scholarly journals Preparation of mitochondrial DNA from long-term preserved and accident carcass organs in animals.

1994 ◽  
Vol 38 (1) ◽  
pp. 19-23
Author(s):  
Michinari Yokohama ◽  
Taisuke Yamazaki ◽  
Yuichi Kameyama ◽  
Yoshirou Ishijima
Keyword(s):  
Mitochondrial Dna

scholarly journals Genetic Consequences of Fence Confinement in a Population of White-Tailed Deer

Diversity ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 126
Author(s):  
Emily K. Latch ◽  
Kenneth L. Gee ◽  
Stephen L. Webb ◽  
Rodney L. Honeycutt ◽  
Randy W. DeYoung ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Mitochondrial Dna ◽  
Wildlife Management ◽  
Field Observations ◽  
Adaptive Potential ◽  
Population Isolation ◽  
Potential Benefits ◽  
Wildlife Populations ◽  
Mtdna Diversity

Fencing wildlife populations can aid wildlife management goals, but potential benefits may not always outweigh costs of confinement. Population isolation can erode genetic diversity and lead to the accumulation of inbreeding, reducing viability and limiting adaptive potential. We used microsatellite and mitochondrial DNA data collected from 640 white-tailed deer confined within a 1184 ha fence to quantify changes in genetic diversity and inbreeding over the first 12 years of confinement. Genetic diversity was sustained over the course of the study, remaining comparable to unconfined white-tailed deer populations. Uneroded genetic diversity suggests that genetic drift is mitigated by a low level of gene flow, which supports field observations that the fence is not completely impermeable. In year 9 of the study, we observed an unexpected influx of mtDNA diversity and drop in inbreeding as measured by FIS. A male harvest restriction imposed that year increased male survival, and more diverse mating may have contributed to the inbreeding reduction and temporary genetic diversity boost we observed. These data add to our understanding of the long-term impacts of fences on wildlife, but also highlight the importance of continued monitoring of confined populations.

Mitochondrial DNA deletions in the peripheral blood of workers at the Mayak PA who were exposed to long-term combined effects of external γ- and internal α-radiation

BIOPHYSICS ◽  
2016 ◽  
Vol 61 (6) ◽  
pp. 1026-1032
Author(s):  
L. V. Malakhova ◽  
M. G. Lomaeva ◽  
M. L. Zakharova ◽  
E. N. Kirillova ◽  
S. N. Sokolova ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Peripheral Blood ◽  
Combined Effects ◽  
Dna Deletions

Abstract 381: Prolonged Renal Failure Leads to Reduced Number of Active Cardiac Mitochondria in a Rat Model for Long Term Chronic Kidney Disease

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Einat A Hertzberg-Bigelman ◽  
Michal Entin-Meer ◽  
Genya Aharon-Hananel ◽  
Ann Saada ◽  
Ran Levy ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Mitochondrial Dna ◽  
Kidney Disease ◽  
Cardiac Function ◽  
Rat Model ◽  
Dna Content ◽  
Cardiac Mitochondria ◽  
Mitochondrial Content ◽  
Mitochondrial Dna Content

Objectives - Cardiorenal syndrome type 4 is characterized by primary chronic kidney disease (CKD) leading to an impairment of cardiac function. We recently showed a reduced expression of several cardiac mitochondrial genes in short-term CKD rat model. We aimed to evaluate whether cardiac mitochondrial structure and function is modified in long-term CKD and if so, to characterize the potential associated mechanisms. Methods - Lewis rats underwent 5/6 nephrectomy for induction of CKD. Upon necroscopy, eight months later, cardiac sections were analyzed by histology and electron microscopy (EM). Mitochondrial DNA content was determined by the mitochondrial gene, cytochrome B. Mitochondrial content was assessed by citrate synthase (CS) activity in tissue homogenate and respiratory chain function was determined by the activity of complexes I-IV in isolated mitochondria. The levels of PGC1a, a transcription factor for mitochondrial biogenesis, Angiotensin II type 1 receptor and cytosolic cytochrome C were assayed by western blot. Cytokine serum profile was determined by microarray. Results - Long-term CKD leads to cardiac hypertrophy and increased interstitial fibrosis. EM analysis revealed a massive spatial disarrangement accompanied by a considerably increased volume of swollen-damaged mitochondria in CKD hearts (32±3%, n=5, 48±6%, n=4; respectively; p<0.05). Total mitochondrial DNA content was decreased in cardiac tissue of CKD rats. Concomitantly, active mitochondrial content was significantly reduced. Conversely, no differences were observed in respiratory chain enzymes’ functions (complexes I-IV) in isolated active mitochondria. Moreover, inflammatory response and activation of Renin-Angiotensin-Aldosterone-System (RAAS) were detected in the CKD setting. Conclusion - CKD results in a marked reduction of active mitochondria in the heart. Inflammatory cytokines and RAAS, may set a deleterious environment to cardiac mitochondria, as suggested in non-CKD models. The data may represent a significant milestone in the personalized medicine strategy for treating CKD patients who present with normal cardiac function accompanied by positive biomarkers for cardiac mitochondria damage.

