scholarly journals Piceatannol Ameliorates Hepatic Oxidative Damage and Mitochondrial Dysfunction of Weaned Piglets Challenged with Diquat

Animals ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1239
Author(s):  
Peilu Jia ◽  
Shuli Ji ◽  
Hao Zhang ◽  
Yanan Chen ◽  
Tian Wang
Keyword(s):  
Oxidative Damage ◽  
Protein Expression ◽  
Complex I ◽  
Sirtuin 1 ◽  
Expression Level ◽  
Control Group ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Protein Expression Level ◽  
Atp Production

The liver is an organ that produces large amounts of reactive oxygen species (ROS). Human infants or piglets are prone to oxidative damage due to their uncompleted development of the antioxidant system, causing liver disease. Piceatannol (PIC) has been found to have significant antioxidant effects. The aim of this experiment was to investigate the effects of PIC on the liver in piglets experiencing oxidative stress caused by diquat (DQ). After weaning, 54 male piglets (Duroc × [Landrace × Yorkshire]) were selected and randomly divided into three treatment groups: the CON group, the DQ-CON group, and the DQ-PIC group. The two challenged groups were injected with DQ and then orally administrated either PIC or another vehicle solution, while the control group was given sterile saline injections and an orally administrated vehicle solution. Compared to the results of the CON group, DQ increased the percentage of apoptosis cells in the liver, also decreased the amount of reduced glutathione (GSH) and increased the concentration of malondialdehyde (MDA). In addition, the adenosine triphosphate (ATP) production, activities of mitochondrial complex I, II, III, and V, and the protein expression level of sirtuin 1 (SIRT1) were inhibited by DQ. Furthermore, PIC supplementation inhibited the apoptosis of hepatic cells caused by DQ. PIC also decreased MDA levels and increased the amount of GSH. Piglets given PIC supplementation exhibited increased activities of mitochondrial complex I, II, III, and V, the protein expression level of SIRT1, and the ATP production in the liver. In conclusion, PIC affected the liver of piglets by improving redox status, preserving mitochondrial function, and preventing excessive apoptosis.

Partial mitochondrial complex I inhibition induces oxidative damage and perturbs glutamate transport in primary retinal cultures.

2006 ◽  
Vol 24 (2) ◽  
pp. 308-317 ◽  
Author(s):  
Simone Beretta ◽  
John P.M. Wood ◽  
Barry Derham ◽  
Gessica Sala ◽  
Lucio Tremolizzo ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Complex I ◽  
Glutamate Transport ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Retinal Cultures

scholarly journals The effect of miR-23b-3p on growth hormone in pituitary cells of Yanbian yellow cattle

2020 ◽  
Author(s):  
Jiuxiu Ji ◽  
Angang Lou ◽  
Rui Zhang ◽  
Taihua Jin ◽  
Siyu Xiang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Control Group ◽  
Pituitary Cells ◽  
Mrna Transcription ◽  
Luciferase Reporter Gene ◽  
Protein Expression Level ◽  
Yellow Cattle ◽  
Reporter Gene System

Abstract Background There is a relationship between miR-23b-3p and GH in pituitary of Yanbian yellow cattle. However, the specific mechanism of the effect of miR-23b-3p on GH in pituitary of Yanbian yellow cattle is still unclear.This study aimed to evaluate the effect of miR-23b-3p on growth hormone (GH) in pituitary cells of Yanbian yellow cattle. Methods The primary culture of Yanbian yellow cattle pituitary cells was carried out, and mimics (miR-23b-3p-mi group), mimics reference substance (NC group), inhibitor (miR-23b-3p-in group) and inhibitor reference substance (iNC group) of miR-23b-3p were transfected into the established pituitary primary cells. After 48 h, the cells were collected and the total RNA and protein were extracted.The mRNA transcription and protein expression level of GH and miR-23b-3p target genes were detected by real time fluorescence quantitative PCR (qPCR) and Western blot, respectively. The target relationship of miR-23b-3p was validated by double luciferase reporter gene system. Results Compared with the NC control group, GH mRNA transcription and protein expression level in pituitary cells of Yanbian yellow cattle was significantly decreased by adding miR-23b-3p minics ( P <0.01), while compared with the iNC control group, GH mRNA transcription and protein expression level were significantly increased by adding miR-23b-3p inhibitor( P <0.05). The result of bioinformatics analysis and double luciferase reporter gene system validation proved that miR-23b-3p targeted 3'UTR of pituitary specific transcription factor 1 (POU1F1). Compared with the NC control group, POU1F1 mRNA transcription and protein expression level were significantly inhibited by the addition of miR-23b-3p minics ( P <0.01), while compared with the iNC control group, POU1F1 mRNA transcription and protein expression level were significantly increased by the addition of miR-23b-3p inhibitor ( P <0.01). Conclusions miR-23b-3p could regulate GH in pituitary cells by regulating POU1F1 gene.

scholarly journals Oxidative Damage to Mitochondrial Complex I Due to Peroxynitrite

2003 ◽  
Vol 278 (39) ◽  
pp. 37223-37230 ◽  
Author(s):  
James Murray ◽  
Steven W. Taylor ◽  
Bing Zhang ◽  
Soumitra S. Ghosh ◽  
Roderick A. Capaldi
Keyword(s):  
Oxidative Damage ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Epigallocatechin-3-Gallate Plus Omega-3 Restores the Mitochondrial Complex I and F0F1-ATP Synthase Activities in PBMCs of Young Children with Down Syndrome: A Pilot Study of Safety and Efficacy

