Relevant bibliographies by topics / Mitochondrial alterations

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mitochondrial alterations'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2024

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Journal articles on the topic "Mitochondrial alterations"

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Shen, Liang, and Xianquan Zhan. "Mitochondrial Dysfunction Pathway Alterations Offer Potential Biomarkers and Therapeutic Targets for Ovarian Cancer." Oxidative Medicine and Cellular Longevity 2022 (April 20, 2022): 1–22. http://dx.doi.org/10.1155/2022/5634724.

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The mitochondrion is a very versatile organelle that participates in some important cancer-associated biological processes, including energy metabolism, oxidative stress, mitochondrial DNA (mtDNA) mutation, cell apoptosis, mitochondria-nuclear communication, dynamics, autophagy, calcium overload, immunity, and drug resistance in ovarian cancer. Multiomics studies have found that mitochondrial dysfunction, oxidative stress, and apoptosis signaling pathways act in human ovarian cancer, which demonstrates that mitochondria play critical roles in ovarian cancer. Many molecular targeted drugs have been developed against mitochondrial dysfunction pathways in ovarian cancer, including olive leaf extract, nilotinib, salinomycin, Sambucus nigra agglutinin, tigecycline, and eupatilin. This review article focuses on the underlying biological roles of mitochondrial dysfunction in ovarian cancer progression based on omics data, potential molecular relationship between mitochondrial dysfunction and oxidative stress, and future perspectives of promising biomarkers and therapeutic targets based on the mitochondrial dysfunction pathway for ovarian cancer.
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Kim, Hyoung Kyu, Won Sun Park, Sung Hyun Kang, et al. "Mitochondrial alterations in human gastric carcinoma cell line." American Journal of Physiology-Cell Physiology 293, no. 2 (2007): C761—C771. http://dx.doi.org/10.1152/ajpcell.00043.2007.

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We compared mitochondrial function, morphology, and proteome in the rat normal gastric cell line RGM-1 and the human gastric cancer cell line AGS. Total numbers and cross-sectional sizes of mitochondria were smaller in AGS cells. Mitochondria in AGS cells were deformed and consumed less oxygen. Confocal microscopy indicated that the mitochondrial inner membrane potential was hyperpolarized and the mitochondrial Ca2+concentration was elevated in AGS cells. Interestingly, two-dimensional electrophoresis proteomics on the mitochondria-enriched fraction revealed high expression of four mitochondrial proteins in AGS cells: ubiquinol-cytochrome c reductase, mitochondrial short-chain enoyl-coenzyme A hydratase-1, heat shock protein 60, and mitochondria elongation factor Tu. The results provide clues as to the mechanism of the mitochondrial changes in cancer at the protein level and may serve as potential cancer biomarkers in mitochondria.
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Lenzi, Paola, Francesca Biagioni, Carla L. Busceti, et al. "Alterations of Mitochondrial Structure in Methamphetamine Toxicity." International Journal of Molecular Sciences 23, no. 16 (2022): 8926. http://dx.doi.org/10.3390/ijms23168926.

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Recent evidence shows that methamphetamine (METH) produces mitochondrial alterations that contribute to neurotoxicity. Nonetheless, most of these studies focus on mitochondrial activity, whereas mitochondrial morphology remains poorly investigated. In fact, morphological evidence about the fine structure of mitochondria during METH toxicity is not available. Thus, in the present study we analyzed dose-dependent mitochondrial structural alterations during METH exposure. Light and transmission electron microscopy were used, along with ultrastructural stoichiometry of catecholamine cells following various doses of METH. In the first part of the study cell death and cell degeneration were assessed and they were correlated with mitochondrial alterations observed using light microscopy. In the second part of the study, ultrastructural evidence of specific mitochondrial alterations of crests, inner and outer membranes and matrix were quantified, along with in situ alterations of mitochondrial proteins. Neurodegeneration induced by METH correlates significantly with specific mitochondrial damage, which allows definition of a scoring system for mitochondrial integrity. In turn, mitochondrial alterations are concomitant with a decrease in fission/mitophagy protein Fis1 and DRP1 and an increase in Pink1 and Parkin in situ, at the mitochondrial level. These findings provide structural evidence that mitochondria represent both direct and indirect targets of METH-induced toxicity
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Ludwig, Rebecca, Bimala Malla, Maria Höhrhan, Carmen Infante-Duarte, and Lina Anderhalten. "Investigating the Mitoprotective Effects of S1P Receptor Modulators Ex Vivo Using a Novel Semi-Automated Live Imaging Set-Up." International Journal of Molecular Sciences 25, no. 1 (2023): 261. http://dx.doi.org/10.3390/ijms25010261.