Denisovan DNA in Late Pleistocene sediments from Baishiya Karst Cave on the Tibetan Plateau

Science ◽  
2020 ◽  
Vol 370 (6516) ◽  
pp. 584-587
Author(s):  
Dongju Zhang ◽  
Huan Xia ◽  
Fahu Chen ◽  
Bo Li ◽  
Viviane Slon ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Amino Acid ◽  
Tibetan Plateau ◽  
Late Pleistocene ◽  
Amino Acid Substitution ◽  
Middle Pleistocene ◽  
The Tibetan Plateau ◽  
Karst Cave ◽  
Late Middle Pleistocene

A late Middle Pleistocene mandible from Baishiya Karst Cave (BKC) on the Tibetan Plateau has been inferred to be from a Denisovan, an Asian hominin related to Neanderthals, on the basis of an amino acid substitution in its collagen. Here we describe the stratigraphy, chronology, and mitochondrial DNA extracted from the sediments in BKC. We recover Denisovan mitochondrial DNA from sediments deposited ~100 thousand and ~60 thousand years ago (ka) and possibly as recently as ~45 ka. The long-term occupation of BKC by Denisovans suggests that they may have adapted to life at high altitudes and may have contributed such adaptations to modern humans on the Tibetan Plateau.

A new species of chameleon (Squamata: Chamaeleonidae) from the Aberdare Mountains in the central highlands of Kenya

Zootaxa ◽  
2012 ◽  
Vol 3391 (1) ◽  
pp. 1 ◽  
Author(s):  
JAN STIPALA ◽  
NICOLA LUTZMANN ◽  
PATRICK K. MALONZA ◽  
PAUL WILKINSON ◽  
BRENDAN GODLEY ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
New Species ◽  
Temporal Region ◽  
New Taxon ◽  
Term Survival ◽  
Long Term Survival ◽  
Distinct Lineage ◽  
Central Highlands ◽  
A New Species

We describe a new species of chameleon, Trioceros kinangopensis sp. nov., from Kinangop Peak in the Aberdare moun-tains, central highlands of Kenya. The proposed new species is morphologically and genetically distinct from other mem-ber of the bitaeniatus-group. It is morphologically most similar to T. schubotzi but differs in the lack of sexual sizedimorphism, smaller-sized females, smoother, less angular canthus rostrales, smaller scales on the temporal region and abright orange gular crest in males. Mitochondrial DNA indicates that the proposed new taxon is a distinct lineage that isclosely related to T. nyirit and T. schubotzi. The distribution of T. kinangopensis sp. nov. appears to be restricted to the afroalpine zone in vicintiy of Kinangop Peak and fires may pose a serious threat to the long-term survival of this species.

scholarly journals Depletion of mitochondrial DNA alters glucose metabolism in SK-Hep1 cells

2001 ◽  
Vol 280 (6) ◽  
pp. E1007-E1014 ◽  
Author(s):  
Kyu-Sang Park ◽  
Kyung-Jay Nam ◽  
Jun-Woo Kim ◽  
Youn-Bok Lee ◽  
Chang-Yeop Han ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Glucose Metabolism ◽  
Nuclear Dna ◽  
Glucose Transporters ◽  
Diabetic Patients ◽  
Human Hepatoma Cells ◽  
Metabolizing Enzymes ◽  
Atp Production ◽  
Protein Levels

Maternally inherited mitochondrial DNA (mtDNA) has been suggested to be a genetic factor for diabetes. Reports have shown a decrease of mtDNA content in tissues of diabetic patients. We investigated the effects of mtDNA depletion on glucose metabolism by use of ρ0 SK-Hep1 human hepatoma cells, whose mtDNA was depleted by long-term exposure to ethidium bromide. The ρ0 cells failed to hyperpolarize mitochondrial membrane potential in response to glucose stimulation. Intracellular ATP content, glucose-stimulated ATP production, glucose uptake, steady-state mRNA and protein levels of glucose transporters, and cellular activities of glucose-metabolizing enzymes were decreased in ρ0 cells compared with parental ρ+ cells. Our results suggest that the quantitative reduction of mtDNA may suppress the expression of nuclear DNA-encoded glucose transporters and enzymes of glucose metabolism. Thus this may lead to diabetic status, such as decreased ATP production and glucose utilization.

