scholarly journals Testosterone Upregulates the Expression of Mitochondrial ND1 and ND4 and Alleviates the Oxidative Damage to the Nigrostriatal Dopaminergic System in Orchiectomized Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Wensheng Yan ◽  
Yunxiao Kang ◽  
Xiaoming Ji ◽  
Shuangcheng Li ◽  
Yingkun Li ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Oxidative Damage ◽  
Mitochondrial Function ◽  
Complex I ◽  
Dopaminergic System ◽  
Male Rats ◽  
Mitochondrial Complex I ◽  
Testosterone Deficiency ◽  
Mitochondrial Complex ◽  
Mitochondrial Nd1

Testosterone deficiency, as a potential risk factor for aging and aging-related neurodegenerative disorders, might induce mitochondrial dysfunction and facilitate the declines of the nigrostriatal dopaminergic system by exacerbating the mitochondrial defects and increasing the oxidative damage. Thus, how testosterone levels influence the mitochondrial function in the substantia nigra was investigated in the study. The present studies showed that testosterone deficiency impaired the mitochondrial function in the substantia nigra and induced the oxidative damage to the substantia nigra as well as the deficits in the nigrostriatal dopaminergic system. Of four mitochondrial respiratory chain complexes, castration of male rats reduced the activity of mitochondrial complex I and downregulated the expression of ND1 and ND4 of 7 mitochondrial DNA- (mtDNA-) encoded subunits of complex I in the substantia nigra. Supplements of testosterone propionate to castrated male rats ameliorated the activity of mitochondrial complex I and upregulated the expression of mitochondrial ND1 and ND4. These results suggest an important role of testosterone in maintaining the mitochondrial function in the substantia nigra and the vulnerability of mitochondrial complex I to testosterone deficiency. Mitochondrial ND1 and ND4, as potential testosterone targets, were implicated in the oxidative damage to the nigrostriatal dopaminergic system.

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 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 DJ-1 Null Dopaminergic Neuronal Cells Exhibit Defects in Mitochondrial Function and Structure: Involvement of Mitochondrial Complex I Assembly

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e32629 ◽  
Author(s):  
Jun Young Heo ◽  
Ji Hoon Park ◽  
Soung Jung Kim ◽  
Kang Sik Seo ◽  
Jeong Su Han ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Complex I ◽  
Neuronal Cells ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Assembly

scholarly journals Inhibition of Mitochondrial Complex I Impairs Release of α-Galactosidase by Jurkat Cells

2019 ◽  
Vol 20 (18) ◽  
pp. 4349
Author(s):  
Jonathan Lambert ◽  
Steven Howe ◽  
Ahad Rahim ◽  
Derek Burke ◽  
Simon Heales
Keyword(s):  
Respiratory Chain ◽  
Mitochondrial Function ◽  
Complex I ◽  
Mitochondrial Respiratory Chain ◽  
Jurkat Cells ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Mitochondrial Respiratory Chain Activity ◽  
Respiratory Chain Activity ◽  
Mitochondrial Respiratory

Fabry disease (FD) is caused by mutations in the GLA gene that encodes lysosomal α-galactosidase-A (α-gal-A). A number of pathogenic mechanisms have been proposed and these include loss of mitochondrial respiratory chain activity. For FD, gene therapy is beginning to be applied as a treatment. In view of the loss of mitochondrial function reported in FD, we have considered here the impact of loss of mitochondrial respiratory chain activity on the ability of a GLA lentiviral vector to increase cellular α-gal-A activity and participate in cross correction. Jurkat cells were used in this study and were exposed to increasing viral copies. Intracellular and extracellular enzyme activities were then determined; this in the presence or absence of the mitochondrial complex I inhibitor, rotenone. The ability of cells to take up released enzyme was also evaluated. Increasing transgene copies was associated with increasing intracellular α-gal-A activity but this was associated with an increase in Km. Release of enzyme and cellular uptake was also demonstrated. However, in the presence of rotenone, enzyme release was inhibited by 37%. Excessive enzyme generation may result in a protein with inferior kinetic properties and a background of compromised mitochondrial function may impair the cross correction process.

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