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In multiple sclerosis (MS), mitochondrial alterations appear to contribute to disease progression. The sphingosine-1-phosphate receptor modulator siponimod is approved for treating secondary progressive MS. Its preceding compound fingolimod was shown to prevent oxidative stress-induced alterations in mitochondrial morphology. Here, we assessed the effects of siponimod, compared to fingolimod, on neuronal mitochondria in oxidatively stressed hippocampal slices. We have also advanced the model of chronic organotypic hippocampal slices for live imaging, enabling semi-automated monitoring of mitochondrial alterations. The slices were prepared from B6.Cg-Tg(Thy1-CFP/COX8A)S2Lich/J mice that display fluorescent neuronal mitochondria. They were treated with hydrogen peroxide (oxidative stress paradigm) ± 1 nM siponimod or fingolimod for 24 h. Afterwards, mitochondrial dynamics were investigated. Under oxidative stress, the fraction of motile mitochondria decreased and mitochondria were shorter, smaller, and covered smaller distances. Siponimod partly prevented oxidatively induced alterations in mitochondrial morphology; for fingolimod, a similar trend was observed. Siponimod reduced the decrease in mitochondrial track displacement, while both compounds significantly increased track speed and preserved motility. The novel established imaging and analysis tools are suitable for assessing the dynamics of neuronal mitochondria ex vivo. Using these approaches, we showed that siponimod at 1 nM partially prevented oxidatively induced mitochondrial alterations in chronic brain slices.
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McCormick, A. Louise, Vanessa L. Smith, Dar Chow, and Edward S. Mocarski. "Disruption of Mitochondrial Networks by the Human Cytomegalovirus UL37 Gene Product Viral Mitochondrion-Localized Inhibitor of Apoptosis." Journal of Virology 77, no. 1 (2003): 631–41. http://dx.doi.org/10.1128/jvi.77.1.631-641.2003.

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ABSTRACT By 24 h after infection with human cytomegalovirus, the reticular mitochondrial network characteristic of uninfected fibroblasts was disrupted as mitochondria became punctate and dispersed. These alterations were associated with expression of the immediate-early (α) antiapoptotic UL37x1 gene product viral mitochondrion-localized inhibitor of apoptosis (vMIA). Similar alterations in mitochondrial morphology were induced directly by vMIA in transfected cells. A 68-amino-acid antiapoptotic derivative of vMIA containing the mitochondrial localization and antiapoptotic domains also induced disruption, whereas a mutant lacking the antiapoptotic domain failed to cause disruption. These data suggest that the fission and/or fusion process that normally controls mitochondrial networks is altered by vMIA. Mitochondrial fission has been implicated in the induction of apoptosis and vMIA-mediated inhibition of apoptosis may occur subsequent to this event.
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Kurt, Yasemin Gulcan, Bulent Kurt, Tuncer Cayci, and Emin Ozgur Akgul. "Mitochondrial DNA alterations in colorectal cancer cell lines." Journal of Nippon Medical School 79, no. 3 (2012): 244. http://dx.doi.org/10.1272/jnms.79.244.

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Gao, Kuo, Meiying Niu, Xing Zhai, Youliang Huang, Xin Tian, and Tiangang Li. "Genetic and non-genetic factors responsible for mitochondrial failure and Alzheimer’s disease." Genetika 46, no. 2 (2014): 631–47. http://dx.doi.org/10.2298/gensr1402631g.

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The objective of this review article is to explain the factors responsible for damaged mitochondria and its association with Alzheimer?s disease. Alzheimer?s disease (AD) is fairly produced by dysfunctional mitochondria that are alternatively caused by excessive reactive oxygen species and mitochondrial dynamic imbalance. In the pathogenesis of AD, there is important role of many factors including amyloid-beta peptide (A ), tau-proteins, and mutations in presenilin-1. Additionally, mitochondrial-targeted antioxidants have also been explained because of their significance to mitochondrial alterations in AD. Moreover, alteration in mitochondrial dynamics is responsible for the generation of segregated, damaged mitochondria that are, later on, destroyed through mitochondrial autophagy in AD. Finally, various novel models used for studying Alzheimer?s disease, have been discussed.
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Simcox, Eve M., Amy Reeve, and Doug Turnbull. "Monitoring mitochondrial dynamics and complex I dysfunction in neurons: implications for Parkinson's disease." Biochemical Society Transactions 41, no. 6 (2013): 1618–24. http://dx.doi.org/10.1042/bst20130189.

