Search results

1

Acidosis inhibits calcium accumulation in intrasynaptosomal mitochondria

100%

Fedorovich S. V., Aksentsev S. L., Konev S. V.

Acta Neurobiologiae Experimentalis

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1996

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vol. 56

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issue 3

703

2

Heteroplasmy in plants

80%

Woloszynska M., Oziemlak A., Janska H.

Biotechnologia

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2001

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issue 1

42-46

EN

Heteroplasmy is the state characterised by the presence of more than one type of mitochondrial or chloroplast genome in one organism. Infrequent recombinations across short repeated sequences often lead to heteroplasmy in higher plant mitochondria. Different Phaseolus species have been examined in order to understand the dynamics of heteroplasmy originating through recombination mediated by the 315 bp repeated sequence. Two techniques were applied to detect heteroplasmy: Souhern hybridization with prolonged autoradiography and PCR amplification followed by hybridization or reamplification. In all examined genomes the four recombination forms were detected. However, these forms do not occur in the same relative amounts. Moreover, in the examined genomes different recombination forms exist at the predominant/substoichiomeric level, but always only two of them are predominant. Based on these results and the previous data, we suggest that the changes in the heteroplasmic population of mitochondrial molecules in plants may offer the source of genetic variation in the course of evolution.

3

The biology and pathology of hypoxia-ischemia: an update

80%

Clarkson A. N., Sutherland B. A., Appleton I.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 3

213-225

EN

After an hypoxic-ischemic (HI) insult, a multi-faceted complex cascade of events occurs that ultimately causes cell death and neurological damage to the central nervous system. The various cascades include, amongst others: immunological changes, such as the activation of the complement system and the generation of antibodies; increased inflammation through the actions of pro-inflammatory cytokines and chemokines; the production of reactive oxygen species leading to oxidative stress; and diminished mitochondrial function leading to the activation of apoptotic pathways and subsequent alteration in the function of neurons within the contralateral hemisphere. This review addresses the immunological aspects following HI, the role of various cytokines (both pro-inflammatory and anti-inflammatory) and chemokines after the induction of HI. In addition, the role of free radicals in producing HI-induced neurodegeneration and the contribution that mitochondrial dysfunction has in neuronal apoptotic cell death will be discussed. This review also covers the changes that the previously assumed 'internal control', the contralateral hemisphere, undergoes due to HI and describes the difficulties associated with therapy intended to prevent neuronal injury associated with HI.

4

The immunopathology of primary biliary cirrhosis: thoughts for the millennium

80%

Sasaki M., Ansari A. A., Nakanuma Y., Coppel R. L., Keeffe E. B., Gershwin M. E.

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vol. 48

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issue 1

1-10

EN

Primary biliary cirrhosis is an organ specific autoimmune disease that produces progressive cholestatic liver failure. It is predominantly a disease of women characterized by chronic progressive destruction of small intrahepatic bile ducts with portal inflammation and ultimately fibrosis. The serologic hallmark of primary biliary cirrhosis (PBC) is the presence of antibodies to mitochondria. The mechanisms by which and if which such antibodies produce liver tissue injury is unknown. However, the presence of these antibodies have allowed detailed immunological definition of the antigenic epitopes, the nature of reacting autoantibodies and the characterization of T cell responses. Several mechanisms may now be proposed regarding the immune mediated bile duct damage in PBC, including the possible role of T cell-mediated cytotoxicity and intracellular interaction between the IgA class of antimitochondrial antibodies (AMA) and mitochondrial autoantigens. The advent of molecular biology, the ability to clone and define epitopes, and the use of in situ nucleic acid hybridization, have all led to advances in understanding the natural history of immunopathology in PBC. There are major questions which remain unanswered, including, of course, etiology, but also including the questions of why there is female predominance, the absence of PBC in children, the relative ineffectiveness of immunosuppressive drugs, and the specific role of mitochondrial antigens. In this review, we focus on these issues and particularly on the immunobiology of patients with this disease.

5

Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models

80%

Albrecht J., Hilgier W., Faff L.

Acta Neurobiologiae Experimentalis

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1996

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vol. 56

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issue 2

545-548

EN

The phosphate-dependent (PAG) and phosphate-independent (PIndG) glutaminase activities were measured in cerebral perikaryal mitochondria derived from rats subjected to ammonium acetate- induced "simple" hyperammonemia (SHA) or thioacetamide-induced hepatic encephalopathy (HE).These two moderately hyperammonemic conditions were previously found to be accoopanied by pronounced changes in virtually all the enzyme activities coupling the tricarboxilic acid cycle to the synthesis and metabolism of the excitatory neurotransmitter glutamate.Both PAG and PIndG remained unaffected by SHA or HE, indicating that htey do not contribute to the cerebral glutamine/glutamate imbalance associated with both conditions.

6

Mitochondrial DNA mutations in human neoplasia

80%

Czarnecka A. M., Golik P., Bartnik E.

