scholarly journals SOD2 Mediates Curcumin-Induced Protection against Oxygen-Glucose Deprivation/Reoxygenation Injury in HT22 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yuqing Wang ◽  
Yuanyuan Zhang ◽  
Liang Yang ◽  
Jin Yuan ◽  
Ji Jia ◽  
...  
Keyword(s):  
Cell Morphology ◽  
Complex I ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Control Group ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Ht22 Cells ◽  
Mitochondrial Superoxide ◽  
Complex I Activity

Curcumin (Cur) induces neuroprotection against brain ischemic injury; however, the mechanism is still obscure. The aim of this study is to explore the potential neuroprotective mechanism of curcumin against oxygen-glucose deprivation/reoxygenation (OGD/R) injury in HT22 cells and investigate whether type-2 superoxide dismutase (SOD2) is involved in the curcumin-induced protection. In the present study, HT22 neuronal cells were treated with 3 h OGD plus 24 h reoxygenation to mimic ischemia/reperfusion injury. Compared with the normal cultured control group, OGD/R treatment reduced cell viability and SOD2 expression, decreased mitochondrial membrane potential (MMP) and mitochondrial complex I activity, damaged cell morphology, and increased lactic dehydrogenase (LDH) release, cell apoptosis, intracellular reactive oxygen species (ROS), and mitochondrial superoxide (P<0.05). Meanwhile, coadministration of 100 ng/ml curcumin reduced the cell injury and apoptosis, inhibited intracellular ROS and mitochondrial superoxide accumulation, and ameliorated intracellular SOD2, cell morphology, MMP, and mitochondrial complex I activity. Downregulating the SOD2 expression by using siRNA, however, significantly reversed the curcumin-induced cytoprotection (P<0.05). These findings indicated that curcumin induces protection against OGD/R injury in HT22 cells, and SOD2 protein may mediate the protection.

Effect of nutritional support on mitochondrial complex I activity in malnourished patients with anorexia nervosa

2013 ◽  
Vol 38 (11) ◽  
pp. 1093-1098
Author(s):  
Beatriz De-Mateo-Silleras ◽  
Sara R. Alonso-Torre ◽  
Paz Redondo-del-Río ◽  
Khursheed Jeejeebhoy ◽  
Alberto Miján-de-la-Torre
Keyword(s):  
Anorexia Nervosa ◽  
Complex I ◽  
Physical Inactivity ◽  
Positive Association ◽  
Fat Free Mass ◽  
Control Group ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Activity ◽  
Healthy Females

Previous studies have shown a reduction in lymphocyte mitochondrial complex I activity (CIA) in malnourished patients, which is restored after refeeding. Our aim was to evaluate the usefulness of CIA as an indicator of nutritional status in anorexia nervosa patients. Twelve malnourished anorexia nervosa females (mean age, 24.5 years) were admitted to the Eating Disorders Unit. Basal and weekly anthropometrics, bioelectric impedance (BIA), body composition, and CIA were performed until discharge. Patients were matched to 25 healthy females and refeeding was adjusted according to the Unit’s protocol. Statistics were used as appropriated and significance was reached at p < 0.05. Patients showed a significant reduction in body mass index, fat mass and fat free mass (FFM), triceps skinfold, and waist circumference on admission as compared with the control group. Parameters improved during hospitalization, but they failed to reach normal values at discharge. Compared with controls, CIA was significantly lower in patients on admission (2.16 vs. 5.68 nmol·min−1·mg protein−1). Refeeding and weight gain did not restore CIA. A positive association (r2 = 0.69) was found between FFM and CIA in patients at discharge. Malnourished females with anorexia nervosa have lower CIA than controls that is not recovered after refeeding. This could be because of a low FFM exacerbated by physical inactivity while in hospital.

CFM6 is an Essential CRM Protein Required for the Splicing of nad5 Transcript in Arabidopsis Mitochondria

2021 ◽  
Author(s):  
Wei-Chih Lin ◽  
Ya-Huei Chen ◽  
Shin-Yuan Gu ◽  
Hwei-Ling Shen ◽  
Kai-Chau Huang ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
High Accumulation ◽  
Stunted Growth ◽  
Growth Defects ◽  
Group I ◽  
Or Genes ◽  
Complex I Activity ◽  
Intron 4

Abstract Plant CRM domain-containing proteins are capable of binding RNA to facilitate the splicing of group I or II introns in chloroplasts, but their functions in mitochondria are less clear. In the present study, Arabidopsis thaliana CFM6, a protein with a single CRM domain, was expressed in most plant tissues, particularly in flower tissues, and restricted to mitochondria. Mutation of CFM6 causes severe growth defects, including stunted growth, curled leaves, delayed embryogenesis, and pollen development. CFM6 functions specifically in the splicing of group II intron 4 of nad5, which encodes a subunit of mitochondrial complex I, as evidenced by the loss of nad5 intron 4 splicing and high accumulation of its pretranscripts in cfm6 mutants. The phenotypic and splicing defects of cfm6 were rescued in transgenic plants overexpressing 35S::CFM6-YFP. Splicing failure in cfm6 also led to the loss of complex I activity and to its improper assembly. Moreover, dysfunction of complex I induced the expression of proteins or genes involved in alternative respiratory pathways in cfm6. Collectively, CFM6, a previously uncharacterized CRM domain-containing protein, is specifically involved in the cis-splicing of nad5 intron 4 and plays a pivotal role in mitochondrial complex I biogenesis and normal plant growth.

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.

Synthesis and Mitochondrial Complex I Activity of Annonaceous Trans and Cis Solamins Precursors

2004 ◽  
Vol 1 (4) ◽  
pp. 316-322 ◽  
Author(s):  
Julie Defretin ◽  
Christophe Gleye ◽  
Diego Cortes ◽  
Xavier Franck ◽  
Reynald Hocquemiller ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Activity
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