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Mitochondrial dynamics are essential for maintaining organelle stability and function. Through fission, fusion and mitophagic events, optimal populations of mitochondria are retained. Subsequently, alterations in such processes can have profound effects on the individual mitochondrion and the cell within which they reside. Neurons are post-mitotic energy-dependent cells and, as such, are particularly vulnerable to alterations in cellular bioenergetics and increased stress that may occur as a direct or indirect result of mitochondrial dysfunction. The trafficking of mitochondria to areas of higher energy requirements, such as synapses, where mitochondrial densities fluctuate, further highlights the importance of efficient mitochondrial dynamics in neurons. PD (Parkinson's disease) is a common progressive neurodegenerative disorder which is characterized by the loss of dopaminergic neurons within the substantia nigra. Complex I, the largest of all of the components of the electron transport chain is heavily implicated in PD pathogenesis. The exact series of events that lead to cell loss, however, are not fully elucidated, but are likely to involve dysfunction of mitochondria, their trafficking and dynamics.
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Gordon, J. A., and V. H. Gattone. "Mitochondrial alterations in cisplatin-induced acute renal failure." American Journal of Physiology-Renal Physiology 250, no. 6 (1986): F991—F998. http://dx.doi.org/10.1152/ajprenal.1986.250.6.f991.

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The mild reversible nonoliguric form of acute renal failure is perhaps the most common of many nephrotoxic side effects that occur secondary to cisplatin administration. The present studies were undertaken to gain insight into mitochondria alterations and morphological abnormalities underlying this form of renal failure. Following a single intraperitoneal injection of 5.5 mg/kg body wt of cisplatin changes in renal function, mitochondrial respiration, and calcium accumulation were measured serially over a 9-day period. Results indicate that reversible functional changes secondary to cisplatin are accompanied by changes in mitochondrial respiration and calcium accumulation. A decline in state 3 mitochondrial respiration precedes mitochondrial calcium accumulation. However, calcium accumulation begins to recover before mitochondrial respiration. At the peak of functional and biochemical injury morphological damage is extensive, and mitochondria are strikingly aberrant. The results demonstrate that changes in mitochondrial respiration and calcium accumulation occur secondary to cisplatin administration. Both of these effects may play a role in the renal cellular injury induced by cisplatin.
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Leão Barros, Mariceli Baia, Danilo do Rosário Pinheiro, and Bárbara do Nascimento Borges. "Mitochondrial DNA Alterations in Glioblastoma (GBM)." International Journal of Molecular Sciences 22, no. 11 (2021): 5855. http://dx.doi.org/10.3390/ijms22115855.

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Glioblastoma (GBM) is an extremely aggressive tumor originating from neural stem cells of the central nervous system, which has high histopathological and genomic diversity. Mitochondria are cellular organelles associated with the regulation of cellular metabolism, redox signaling, energy generation, regulation of cell proliferation, and apoptosis. Accumulation of mutations in mitochondrial DNA (mtDNA) leads to mitochondrial dysfunction that plays an important role in GBM pathogenesis, favoring abnormal energy and reactive oxygen species production and resistance to apoptosis and to chemotherapeutic agents. The present review summarizes the known mitochondrial DNA alterations related to GBM, their cellular and metabolic consequences, and their association with diagnosis, prognosis, and treatment.
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Dissertations / Theses on the topic "Mitochondrial alterations"

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Marmolino, Daniele. "Alterations of mitochondrial biogenesis and alterations of mitochondrial antioxidant defense in Friedreich's ataxia." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209972.