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 469
Author(s):  
Iris Scala ◽  
Daniela Valenti ◽  
Valentina Scotto D’Aniello ◽  
Maria Marino ◽  
Maria Pia Riccio ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mitochondrial Dysfunction ◽  
Atp Synthase ◽  
Complex I ◽  
Antioxidant Properties ◽  
Control Group ◽  
Mitochondrial Complex I ◽  
Omega 3 ◽  
Mitochondrial Complex ◽  
F0f1 Atp Synthase

Down syndrome (DS) is a major genetic cause of intellectual disability. DS pathogenesis has not been fully elucidated, and no specific pharmacological therapy is available. DYRK1A overexpression, oxidative stress and mitochondrial dysfunction were described in trisomy 21. Epigallocatechin-3-gallate (EGCG) is a multimodal nutraceutical with antioxidant properties. EGCG inhibits DYRK1A overexpression and corrects DS mitochondrial dysfunction in vitro. The present study explores safety profiles in DS children aged 1–8 years treated with EGCG (10 mg/kg/die, suspended in omega-3, per os, in fasting conditions, for 6 months) and EGCG efficacy in restoring mitochondrial complex I and F0F1-ATP synthase (complex V) deficiency, assessed on PBMCs. The Griffiths Mental Developmental Scales—Extended Revised (GMDS-ER) was used for developmental profiling. Results show that decaffeinated EGCG (>90%) plus omega-3 is safe in DS children and effective in reverting the deficit of mitochondrial complex I and V activities. Decline of plasma folates was observed in 21% of EGCG-treated patients and should be carefully monitored. GMDS-ER scores did not show differences between the treated group compared to the DS control group. In conclusion, EGCG plus omega-3 can be safely administered under medical supervision in DS children aged 1–8 years to normalize mitochondria respiratory chain complex activities, while results on the improvement of developmental performance are still inconclusive.

scholarly journals A Mandibular Advancement Device Attenuates the Abnormal Morphology and Function of Mitochondria from the Genioglossus in OSAHS Rabbits

2021 ◽  
Author(s):  
Chunyan Liu ◽  
Shilong Zhang ◽  
Dechao Zhu ◽  
Dengying Fan ◽  
Yahui Zhu ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Complex I ◽  
Mitochondrial Membrane ◽  
Mandibular Advancement Device ◽  
Mandibular Advancement ◽  
Control Group ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
And Function

Abstract Background: To examine the morphology and function of mitochondria from the genioglossus in a rabbit model of obstructive sleep apnea-hypopnea syndrome (OSAHS), as well as these factors after insertion of a mandibular advancement device (MAD). Methods: Thirty male New Zealand white rabbits were randomized into three groups: control, OSAHS and MAD, with 10 rabbits in each group. Animals in Group OSAHS and Group MAD were induced to develop OSAHS by injection of gel into the submucosal muscular layer of the soft palate. The rabbits in Group MAD were fitted with a MAD. The animals in the control group were not treated. Further, polysomnography (PSG) and CBCT scan were used to measure MAD effectiveness. CBCT of the upper airway and PSG suggested that MAD was effective. Rabbits in the three groups were induced to sleep for 4–6 hours per day for 8 consecutive weeks. The genioglossus was harvested and detected by optical microscopy and transmission electron microscopy. The mitochondrial membrane potential was determined by laser confocal microscopy and flow cytometry. Mitochondrial complex I and IV activities were detected by mitochondrial complex assay kits.Results: OSAHS-like symptoms were induced successfully in Group OSAHS and rescued by MAD treatment. The relative values of the mitochondrial membrane potential, mitochondrial complex I activity and complex IV activity were significantly lower in Group OSAHS than in the control group; however, there was no significant difference between Group MAD and the control group. The OSAHS-induced injury and the dysfunctional mitochondria of the genioglossus muscle were reduced by MAD treatment.Conclusion: Damaged mitochondrial structure and function were induced by OSAHS and could be attenuated by MAD treatment.

scholarly journals A high mutation load of m.14597A>G in MT-ND6 causes Leigh syndrome

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoshihito Kishita ◽  
Kaori Ishikawa ◽  
Kazuto Nakada ◽  
Jun-Ichi Hayashi ◽  
Takuya Fushimi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Complex I ◽  
Neurodegenerative Disorder ◽  
Rflp Analysis ◽  
Leigh Syndrome ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Mutation Load ◽  
Atp Production ◽  
Cybrid Cell

AbstractLeigh syndrome (LS) is an early-onset progressive neurodegenerative disorder associated with mitochondrial deficiency. m.14597A>G (p.Ile26Thr) in the MT-ND6 gene was reported to cause Leberʼs hereditary optic neuropathy (LHON) or dementia/dysarthria. In previous reports, less than 90% heteroplasmy was shown to result in adult-onset disease. Here, by whole mitochondrial sequencing, we identified m.14597A>G mutation of a patient with LS. PCR–RFLP analysis on fibroblasts from the patient revealed a high mutation load (> 90% heteroplasmy). We performed functional assays using cybrid cell models generated by fusing mtDNA-less rho0 HeLa cells with enucleated cells from patient fibroblasts carrying the m.14597A>G variant. Cybrid cell lines bearing the m.14597A>G variant exhibited severe effects on mitochondrial complex I activity. Additionally, impairment of cell proliferation, decreased ATP production and reduced oxygen consumption rate were observed in the cybrid cell lines bearing the m.14597A>G variant when the cells were metabolically stressed in medium containing galactose, indicating mitochondrial respiratory chain defects. These results suggest that a high mutation load of m.14597A>G leads to LS via a mitochondrial complex I defect, rather than LHON or dementia/dysarthria.

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