Relationship between nuclear DNA fragmentation, mitochondrial DNA damage and standard sperm parameters in spermatozoa of fertile and sub‐fertile men before and after freeze‐thawing procedure

Andrologia ◽  
2018 ◽  
Vol 50 (5) ◽  
Author(s):  
H. Amor ◽  
A. Zeyad ◽  
Y. Alkhaled ◽  
M. Laqqan ◽  
A. Saad ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Dna Fragmentation ◽  
Nuclear Dna ◽  
Sperm Parameters ◽  
Mitochondrial Dna Damage ◽  
Before And After ◽  
Nuclear Dna Fragmentation ◽  
Thawing Procedure

scholarly journals Viscum albumL. Extracts Protects HeLa Cells against Nuclear and Mitochondrial DNA Damage

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Evren Önay-Uçar ◽  
Özlem Erol ◽  
Başak Kandemir ◽  
Elif Mertoğlu ◽  
Ali Karagöz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Hela Cells ◽  
Oxidative Dna Damage ◽  
Nuclear Dna ◽  
Viscum Album ◽  
Mitochondrial Dna Damage ◽  
Methanolic Extracts ◽  
Host Trees ◽  
Lime Tree

Viscum albumL. is a semiparasitic plant grown on trees and widely used for the treatment of many diseases in traditional and complementary therapy. It is well known that some activities ofViscum albumextracts are varied depending on the host trees, such as antioxidant, apoptosis-inducing, anticancer activities of the plant. The aim of the present study is to examine the comparative effects of methanolic extracts ofV. albumgrown on three different host trees (locust tree, lime tree, and hedge maple tree) on H2O2-induced DNA damage in HeLa cells. Oxidative damage in mitochondrial DNA and two nuclear regions was assessed by QPCR assay. The cells were pretreated with methanolic extracts (10 μg/mL) for 48 h, followed by the treatment with 750 μM H2O2for 1 hour. DNA damage was significantly induced by H2O2while it was inhibited byV. albumextracts. All extracts completely protected against nuclear DNA damage. While the extract from lime tree or white locust tree entirely inhibited mitochondrial DNA damage, that from hedge maple tree inhibited by only 50%. These results suggest that methanolic extracts ofV. albumcan prevent oxidative DNA damage, and the activity is dependent on the host tree.

scholarly journals PCR‐Based Analysis of Mitochondrial DNA Copy Number, Mitochondrial DNA Damage, and Nuclear DNA Damage

2016 ◽  
Vol 67 (1) ◽  
Author(s):  
Claudia P. Gonzalez‐Hunt ◽  
John P. Rooney ◽  
Ian T. Ryde ◽  
Charumathi Anbalagan ◽  
Rashmi Joglekar ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Nuclear Dna ◽  
Dna Copy Number ◽  
Mitochondrial Dna Damage ◽  
Mitochondrial Dna Copy Number

scholarly journals Asbestos induces mitochondrial DNA damage and dysfunction linked to the development of apoptosis

2003 ◽  
Vol 285 (5) ◽  
pp. L1018-L1025 ◽  
Author(s):  
Arti Shukla ◽  
Michael Jung ◽  
Maria Stern ◽  
Naomi K. Fukagawa ◽  
Douglas J. Taatjes ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Cell Injury ◽  
Nuclear Dna ◽  
Oxidant Stress ◽  
Mesothelial Cells ◽  
Confocal Scanning Laser Microscopy ◽  
Mrna Levels ◽  
Mitochondrial Dna Damage ◽  
Induced Apoptosis

To test the hypothesis that asbestos-mediated cell injury is mediated through an oxidant-dependent mitochondrial pathway, isolated mesothelial cells were examined for mitochondrial DNA damage as determined by quantitative PCR. Mitochondrial DNA damage occurred at fourfold lower concentrations of crocidolite asbestos compared with concentrations required for nuclear DNA damage. DNA damage by asbestos was preceded by oxidant stress as shown by confocal scanning laser microscopy using MitoTracker Green FM and the oxidant probe Redox Sensor Red CC-1. These events were associated with dose-related decreases in steady-state mRNA levels of cytochrome c oxidase, subunit 3 (COIII), and NADH dehydrogenase 5. Subsequently, dose-dependent decreases in formazan production, an indication of mitochondrial dysfunction, increased mRNA expression of pro- and antiapoptotic genes, and increased numbers of apoptotic cells were observed in asbestos-exposed mesothelial cells. The possible contribution of mitochondrial-derived pathways to asbestos-induced apoptosis was confirmed by its significant reduction after pretreatment of cells with a caspase-9 inhibitor. Apoptosis was decreased in the presence of catalase. Last, use of HeLa cells transfected with a mitochondrial transport sequence targeting the human DNA repair enzyme 8-oxoguanine DNA glycosylase to mitochondria demonstrated that asbestos-induced apoptosis was ameliorated with increased cell survival. Studies collectively indicate that mitochondria are initial targets of asbestos-induced DNA damage and apoptosis via an oxidant-related mechanism.

