scholarly journals Impaired mitochondrial complex III and melatonin responsive reactive oxygen species generation in kidney mitochondria of db/db mice

2011 ◽  
Vol 51 (3) ◽  
pp. 338-344 ◽  
Author(s):  
Hua Zhang ◽  
Hong-Mei Zhang ◽  
Li-Ping Wu ◽  
Dun-Xian Tan ◽  
Amrita Kamat ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Kidney Mitochondria

scholarly journals Mitochondria protection from hypoxia/reoxygenation injury with mitochondria heat shock protein 70 overexpression

2008 ◽  
Vol 294 (1) ◽  
pp. H249-H256 ◽  
Author(s):  
Courtney L. Williamson ◽  
Erinne R. Dabkowski ◽  
Wolfgang H. Dillmann ◽  
John M. Hollander
Keyword(s):  
Reactive Oxygen Species ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Neonatal Rat ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Simulated Ischemia

The majority of mitochondrial proteins are encoded by nuclear genes and synthesized in the cytosol as preproteins containing a mitochondria import sequence. Preproteins traverse the outer mitochondrial membrane in an unfolded state and then translocate through the inner membrane into the matrix via import machinery that includes mitochondrial heat shock protein 70 (mtHSP70). Neonatal rat cardiac myocytes (NCM) infected with an adenoviral vector expressing mtHSP70 or an empty control (Adv−) for 48 h were submitted to 8 h of simulated ischemia (hypoxia) followed by 16 h of reperfusion (reoxygenation). Infection with mtHSP70 virus yielded an increase in mtHSP70 protein in NCM mitochondria compared with Adv−( P < 0.05). Cell viability after simulated ischemia/reperfusion (I/R) was decreased in both Adv−and mtHSP70 groups, relative to control ( P < 0.05), but mtHSP70-infected NCM had enhanced viability after I/R relative to Adv-infected NCM ( P < 0.05). Simulated I/R caused an increase in reactive oxygen species generation and lipid peroxidation in Adv-infected NCM ( P < 0.05, for both) that was not observed in mtHSP70-infected NCM. Mitochondrial complex III and IV activities were greater in mtHSP70-infected NCM after simulated I/R compared with Adv−( P < 0.05 for both). After simulated I/R, ATP content increased in mtHSP70-infected NCM, compared with Adv−( P < 0.05). Apoptotic markers were decreased in mtHSP70-infected NCM compared with Adv−after simulated I/R ( P < 0.05). These results indicate that overexpression of mtHSP70 protects the mitochondria against damage from simulated I/R that may be due to a decrease in reactive oxygen species leading to preservation of mitochondrial complex function activities and ATP formation.

scholarly journals Reactive Oxygen Species Generated at Mitochondrial Complex III Stabilize Hypoxia-inducible Factor-1α during Hypoxia

2000 ◽  
Vol 275 (33) ◽  
pp. 25130-25138 ◽  
Author(s):  
Navdeep S. Chandel ◽  
David S. McClintock ◽  
Carlos E. Feliciano ◽  
Teresa M. Wood ◽  
J. Andres Melendez ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Hypoxia Inducible Factor 1Α

scholarly journals Metabolic determinants of cellular fitness dependent on mitochondrial reactive oxygen species

2020 ◽  
Vol 6 (45) ◽  
pp. eabb7272
Author(s):  
Hyewon Kong ◽  
Colleen R. Reczek ◽  
Gregory S. McElroy ◽  
Elizabeth M. Steinert ◽  
Tim Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cancer Cells ◽  
Complex I ◽  
Lymphoblastic Leukemia ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex

Mitochondria-derived reactive oxygen species (mROS) are required for the survival, proliferation, and metastasis of cancer cells. The mechanism by which mitochondrial metabolism regulates mROS levels to support cancer cells is not fully understood. To address this, we conducted a metabolism-focused CRISPR-Cas9 genetic screen and uncovered that loss of genes encoding subunits of mitochondrial complex I was deleterious in the presence of the mitochondria-targeted antioxidant mito-vitamin E (MVE). Genetic or pharmacologic inhibition of mitochondrial complex I in combination with the mitochondria-targeted antioxidants, MVE or MitoTEMPO, induced a robust integrated stress response (ISR) and markedly diminished cell survival and proliferation in vitro. This was not observed following inhibition of mitochondrial complex III. Administration of MitoTEMPO in combination with the mitochondrial complex I inhibitor phenformin decreased the leukemic burden in a mouse model of T cell acute lymphoblastic leukemia. Thus, mitochondrial complex I is a dominant metabolic determinant of mROS-dependent cellular fitness.

scholarly journals Mammalian Mitochondrial Complex I: Biogenesis, Regulation, and Reactive Oxygen Species Generation

2010 ◽  
Vol 12 (12) ◽  
pp. 1431-1470 ◽  
Author(s):  
Werner J.H. Koopman ◽  
Leo G.J. Nijtmans ◽  
Cindy E.J. Dieteren ◽  
Peggy Roestenberg ◽  
Federica Valsecchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex
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