scholarly journals Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Guang-xing Shui ◽  
Dong Sang ◽  
Xun Yin ◽  
Yun Cai ◽  
Wei Sun
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Renal Fibrosis ◽  
Aristolochic Acid ◽  
Treated Group ◽  
Ros Production ◽  
Atp Content ◽  
Copy Numbers ◽  
Collagen Iii ◽  
Dna Copy Numbers

Objectives. The effects of the traditional formula Dahuang Fuzi Decoction (DFD) on chronic aristolochic acid nephropathy (AAN) in mice and its underlying mechanisms were studied. Methods. Mice were randomly divided into the following six groups: the control group, the model group (AAN), the saline-treated group (AAN + vehicle), the normal dose DFD-treated group (AAN + NDFD), the high dose DFD-treated group (AAN + HDFD), and the rosiglitazone treated group (AAN + Rosi). After treating for 8 weeks, 24 h urine and blood samples were collected and the mice sacrificed to study the biochemical parameters associated with renal function. The samples were analyzed for renal fibrosis and mitochondrial dysfunction (MtD) markers. To achieve that, collagen III, collagen I, mitochondrial DNA copy numbers (mtDNA), mitochondrial membrane potential (MMP), ATP content, and ROS production were evaluated. Results. Our results showed that proteinuria, kidney function, and the renal pathological characteristics were improved by DFD and rosiglitazone. The expression of collagen III and collagen I decreased after treating with either DFD or rosiglitazone. Mitochondrial dysfunction based on the increase in ROS production, decrease in mitochondrial DNA copy numbers, and reduction of MMP and ATP content was improved by DFD and rosiglitazone. Conclusions. DFD could protect against renal impairments and ameliorate mitochondrial dysfunction in chronic AAN mice.

scholarly journals Effect of bariatric surgery on circulating and urinary mitochondrial DNA copy numbers in obesity with or without diabetes

2020 ◽  
Vol 8 (1) ◽  
pp. e001372
Author(s):  
Mihae Seo ◽  
Hyoungnae Kim ◽  
Hyunjin Noh ◽  
Jin Seok Jeon ◽  
Dong Won Byun ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Control Group ◽  
Copy Numbers ◽  
Patient Groups ◽  
Dna Copy Numbers ◽  
Nicotinamide Adenine Dinucleotide Dehydrogenase ◽  
Design And Methods ◽  
Obesity Patient

IntroductionRecent studies have suggested that extracellular circulating and urinary mitochondrial DNA (mtDNA) are associated with mitochondrial dysfunction in obesity and type 2 diabetes mellitus (T2DM). However, the changes to cell-free serum and urinary mtDNA after bariatric surgery in patients with obesity with T2DM have not been investigated to date.Research design and methodsWe prospectively recruited patients with obesity (n=18), and with obesity and T2DM (n=14) who underwent bariatric surgery, along with healthy volunteers (HV) as a control group (n=22). Serum and urinary mitochondrial nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) copy numbers were measured using quantitative PCR (qPCR). The mtDNA copy numbers of patients with obesity (with and without T2DM) were followed up 6 months after surgery.ResultsThe copy numbers of urinary mtND-1 and mtCOX-3 in patients with obesity, with or without T2DM, were higher than those in the HVs. Moreover, urinary mtCOX-3 copy number increased in patients with obesity with T2DM compared with patients with obesity without T2DM (p=0.018). Meanwhile, serum mtCOX-3 copy numbers in HV were higher in both obesity patient groups (p=0.040). Bariatric surgery reduced urinary mtND-1 and mtCOX-3 copy numbers, as well as serum mtCOX-3 copy numbers only in patients with obesity with T2DM.ConclusionThese results suggest that T2DM induces greater kidney mitochondrial dysfunction in patients with obesity, which can be effectively restored with bariatric surgery.

scholarly journals Mitochondrial dysfunction in sepsis is associated with diminished intramitochondrial TFAM despite its increased cellular expression

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tim Rahmel ◽  
Britta Marko ◽  
Hartmuth Nowak ◽  
Lars Bergmann ◽  
Patrick Thon ◽  
...  
Keyword(s):  
Immune Response ◽  
Mitochondrial Dysfunction ◽  
Healthy Volunteers ◽  
Transcription Initiation ◽  
Atp Content ◽  
Initiation Complex ◽  
Cellular Expression ◽  
Copy Numbers ◽  
Transcription Initiation Complex ◽  
Dna Copy Numbers

AbstractSepsis is characterized by a dysregulated immune response, metabolic derangements and bioenergetic failure. These alterations are closely associated with a profound and persisting mitochondrial dysfunction. This however occurs despite increased expression of the nuclear-encoded transcription factor A (TFAM) that normally supports mitochondrial biogenesis and functional recovery. Since this paradox may relate to an altered intracellular distribution of TFAM in sepsis, we tested the hypothesis that enhanced extramitochondrial TFAM expression does not translate into increased intramitochondrial TFAM abundance. Accordingly, we prospectively analyzed PBMCs both from septic patients (n = 10) and lipopolysaccharide stimulated PBMCs from healthy volunteers (n = 20). Extramitochondrial TFAM protein expression in sepsis patients was 1.8-fold greater compared to controls (p = 0.001), whereas intramitochondrial TFAM abundance was approximate 80% less (p < 0.001). This was accompanied by lower mitochondrial DNA copy numbers (p < 0.001), mtND1 expression (p < 0.001) and cellular ATP content (p < 0.001) in sepsis patients. These findings were mirrored in lipopolysaccharide stimulated PBMCs taken from healthy volunteers. Furthermore, TFAM-TFB2M protein interaction within the human mitochondrial core transcription initiation complex, was 74% lower in septic patients (p < 0.001). In conclusion, our findings, which demonstrate a diminished mitochondrial TFAM abundance in sepsis and endotoxemia, may help to explain the paradox of lacking bioenergetic recovery despite enhanced TFAM expression.

scholarly journals Sperm mitochondrial DNA copy numbers in normal and abnormal semen analysis: a systematic review and meta-analysis.