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Friedreich’s ataxia (FRDA) is an autosomal recessive inherited disorder affecting approximately 1 every 40,000 individuals in Western Europe, is characterized by progressive gait and limb ataxia, dysarthria, areflexia, loss of vibratory and position sense, and a progressive weakness of central origin. Additional features particularly include an hypertrophic cardiomyopathy that can cause premature death. A large GAA repeat expansion in the first intron of the FXN gene is the most common mutation underlying FRDA. Patients show severely reduced levels of the FXN-encoded mitochondrial protein frataxin.<p>Frataxin function is not yet completely elucidated. In frataxin deficiency conditions abnormalities of iron metabolism occur: decreased activities of iron-sulfur cluster (ISC) containing proteins, accumulation of iron in mitochondria and depletion in the cytosol, enhanced cellular iron uptake, and, in some models, reduced heme synthesis. <p>Evidence of oxidative stress has also been found in most though not all models of frataxin deficiency. Accordingly, yfh1-deficient yeast and cells from FRDA patients are highly sensitive to oxidants. Respiratory chain dysfunction further aggravate oxidative stress by increasing leakage of electrons and the formation of superoxide. Frataxin deficient cells not only generate more free radicals, but, they also show a reduced ability to mobilize antioxidant defenses, in particular to induce superoxide dismutase 2 (SOD2).<p>Peroxisome proliferator-activated receptor (PPAR) isoform-gamma play a key role in numerous cellular functions and is a key regulator of mitochondrial biogenesis and of the ROS metabolism. Recruitment of the PPAR coactivator-1a (PGC-1a) mediates many effects of the PPAR-γ activation.<p>In a first work we assessed the potential beneficial effects of a potent PPAR-gamma agonist on frataxin expression in primary fibroblasts from healthy controls and FRDA patients, and Neuroblastoma cells. We used the APAF molecule (1-0-hexadecyl-2-azelaoyl-sn-glycero-3-phosphocoline; C33H66NO9P). Our results show that this compound is able to increase frataxin amount both at transcriptional and post-transcriptional level. At a dose of 20µM frataxin mRNA significantly increases in both controls (p=0.03) and FRDA patients (p=0.002) fibroblasts (1). The finding was confirmed in Neuroblastoma cells (p=0.042). According to previous publications APAF, as others PPAR-gamma agonists is able to up-regulate PGC-1a transcription.<p>In a second part of the study we investigate the role of the PPAR-gamma/PGC-1a pathway in the pathogenesis of FRDA. We performed a microarray analysis of heart and skeletal muscle in a mouse model of frataxin deficiency and we found molecular evidence of increased lipogenesis in skeletal muscle and alteration of fiber-type composition in heart, consistent with insulin resistance and cardiomyopathy, respectively. Since the PPAR-gamma pathway is known to regulate both processes, we hypothesized that dysregulation of this pathway could play a key role in frataxin deficiency. We confirmed this by showing a coordinate dysregulation of Pgc1a and the transcription factor Srebp1 in cellular and animal models of frataxin deficiency, and in cells from FRDA patients, who have marked insulin resistance. Particularly, PGC-1a was found significantly reduced (2) in primary fibroblasts and lymphocytes from FRDA patients (p<0.05). Furthermore, PGC-1a mRNA levels strongly correlate with frataxin relative mRNA levels (r2=0.9, p<0.001). According to this observation, in C2C12 myoblasts, PGC-1a and a reporter gene under the control of the PGC-1a promoter are rapidly down-regulated (p<0.05) when frataxin expression is inhibited by an shRNA in vitro. To further investigate this relation, we then generate PGC-1a deficient fibroblasts cells using a specific siRNA; at 72 hours of transfection frataxin was found down-regulate (p<0.05) in control cells. <p>Taken together those data indicate that some mechanism directly links an early effect of frataxin deficiency with reduced PGC-1a transcription in this cell type, and presumably in other cells that also down-regulate PGC-1α when frataxin levels are low.<p>Finally, since PGC-1a has also emerged as a key factor in the induction of many antioxidant programs in response to oxidative stress, both in vivo and in vitro, in particular in neurons, we tested whether the PGC-1a down-regulation occurring in FRDA cells could be in part responsible for the blunted antioxidant response observed in frataxin deficiency.<p>Using primary fibroblasts from FRDA patients we found reduced SOD2 levels (p<0.05), according to PGC1&<br>Doctorat en Sciences biomédicales et pharmaceutiques<br>info:eu-repo/semantics/nonPublished
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Moorehead, Roger A. "Mitochondrial alterations in tumour cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ30106.pdf.

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Meierhofer, David. "Mitochondrial alterations in solid carcinomas relationship between tumorgenesis of human kidney carcinomas and mitochondrial DNA (mtDNA) alterations." Saarbrücken VDM Verlag Dr. Müller, 2005. http://d-nb.info/989166570/04.

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Stringer, Henry. "Mitochondrial DNA alterations and statin-induced myopathy." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/9949.