scholarly journals Mitochondrial DNA damage associated with lipid peroxidation of the mitochondrial membrane induced by Fe2+-citrate

2006 ◽  
Vol 78 (3) ◽  
pp. 505-514 ◽  
Author(s):  
Andréa M. Almeida ◽  
Clélia R.A. Bertoncini ◽  
Jiri Borecký ◽  
Nadja C. Souza-Pinto ◽  
Aníbal E. Vercesi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Dna Fragmentation ◽  
Hereditary Hemochromatosis ◽  
Beta Thalassemia ◽  
Rat Liver Mitochondria ◽  
Small Molecular Weight ◽  
Mitochondrial Dna Damage

Iron imbalance/accumulation has been implicated in oxidative injury associated with many degenerative diseases such as hereditary hemochromatosis, beta-thalassemia, and Friedreich's ataxia. Mitochondria are particularly sensitive to iron-induced oxidative stress - high loads of iron cause extensive lipid peroxidation and membrane permeabilization in isolated mitochondria. Here we detected and characterized mitochondrial DNA damage in isolated rat liver mitochondria exposed to a Fe2+-citrate complex, a small molecular weight complex. Intense DNA fragmentation was induced after the incubation of mitochondria with the iron complex. The detection of 3' phosphoglycolate ends at the mtDNA strand breaks by a 32P-postlabeling assay, suggested the involvement of hydroxyl radical in the DNA fragmentation induced by Fe2+-citrate. Increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine also suggested that Fe2+-citrate-induced oxidative stress causes mitochondrial DNA damage. In conclusion, our results show that iron-mediated lipid peroxidation was associated with intense mtDNA damage derived from the direct attack of reactive oxygen species.

scholarly journals Mitochondrial DNA deletions and nuclear DNA fragmentation in testicular and epididymal human sperm

2002 ◽  
Vol 17 (6) ◽  
pp. 1565-1570 ◽  
Author(s):  
M. O'Connell ◽  
N. McClure ◽  
S.E.M. Lewis
Keyword(s):  
Mitochondrial Dna ◽  
Dna Fragmentation ◽  
Nuclear Dna ◽  
Human Sperm ◽  
Dna Deletions ◽  
Nuclear Dna Fragmentation

Flow cytometric measurement of sperm nuclear DNA fragmentation in infertile men with normal standard sperm parameters

2009 ◽  
Vol 6 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Tzvetan H. Lukanov ◽  
Danail I. Lichev ◽  
Emiliana I. Konova ◽  
Alkan I. Emin ◽  
Nina P. Ayvazova ◽  
...  
Keyword(s):  
Dna Fragmentation ◽  
Nuclear Dna ◽  
Sperm Parameters ◽  
Flow Cytometric ◽  
Infertile Men ◽  
Flow Cytometric Measurement ◽  
Nuclear Dna Fragmentation ◽  
Normal Standard

scholarly journals p53 is required for nuclear but not mitochondrial DNA damage-induced degeneration

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Matthew J. Geden ◽  
Selena E. Romero ◽  
Mohanish Deshmukh
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Nuclear Dna ◽  
Neuronal Cell ◽  
Axon Degeneration ◽  
Whole Cell ◽  
Axon Pruning ◽  
Mtdna Damage ◽  
Mitochondrial Dna Damage ◽  
Neuronal Cell Bodies

AbstractWhile the consequences of nuclear DNA damage have been well studied, the exact consequences of acute and selective mitochondrial DNA (mtDNA) damage are less understood. DNA damaging chemotherapeutic drugs are known to activate p53-dependent apoptosis in response to sustained nuclear DNA damage. While it is recognized that whole-cell exposure to these drugs also damages mtDNA, the specific contribution of mtDNA damage to cellular degeneration is less clear. To examine this, we induced selective mtDNA damage in neuronal axons using microfluidic chambers that allow for the spatial and fluidic isolation of neuronal cell bodies (containing nucleus and mitochondria) from the axons (containing mitochondria). Exposure of the DNA damaging drug cisplatin selectively to only the axons induced mtDNA damage in axonal mitochondria, without nuclear damage. We found that this resulted in the selective degeneration of only the targeted axons that were exposed to DNA damage, where ROS was induced but mitochondria were not permeabilized. mtDNA damage-induced axon degeneration was not mediated by any of the three known axon degeneration pathways: apoptosis, axon pruning, and Wallerian degeneration, as Bax-deficiency, or Casp3-deficiency, or Sarm1-deficiency failed to protect the degenerating axons. Strikingly, p53, which is essential for degeneration after nuclear DNA damage, was also not required for degeneration induced with mtDNA damage. This was most evident when the p53-deficient neurons were globally exposed to cisplatin. While the cell bodies of p53-deficient neurons were protected from degeneration in this context, the axons farthest from the cell bodies still underwent degeneration. These results highlight how whole cell exposure to DNA damage activates two pathways of degeneration; a faster, p53-dependent apoptotic degeneration that is triggered in the cell bodies with nuclear DNA damage, and a slower, p53-independent degeneration that is induced with mtDNA damage.

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