p<۰.۰۵) prevented lipid peroxidation, modulated the opening of mitochondrial permeability transition (mPT) pores and caused no significant release of cytochrome c. However, CoQ۱۰ showed a mild inductive effect on mPT pores at higher concentrations. PCK and CoQ۱۰ also enhanced mitochondrial ATPase activity. The findings from this study suggest that both PCK and CoQ۱۰ could be useful in the management of diseases in which excessive apoptosis is characterized by excessive tissue degeneration, such as neurodegenerative conditions.
کلیدواژه ها:
نویسندگان
Akinwunmi Adeoye
Department of Biochemistry, Faculty of Science, Federal University Oye-Ekiti
John Olanlokun
Department of Biochemistry, University of Ibadan
Daniela Porta
۱INICSA, Enrique Barros Pabellón Biología Celular, Ciudad Universitaria, X۵۰۰۰, Córdoba, Argentina
Jude Akinyelu
Department of Biochemistry, Federal University Oye-Ekiti, Nigeria
Maria Rivoira
۱INICSA, Enrique Barros Pabellón Biología Celular, Ciudad Universitaria, X۵۰۰۰, Córdoba, Argentina
Nestor Garcia
۱INICSA, Enrique Barros Pabellón Biología Celular, Ciudad Universitaria, X۵۰۰۰, Córdoba, Argentina
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