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Background/Objectives: Statins are widely used to treat hyperlipidemia and lower cardiovascular disease risk. While statins are generally well tolerated, ~10-15% of patients experience statin-induced myopathy (SIM), a potentially fatal complication. Statin treatment has been associated with mitochondrial dysfunction. High-dose simvastatin treatment has been associated with skeletal muscle mitochondrial DNA (mtDNA) depletion. The contribution of mitochondrial dysfunction to the development and exacerbation of SIM may be important. The goal of this project was to examine the effects of statins on mtDNA to provide further insight into the etiology and severity of mitochondrial myotoxicity in SIM. Methods/Results: Two studies were performed. PCR quantification of mtDNA and nuclear DNA was used to measure mtDNA content. Long-template PCR was used to amplify the mitochondrial genome and score mtDNA deletion burden. In an in vitro study, rhabdomyosarcoma cells were exposed to simvastatin and atorvastatin for over 70 days. Both mtDNA content and deletion burden were measured longitudinally and remained unchanged amongst statin treated cells. In an in vivo study, skeletal muscle biopsies from patients diagnosed with SIM (n=24) and comparators showing no pathologic findings (n=23) were retrospectively reviewed from stored clinical samples. The pathologic features and degree of pathology within each biopsy were scored. MtDNA content and deletion score was compared between groups. Two genotypes that are associated with changes in statin response and SIM risk, apolipoprotein E and SLCO1B1, were examined. No difference in genotype frequency between groups was detected. Controlling for age, gender, biopsy year and apolipoprotein E genotype, SIM subject mtDNA/nDNA (mean±SD, 2036±1146) was significantly lower than the comparators (3220±1594) (p=0.042). No difference was observed in mtDNA deletion score (0-200) between SIM subjects (21.2±19.2) and comparators (19.4±30.0). There was an inverse correlation between mtDNA content and degree of pathology (p=006 r=-0.399). Conclusions: We found decreased in vivo skeletal muscle mtDNA content in association with SIM. How this relates to the pathogenesis of SIM remains unclear. As the mtDNA deletion score was not associated with SIM, quantitative rather than qualitative mtDNA alterations are suggested. MtDNA content should be further investigated as a potential marker of statin drug myotoxicity.
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Bartho, Lucy A. "Mitochondrial Alterations Through Gestation and in Placental Pathologies." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/411262.

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The placenta is a transient organ, essential for the growth and development of the fetus throughout pregnancy. This temporary organ brings maternal and fetal blood circulation into close proximity, which allows for the exchange of oxygen, carbon dioxide, waste, and other essential nutrients. Despite constant influences by internal and external factors, the human placenta has a defined life span of approximately 280 days. From conception, through to term, the placenta undergoes chronological aging, which is regulated by a range of cellular processes. Advanced placental aging and cellular senescence have been known to contribute to the pathophysiology of preterm birth, fetal growth restriction and may cause an increased risk of stillbirth. However, the molecular mechanisms behind placental aging are still poorly understood. As a key regulator of cell homeostasis, mitochondria have been recognised as an important mediator of age-related disease processes through the production of reactive oxygen species which activate mechanisms that induce cellular senescence. Currently, we do not understand the molecular link between cellular aging processes and the role of mitochondria in chronological and pathological placental aging. Therefore, this research aimed to, 1) identify key areas of mitochondrial physiology that change with placental development, 2) characterise a set of markers that define aging in the human placenta, 3) assess the role of the mitochondria in the placenta as it develops throughout a healthy pregnancy, 4) to measure the chosen markers of aging in placentas complicated by pregnancy pathologies. Chapter 1 presents a comprehensive review of the literature to date and highlights key gaps in our current knowledge. It sets the scene for the experimental chapters to follow. Chapter 2 provides the details of the methods and materials that have been used in the laboratory to generate the data presented in the results chapters. Chapter 3 explored the molecular changes within healthy and pathological placentas, through analysing large publicly available datasets. This chapter aimed to establish an understanding of placental aging and mitochondrial physiology through measuring mitochondrial biogenesis, dynamics, mitophagy, apoptosis and senescence transcripts. Furthermore, this chapter measured altered transcripts in an additional validation cohort consisting of placentas affected by term, preterm, post-term and FGR pregnancies. This study was a large-scale investigation across multiple datasets that identified altered TOMM2020, MFN1, and MFN2 expression throughout preterm, post-term and FGR pregnancies, which may be a contributing factor to placental insufficiency. It established key markers that influence mitochondrial physiology in placental aging, which informed future studies in this thesis. Chapter 4 focused on understanding healthy aging by measuring mitochondrial and senescent changes in term and post-term placenta. Post-term placentae from healthy pregnancies selectively retain highly functioning mitochondria through increases in mitochondrial dynamics proteins MFN1, MFN2 and mitochondrial complex specific proteins. This study directly associated mitochondrial adaptions with increases in cellular senescence in the placenta and may be the reason why some post-term pregnancies are healthy, whilst others turn pathological. These findings have helped to expand our knowledge of the role of mitochondria and healthy aging in the placenta. The current literature on placental aging has focused on comparing the differences between two timepoints in pregnancy, or healthy and complicated pregnancies. The reason being that it is nearly impossible to ethically collect healthy placental tissue from early in pregnancy. Even when these samples are collected, they are inherently impacted by factors which lead to early termination. Therefore, Chapter 5 used placental samples from an established rodent ontogeny model that were collected between mid- and term gestation, without pathologies. These placentas were used to understand the role of mitochondrial biology, senescence, and the ER and in the developing placenta. Markers associated with mitochondrial biogenesis, dynamics and senescence were differentially altered in healthy placentas collected throughout gestation, which was different to what was identified in previous chapters. Therefore, throughout different stages of pregnancy, mitochondria function differently compared to placentas from post-term and growth restricted pregnancies. Lastly, Chapter 6 measured the most differentially expressed genes from previous chapters in placentas complicated by preterm, term, post-term, fetal growth restriction (FGR), preterm preeclampsia (PE), FGR/ PE pregnancies. The aim of this chapter was to utilise MetaboAnalyst data software to identify relationships between genes related to mitochondria, ER and cellular senescence. This study revealed that placentas complicated by pathologies, PE and FGR have tremendously different transcription patterns, compared to the healthy controls. Although this study only investigated a small number of genes in a relatively small sample size, it revealed that the TOMM20/PARK2 ratio is a promising marker to discriminate between healthy placenta and placenta that have been affected by pregnancy pathologies. Overall, the findings in this thesis highlight the importance of mitochondrial alterations and cellular senescence within chronological and pathological aging of the placenta. Whilst the exact mechanisms of mitochondrial aging in the placenta still requires further investigation, MFN1, MFN2, TOMM20 and PARK2 are promising markers of placental aging and should be investigated in further models of placental insufficiency. This work provides the foundation for future work in mitochondrial aging within the human placenta.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Pharmacy & Med Sci<br>Griffith Health<br>Full Text
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Wang, Yue. "Molecular analysis of mitochondrial DNA alterations in endometrial carcinomas." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32059127.

