Antioxidant Effect of CoQ10 on N-nitrosodiethylamine-induced Oxidative Stress in Mice

Song, Ho Sun; Kim, Hee Rae; Park, Tae Wook; Cho, Bong Jae; Choi, Mi Young; Kim, Chang Jong; Sohn, Uy Dong; Sim, Sang Soo

doi:10.4196/kjpp.2009.13.4.321

Cited by 7 publications

(5 citation statements)

References 26 publications

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“…CoQ10 was solube in corn oil. The mice of CoQ10 and HF+CoQ10 group were given CoQ10 (100 mg/kg) once a day for 8 weeks [18]. Mice in all groups were fed the appropriate diet for eight weeks.…”

Section: Methodsmentioning

confidence: 99%

CoQ10 Improves Myocardial Damage in Doxorubicin-Induced Heart Failure in C57BL/6 Mice

Pei¹,

Li²,

Li³

et al. 2022

Front. Biosci. (Landmark Ed)

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Background: Cardiovascular disease is associated with high morbidity and mortality. Doxorubicin (DOX) is an effective adjunct to cancer chemotherapy but leads to cardiovascular-related side effects. Because coenzyme Q10 (CoQ10) has been shown to protect against cardiac damage, this study was conducted to investigate the protective effects of CoQ10 against cardiac damage in mice. Methods: We randomly divided six-week-old male C57BL/6 mice into four groups: control (n = 7), CoQ10 (n = 7), heart failure (HF) (n = 7), and HF+CoQ10 (n = 6) groups. HF group was induced via intraperitoneal injections with DOX (5 mg/kg) once weekly for 4 weeks. CoQ10 was solube in corn oil. The mice of CoQ10 and HF+CoQ10 group were given CoQ10 (100 mg/kg) once a day for 8 weeks. All mice were subjected to different treatment regimens for eight weeks. Metabolic characteristics, cardiac damage, oxidative stress markers (SIRT1, SIRT3, eNOS, TE, P53, SIRT5, CAT, HO-1, and SOD), energy metabolism markers (PARP-1 and PPAR-γ), myocardial fibrosis markers (Smad3 and TGF-β), and apoptosis markers (BAK, BCL-XL, and caspase-8) were analyzed at eight weeks after the different treatments. Results: CoQ10 reduced the levels of molecules related to cardiac damage, oxidative stress, energy metabolism, and myocardial fibrosis in mice with doxorubicin-induced HF. CoQ10 also exerted anti-apoptotic effects in HF mice. Conclusions: CoQ10 may be useful for preventing cardiac damage in DOX-induced HF.

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Section: Methodsmentioning

confidence: 99%

CoQ10 Improves Myocardial Damage in Doxorubicin-Induced Heart Failure in C57BL/6 Mice

Pei¹,

Li²,

Li³

et al. 2022

Front. Biosci. (Landmark Ed)

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“…Both doses are much lower than oral LD 50 for mice (457 mg/kg) ( 29 ), and their choice was based on considerations of similar studies published earlier ( 30 , 31 , 32 , 33 ). Antioxidant control groups were receiving 100 mg/kg bw of taurine or 50 mg/kg bw of CoQ 10 for 5 days and dose selection was based on effective doses reported by previous studies investigating chemically induced oxidative stress in mice ( 34 , 35 , 36 , 37 ). Finally, two groups of animals first received taurine or CoQ 10 for five days and then PFOA (30 mg/kg bw) for another 10 days.…”

Section: Methodsmentioning

confidence: 99%

Perfluorooctanoic acid affects mouse brain and liver tissue through oxidative stress

Endirlik

Eken

Canpınar

et al. 2022

Archives of Industrial Hygiene and Toxicology

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The aim of this study was to investigate oxidative stress induced by perfluorooctanoic acid (PFOA) in the brain and liver tissues of Balb/c mice as well as protective effects of taurine and coenzyme Q10 (CoQ10) in both organs. For this purpose, animals were treated with PFOA (15 and 30 mg/kg) orally and their lipid peroxidation, total glutathione levels (GSH), and antioxidant enzyme activities measured and both tissues analysed for histopathological changes. Our results showed a dose-dependent decrease in body weight and increase in relative brain and liver weights, PFOA-induced lipid peroxidation and reduced glutathione peroxidase (GPx) activity in the brain tissue, and changes in GSH levels, GPx, superoxide dismutase (Cu-Zn SOD), and catalase (CAT) activities in the liver tissue. Pre-treatment with taurine or CoQ10 provided protection against PFOA-induced Cu-Zn SOD reduction in the liver tissue. Our findings evidence the depleting effect of PFOA on antioxidative systems and confirm that PFOA exerts its (neuro)toxicity through oxidative stress, but further research is needed to identify the exact toxicity mechanisms, especially in the brain.

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“…Based on previously published data, where different doses of NDEA were investigated (dose range 75 to 200 µg/g) to cause tumor formation in non-transgenic rodents [23] , [24] , [25] , [26] , a dose of 75 µg/g body weight was selected and given once weekly for 6 weeks by intraperitoneal administration. In the case of BHT a dose of 300 µg/g bodyweight was administered.…”

Section: Methodsmentioning

confidence: 99%

PET/CT Imaging of c-Myc Transgenic Mice Identifies the Genotoxic N-Nitroso-Diethylamine as Carcinogen in a Short-Term Cancer Bioassay

et al. 2012

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BackgroundMore than 100,000 chemicals are in use but have not been tested for their safety. To overcome limitations in the cancer bioassay several alternative testing strategies are explored. The inability to monitor non-invasively onset and progression of disease limits, however, the value of current testing strategies. Here, we report the application of in vivo imaging to a c-Myc transgenic mouse model of liver cancer for the development of a short-term cancer bioassay.Methodology/Principal FindingsμCT and 18F-FDG μPET were used to detect and quantify tumor lesions after treatment with the genotoxic carcinogen NDEA, the tumor promoting agent BHT or the hepatotoxin paracetamol. Tumor growth was investigated between the ages of 4 to 8.5 months and contrast-enhanced μCT imaging detected liver lesions as well as metastatic spread with high sensitivity and accuracy as confirmed by histopathology. Significant differences in the onset of tumor growth, tumor load and glucose metabolism were observed when the NDEA treatment group was compared with any of the other treatment groups. NDEA treatment of c-Myc transgenic mice significantly accelerated tumor growth and caused metastatic spread of HCC in to lung but this treatment also induced primary lung cancer growth. In contrast, BHT and paracetamol did not promote hepatocarcinogenesis.Conclusions/SignificanceThe present study evidences the accuracy of in vivo imaging in defining tumor growth, tumor load, lesion number and metastatic spread. Consequently, the application of in vivo imaging techniques to transgenic animal models may possibly enable short-term cancer bioassays to significantly improve hazard identification and follow-up examinations of different organs by non-invasive methods.

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Antioxidant Effect of CoQ10 on N-nitrosodiethylamine-induced Oxidative Stress in Mice

Cited by 7 publications

References 26 publications

CoQ10 Improves Myocardial Damage in Doxorubicin-Induced Heart Failure in C57BL/6 Mice

CoQ10 Improves Myocardial Damage in Doxorubicin-Induced Heart Failure in C57BL/6 Mice

Perfluorooctanoic acid affects mouse brain and liver tissue through oxidative stress

PET/CT Imaging of c-Myc Transgenic Mice Identifies the Genotoxic N-Nitroso-Diethylamine as Carcinogen in a Short-Term Cancer Bioassay

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