2021 ◽  
Author(s):  
Daria Popova ◽  
Priya Bhide ◽  
Francesco DAntonio ◽  
Purusotam Basnet ◽  
Ganesh Acharya
Keyword(s):  
Mitochondrial Dna ◽  
Sperm Motility ◽  
Semen Quality ◽  
Semen Analysis ◽  
Meta Analysis ◽  
Semen Parameters ◽  
Spermatozoa Motility ◽  
Standard Methodology ◽  
Copy Numbers ◽  
Dna Copy Numbers

Background: Normal mature sperm have a considerably reduced number of mitochondria which provide the energy required for progressive sperm motility. Literature suggests that disorders of sperm motility may be linked to abnormal sperm mitochondrial number and function. Objectives: To summarise the evidence from literature regarding the association of mitochondrial DNA copy numbers and semen quality with a particular emphasis on the spermatozoa motility. Search strategy: Standard methodology recommended by Cochrane. Selection criteria: All published primary research reporting on differences in mitochondrial DNA copy numbers between the sperm of males with a normal and abnormal semen analysis. Data collection and analysis: Using standard methodology recommended by Cochrane we pooled results using a random effects model and the findings were reported as a standardised mean difference. Main results: We included 10 trials. The primary outcome was sperm mitochondrial DNA copy numbers. A meta-analysis including five studies showed significantly higher mitochondrial DNA copy numbers in abnormal semen analysis as compared to normal semen analysis(SMD 1.08, 95% CI 0.74-1.43). Three other studies not included in the meta-analysis showed a significant negative correlation between mitochondrial DNA copy numbers and semen parameters. The quality of evidence was assessed as good to very good in 60% of studies. Conclusions: Our review demonstrates significantly higher mitochondrial DNA in human sperm cells of men with abnormal semen analysis in comparison to men with normal semen analysis. PROSPERO registration: CRD42019118841 Funding None received

Variations in Mitochondrial DNA Copy Numbers in MS Brains

2008 ◽  
Vol 35 (3) ◽  
pp. 283-287 ◽  
Author(s):  
Andrei Blokhin ◽  
Tamara Vyshkina ◽  
Samuel Komoly ◽  
Bernadette Kalman
Keyword(s):  
Mitochondrial Dna ◽  
Copy Numbers ◽  
Dna Copy Numbers

Effects of Micronucleus Frequencies and Mitochondrial DNA Copy Numbers among Benzene‐Exposed Workers in China

2020 ◽  
Vol 61 (3) ◽  
pp. 355-360 ◽  
Author(s):  
Anqi Li ◽  
Yuan Sun ◽  
Tongshuai Wang ◽  
Kan Wang ◽  
Tuanwei Wang ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Copy Numbers ◽  
Exposed Workers ◽  
Dna Copy Numbers

scholarly journals Deep sequencing shows that accumulation of potentially pathogenic mtDNA mutations rather than mtDNA copy numbers may be associated with early embryonic loss

2020 ◽  
Vol 37 (9) ◽  
pp. 2181-2188
Author(s):  
Licheng Ji ◽  
Tingting Liao ◽  
Juan Yang ◽  
Houming Su ◽  
Jianyuan Song ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Spontaneous Abortion ◽  
Missense Mutations ◽  
Mtdna Copy Number ◽  
Mtdna Mutations ◽  
Pathogenic Mutations ◽  
Copy Numbers ◽  
Significant Difference ◽  
Embryonic Loss ◽  
Dna Copy Numbers

Abstract Purpose To explore the relationship between mitochondrial DNA quantity and heteroplasmy and early embryonic loss. Methods A total of 150 villous samples from patients with spontaneous abortion (SA, n = 75) or induced abortion (IA, n = 75) were collected. qPCR and next-generation sequencing (NGS) were used to test mitochondrial DNA quantity and heteroplasmy. Missense mutations with a CADD score > 15 and heteroplasmy ≥ 70% were defined as potentially pathogenic mutations. Results With respect to mitochondrial DNA copy numbers, there was no significant difference between the SA and IA groups (median (IQR), 566 (397–791) vs. 614 (457–739); P = 0.768) or between the euploid and aneuploid groups (median (IQR), 516 (345–730) vs. 599 (423–839); P = 0.107). mtDNA copy numbers were not associated with spontaneous abortion using logistic regression analysis (P = 0.196, 95% CI 1.000–1.001). In addition, more patients harbored possibly pathogenic mtDNA mutations in their chorionic villi in the SA group (70.7%, 53/75) compared with the IA group (54.7%, 41/75; P < 0.05). However, there was no statistical difference between the euploid (80%, 24/30) and aneuploid groups (64.4%, 29/45; p = 0.147). Conclusion Early embryonic loss and the formation of aneuploidy were not related to mtDNA copy number. Patients with spontaneous abortion were more likely to have possibly pathogenic mutations in their mtDNA, and this may assist in purifying pathogenic mtDNA. However, whether the accumulation of these potentially morbific mtDNA mutations caused early embryonic loss requires further investigation.

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