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Wang, Yue, and 王悦. "Molecular analysis of mitochondrial DNA alterations in endometrial carcinomas." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32059127.

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Scheibe, Frederik [Verfasser]. "Mitochondrial alterations in different Alzheimers disease mouse models / Frederik Scheibe." Ulm : Universität Ulm. Medizinische Fakultät, 2015. http://d-nb.info/1073211975/34.

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Kiebish, Michael Andrew. "Mitochondrial lipidome and genome alterations in mouse brain and experimental brain tumors." Thesis, Boston College, 2008. http://hdl.handle.net/2345/27.

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Thesis advisor: Thomas N. Seyfried<br>Mitochondria are the key regulators of the bioenergetic state of the cell. Damage to mitochondrial protein, DNA, or membrane lipids can result as the cause or affect of disease pathology. Regardless, this damage can impair mitochondrial function resulting in a decreased ability to produce ATP to support cellular viability. This thesis research examined the mitochondrial lipidome by shotgun lipidomics in different populations of C57BL/6J (B6) brain mitochondria (non-synaptic and synaptic) and correlated lipid changes to differences in electron transport chain (ETC) activities. Furthermore, a comparison was made for non-synaptic mitochondria between the B6 and the VM mouse strain. The VM strain has a 1.5% incidence of spontaneous brain tumors, which is 210 fold greater than the B6 strain. I determined that differences in the brain mitochondrial lipidome existed in the VM strain compared to the B6 strain, likely corresponding to an increased rate of spontaneous brain tumor formation. Analysis of the mitochondrial genome in the CT-2A, EPEN, VM-NM1, and VM-M3 brain tumors compared to their syngeneic controls mouse strains, C57BL/6J (B6) and VM mice, was examined to determine if mutations existed in experimental brain cancer models. No pathogenic mtDNA mutations were discovered that would likely cause a decrease in the mitochondrial functionality. A novel hypothesis was devised to examine the tumor mitochondrial lipidome to determine if quantitative or molecular species differences existed that could potentially alter the functionality of the ETC. Brain tumor mitochondria were examined from tumors grown in vivo as well as in vitro. Numerous lipid differences were found in the mitochondria of brain tumors, of which the most interesting involved the unique molecular speciation of cardiolipin. ETC activities were significantly decreased in the primary ETC complexes which contribute protons to the gradient as well as the linked complexes of brain tumor mitochondria compared to controls. Taken together, it is likely that differences in the mitochondrial lipidome of brain tumors results in severe impairment of the mitochondria’s ability to produce ATP through the ETC. This research has provided a new understanding of the role of mitochondrial lipids in brain as well as brain cancer and offers an alternative explanation for metabolic dysfunction in cancer<br>Thesis (PhD) — Boston College, 2008<br>Submitted to: Boston College. Graduate School of Arts and Sciences<br>Discipline: Biology
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Pfeiffer, Annika I. [Verfasser]. "Alterations of mitochondrial form and function caused by resistance against oxidative stress and cytoprotective, mitochondrial proteins / Annika I. Pfeiffer." Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/113615440X/34.