Mitochondrial DNA haplogroups and incidence of lipodystrophy in HIV-infected patients on long-term antiretroviral therapy

2012 ◽  
pp. 1 ◽  
Author(s):  
Andrea De Luca ◽  
Milena Nasi ◽  
Simona Di Giambenedetto ◽  
Alessandro Cozzi-Lepri ◽  
Marcello Pinti ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Antiretroviral Therapy

Frequent Mitochondrial DNA Mutations and Polymorphisms in Long-Term Survivors of Childhood Acute Lymphoblastic Leukemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2800-2800 ◽  
Author(s):  
Steven E. Lipshultz ◽  
Vernon E. Walker ◽  
Salina M. Torres ◽  
Dale M. Walker ◽  
Elly Barry ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Acute Lymphoblastic Leukemia ◽  
Myocardial Dysfunction ◽  
Lymphoblastic Leukemia ◽  
Negative Control ◽  
Trna Genes ◽  
Childhood All ◽  
Mtdna Mutations ◽  
Multi Agent

Abstract Progressive myocardial dysfunction, which can lead to cardiomyopathy, congestive heart failure, and sudden cardiac death, is a well-recognized late effect of several agents used in the treatment of childhood cancer. While the mechanism of this damage is not yet fully characterized, mounting data from rodent models implicate treatment-induced mitochondrial DNA (mtDNA) mutations as one potential mechanism of late cardiotoxicity. In the current study, the Dana-Farber Cancer Institute Acute Lymphoblastic Leukemia (ALL) Consortium collected peripheral blood mononuclear cell samples from 93 long-term ALL survivors who were 4 or more years post-doxorubicin and other multi-agent therapy including asparaginase, corticosteroids, vincristine, and methotrexate, as well as radiation therapy. Data from healthy newborn children (n=45) represented a negative control and data from children receiving highly active antiretroviral therapy (HAART) (mean age=11.3 years; SD=2.61; n=51) provided a positive control for mtDNA mutations. Maximum cumulative doxorubicin dose varied among patients by treatment protocol (median=300 mg/m2; range 45 mg/m2 to 470 mg/m2). Median age at treatment was 4.5 years (range=0.5 to 20.8 years) and at mtDNA screening, 14.9 years (range=6.0 to 41.1 years). The mitochondrial tRNA genes and flanking regions were screened via PCR-based denaturing gradient gel electrophoresis (DGGE). Preliminary data showed 47 confirmed polymorphisms or mutations in 39 of 93 ALL survivors screened (42%), occurring in PCR products from 6 of 13 primer sets. The mutation incidence in HIV positive controls receiving HAART was 35 changes in 25 of 51 patients (49%). To date, the negative control population data suggest the occurrence of very few to no polymorphisms or mutations. Most mtDNA changes in ALL survivors were distinct from those in children receiving HAART, and included some sequence variants with suggested pathogenic characteristics. Analysis of cardiac function is ongoing. These data suggest that childhood ALL and its treatment may lead to mutations, over-expression of rare polymorphisms, and the induction of persistent changes that when spontaneously occurring have been associated with clinically significant cardiac effects. Conclusive evidence that doxorubicin-containing multi-agent therapy leads to persistent mtDNA mutations fundamental to cardiac dysfunction might allow for the isolation and prevention of these cardiotoxic effects.

Mutations of the mitochondrial genome: clinical overview and possible pathophysiology of cell damage

1999 ◽  
Vol 66 ◽  
pp. 111-122 ◽  
Author(s):  
Steven M. Rothman
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Cell Damage ◽  
Genetic Research ◽  
Cellular Mechanisms ◽  
Cultured Fibroblasts ◽  
Dna Mutations ◽  
Physiological Abnormalities ◽  
Nuclear Mutations

Mitochondria possess their own DNA and transcription and translation machinery for the synthesis of 13 protein subunits for the oxidative phosphorylation system, two rRNAs and 22 tRNAs. In 1988 the first human neurodegenerative diseases associated with mutations in the mitochondrial genome were described. The most recent biochemical and genetic research suggests that mitochondrial disorders are best categorized as: (i) primary mutations of the mitochondrial DNA, either sporadic or maternally inherited; (ii) nuclear mutations that result in alterations in mitochondrial DNA or intergenomic signalling defects; or (iii) Mendelian defects that affect the respiratory chain in the absence of mitochondrial DNA mutations. There is still little information about the pathophysiology of these different disorders. In order to obtain some insight into the cellular mechanisms of neurodegeneration, we examined cultured fibroblasts from patients with the MELAS (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes) syndrome, which is most frequently caused by a mutation in the mitochondrial tRNA for leucine. We found that their basal level of ionized calcium was elevated and that they could not normally sequester calcium influxes induced by depolarization. In addition, they were unable to maintain normal mitochondrial membrane potentials, as determined using a voltage-sensitive fluorescent indicator. Despite these physiological perturbations, the MELAS fibroblasts had normal concentrations of ATP. If neurons in MELAS patients have similar physiological abnormalities, their functional properties and long-term viability may be compromised.

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