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Books on the topic "Mitochondrial alterations"

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Lieberman, Pamela. Response of brain and heart mitochondrial cardiolipin fatty acid profiles to alterations in dietary polyunsaturated fatty acids. National Library of Canada, 1991.

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Agrawal, Rishi Raj. Neurometabolic alterations after traumatic brain injury: Links to mitochondria-associated ER membranes and Alzheimer’s disease. [publisher not identified], 2021.

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Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
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Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Pathophysiological changes of ageing and their relevance to anaesthesia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0002.

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The molecular basis of ageing is reviewed. This includes the concept of a summation of DNA damage over a lifetime causing genome instability. Epigenetic alterations, telomeric shortening, and the possibility of their modification are discussed. Oxidative and mitochondrial DNA damage and the resulting dysfunction leading to senescence are briefly described. Systemic problems and resultant behavioural adaptation may mask the decline in functional reserve and cause some of the difficulties in identifying its presence in ill elderly patients. Specific organ system changes are then described in some detail. These include the major concerns with the cardiovascular, respiratory, renal, hepatic, neurologic, endocrine, and musculoskeletal systems. The effect of ageing on the special senses of vision and hearing are covered, with emphasis on issues of informed consent.
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Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.

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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.
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Lumb, Andrew B., and Natalie Drury. Respiratory physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0002.

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Moving away from the structure of traditional texts, this chapter follows the journey of oxygen molecules as they move from inspired air to their point of use in mitochondria, with some digressions along the way to cover other relevant aspects of respiratory physiology. The chapter encompasses all the key aspects of respiratory physiology and also highlights physiological alterations that occur under both general and regional anaesthesia, moving the physiological principles discussed into daily anaesthetic practice. The chapter explores relevant anatomy of the airways, lungs, and pleura. The histology and function of the airway lining and alveoli are described, so illustrating the importance of pulmonary defence mechanisms for protecting the internal milieu of the body from this large and fragile interface with the outside world. Key principles and concepts including resistance, compliance, and diffusion are all discussed in their clinical context. Concepts relating to the mechanics of breathing and the control of airway diameter are considered along with lung volumes and their measurement. Both the central and peripheral mechanisms involved in the control of breathing are discussed with particular attention to the impact of anaesthesia. The relationship between ventilation and perfusion and the carriage of oxygen and carbon dioxide are all discussed in detail. The principles behind key respiratory measurements such as dead space, lung volumes, diffusing capacity, and shunt are all described. Overall the chapter provides a comprehensive review of respiratory physiology as well as including additional aspects of variation that occur under anaesthesia.
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Book chapters on the topic "Mitochondrial alterations"

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Dakubo, Gabriel D. "Mitochondrial Genetic Alterations in Cancer I." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_6.

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Dakubo, Gabriel D. "Mitochondrial Genetic Alterations in Cancer II." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_7.

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Dakubo, Gabriel D. "Analysis of Mitochondrial Genome Alterations in Cancer." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_13.

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Dakubo, Gabriel D. "Types of Mitochondrial Genetic Alterations in Cancer." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_5.

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Dakubo, Gabriel D. "Functional Importance of Mitochondrial Genetic Alterations in Cancer." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_9.

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Dakubo, Gabriel D. "The Warburg Phenomenon and Other Metabolic Alterations of Cancer Cells." In Mitochondrial Genetics and Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_2.

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Dörner, A., K. Schulze, U. Rauch, and H. P. Schultheiss. "Adenine nucleotide translocator in dilated cardiomyopathy: Pathophysiological alterations in expression and function." In Detection of Mitochondrial Diseases. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_41.

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McMillin, Jeanie B., Daniel F. Pauly, and Kiminori Kajiyama. "Ischemic Alterations in Mitochondrial Calcium Transport Kinetics." In Cell Calcium Metabolism. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_58.

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Macedo, Denise V., Valmir L. Ferraz, Lucia Pereira-da-Silva, and Anibal E. Vercesi. "Ca2+-Dependent NAD(P)+-Induced Alterations in Membrane Permeability of Rat Liver Mitochondria." In Integration of Mitochondrial Function. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_52.

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Hussain, Salik. "Measurement of Nanoparticle-Induced Mitochondrial Membrane Potential Alterations." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8916-4_7.

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Conference papers on the topic "Mitochondrial alterations"

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Otto, Neil. "Abstract 4802: Functional analysis of cancer associated mitochondrial genome alterations." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4802.

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Eslamizadeh, Sara, Massoud Ghaffarpour, Mohammad Arabzadeh, and Massoud Houshmand. "Abstract 4323: Mitochondrial 22 tRNAs alterations in Iranian breast cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4323.

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Pak, Oleg, Natascha Sommer, Sharon Waisbrod, et al. "Mitochondrial Alterations Of Pulmonary Arterial Smooth Muscle Cells In Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3414.

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Balasubramanian Lakshmi, Vidya Srokshna, Thilo Berger, Claudia Garcia Castro, et al. "Mitochondrial alterations in T cells after invivo and invitro smoke exposure." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.128.

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Aghapour, M., A. Jeron, and D. Bruder. "Streptococcus pneumoniae induces broad alterations in mitochondrial functions in human airway epithelial cells." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.34.

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Pardo Semo, Annie, Erikal Rubí Luis-Garcia, Carina Becerril, et al. "Alterations in mitochondrial permeability transition pore contribute to apoptosis resistance in IPF fibroblasts." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa584.

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Gesualdi, Luisa, Marika Berardini, Francesca Ferranti, et al. "Microgravity Exposure Induces Antioxidant Barrier Deregulation and Mitochondrial Structure Alterations in TCam-2 Cells." In Cells 2023. MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021006.

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"LSC - 2020 - Streptococcus pneumoniae induces broad alterations in mitochondrial functions in human airway epithelial cells." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1056.

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Evans, William, Jazmine Eccles, and William Baldwin. "Changes in Energy Metabolism Induced by PFOS and Dietary Oxylipins." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/jnpe5541.

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CYP2B6 is a drug metabolizing cytochrome P450 (CYP) that has anti-obesity properties, but also increases non-alcoholic fatty liver disease (NAFLD) in hCYP2B6-transgenic mice compared to Cyp2b-null mice. hCYP2B6-transgenic mice are also more susceptible to perfluorooctane sulfonic acid (PFOS) toxicity, a lipid-like toxicant used in stains, varnishes and firefighting foams that increase NAFLD. Our recent research demonstrates that CYP2B6 metabolizes dietary polyunsaturated fatty acids into the oxylipins, 9-HODE and 9-HOTre, which are strong peroxisome proliferator activated receptor alpha (PPARa) agonists and weak PPARg agonists. The purpose of our studies is to better understand the mechanisms behind PFOS and oxylipin-mediated hepatic steatosis. To test whether PFOS, 9-HODE or 9-HOTrE alter mitochondrial metabolism, Seahorse Mitostress assays were performed using HepG2 cells treated with 0.2, 1 and 5mM PFOS, 9-HODE and 9-HOTrE for 24 hours (n=5). Both PFOS and 9-HOTrE increased spare respiratory capacity in a concentration-dependent manner with lesser effects by 9-HODE. qPCR was performed following exposure of HepG2 cells to 1 and 5 mM of each compound to investigate changes in gene expression that may explain alterations in mitochondrial respiration or hepatic steatosis. PFOS repressed expression of ANGPTL4, a biomarker of PPARgactivation. 9-HODE induced CD36 and FASN expression, genes involved in fatty acid uptake and synthesis. 9-HOTrE induced SREBF1 and Cpt1a expression, genes involved in sterol synthesis and fatty acid transport into the mitochondria and may partially explain the increase in SRC. Thus, based on current results, PFOS is associated with reduced transport of lipids from the liver and 9-HODE increases lipid uptake; both would increase steatosis through different mechanisms. 9-HOTre may increase metabolism and therefore reduce steatosis.
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"Mitochondrial dysfunction and redox balance alterations in the development of AD-like pathology in OXYS rats." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-334.

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Reports on the topic "Mitochondrial alterations"

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Palmeira, Carlos. Low-dose, Chronic Exposure to Silver Nanoparticles Causes Mild Mitochondrial Alterations in the Liver of Sprague-Dawley Rat. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada611639.

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Izhar, Shamay, Maureen Hanson, and Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, 1996. http://dx.doi.org/10.32747/1996.7604933.bard.

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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.
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