Journal of Applied Genetics

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2006

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vol. 47

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issue 1

67-78

EN

Many models of tumour formation have been put forth so far. In general they involve mutations in at least three elements within the cell: oncogenes, tumour suppressors and regulators of telomere replication. Recently numerous mutations in mitochondria have been found in many tumours, whereas they were absent in normal tissues from the same individual. The presence of mutations, of course, does not prove that they play a causative role in development of neoplastic lesions and progression; however, the key role played by mitochondria in both apoptosis and generation of DNA-damaging reactive oxygen species might indicate that the observed mutations contribute to tumour development. Recent experiments with nude mice have proven that mtDNA mutations are indeed responsible for tumour growth and exacerbated ROS production. This review describes mtDNA mutations in main types of human neoplasia.

7

Mitochondria and aging: innocent bystanders or guilty parties?

80%

Tonska K., Solyga A., Bartnik E.

Journal of Applied Genetics

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2009

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vol. 50

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issue 1

55-62

EN

. There are many theories of aging and a number of them encompass the role of mitochondria in this process. Mitochondrial DNA mutations and deletions have been shown to accumulate in many tissues in mammals during aging. However, there is little evidence that these mutations could affect the functioning of aging tissues.

8

Human mitochondria in health, disease, ageing and cancer

80%

Bartnik E., Lorenc A., Mroczek K.

Journal of Applied Genetics

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2001

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vol. 42

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issue 1

65-71

EN

In every human cell there are hundreds of mitochondria, which are required for oxidative phosphorylation as well as many other metabolic processes. Each mitochondrion contains approximately 5 mitochondrial DNA molecules. These circular DNAs of 16.5 kb in size contain only 39 genes . Mutations in mitochondrial DNA are responsible for many diseases. Alterations in these molecules may also play a role in ageing and in tumour formation.

9

Intracellular ion channels: properties, function and experimental methodology

80%

Kicinska A., Debska G., Szewczyk A.

Postępy Higieny i Medycyny Doświadczalnej

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2000

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vol. 54

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issue 3

307-316

EN

Ion channels selective for potassium or chloride ions are present in membranes of intracellular organelles such as mitochondria, sarcoplastic (endoplastic) reticulum, nucleus, synaptic vesicles, and chromaffin, and zymogen granules. They are probably important in cellular events such as compensation of electrical charges during intracellular transport of Ca 2+ and H+ and regulation of organelle volume changes. This review describes the basic properties, and current hypotheses concerning the functional role, and some aspects of experimental methodology of intracellular ion channels studies.

10

Dysregulation of calcium in Alzheimer's disease

70%

Brzyska M., Danek E.

Acta Neurobiologiae Experimentalis

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2003

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vol. 63

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issue 3

171-183

EN

Multiple efforts has underlined importance of calcium dependent cellular processes in the biochemical characterisation of Alzheimer?s disease (AD), suggesting that abnormalities in calcium (Ca2+) homeostasis might be involved in the pathophysiology of the disease. Studies of the pathogenic mutations in presenilins 1 and 2 (PS1 and PS2) and amyloid precursor protein (APP) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis. Studies of apolipoprotein E (ApoE) neurotoxic effects in AD confirmed involvement of Ca2+-mediated mechanisms. Futher consequences of Ca2+ alterations in AD underline the importance of the ER and mitochondria as the regulatory sites involved in the pathogenesis of neuronal degeneration. Alterations of Ca2+ homeostasis include cells from peripheral tissues, including lymphocytes and fibroblasts from AD donors.

11

Reconstitution of brain mitochondria inner membrane into planar lipid bilayer

61%

Kulawiak B., Bednarczyk P.

Acta Neurobiologiae Experimentalis

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2005

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vol. 65

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issue 3

271-276

EN

Ion channels are present in the inner mitochondrial membrane. They play an important role in cellular processes. Potassium and chloride channels are involved in regulation of mitochondrial volume, membrane potential and acidification. The mitochondrial potassium channels have been suggested as triggers and end effectors in cytoprotection. In our study we measured single channel activities after reconstitution of submitochondrial particles from rat brain mitochondria into planar lipid membranes. After incorporation, two different potassium selective currents were recorded with single channel conductance from 260 to 320 pS and from 70 to 90 pS in gradient (cis/trans) 50/450 and 50/150 mM KC1 solutions, respectively. We also observed activity of the chloride ion channel. The measured single channel conductance was from 80 to 90 pS in gradient {cis/trans) 50/450 mM KC1 solution. Our results suggest that various ion channels are present in the inner mitochondrial membrane of brain mitochondria.

Refine search results

Acidosis inhibits calcium accumulation in intrasynaptosomal mitochondria

Heteroplasmy in plants

The biology and pathology of hypoxia-ischemia: an update

The immunopathology of primary biliary cirrhosis: thoughts for the millennium

Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models

Mitochondrial DNA mutations in human neoplasia

Mitochondria and aging: innocent bystanders or guilty parties?

Human mitochondria in health, disease, ageing and cancer

Intracellular ion channels: properties, function and experimental methodology

Dysregulation of calcium in Alzheimer's disease

Reconstitution of brain mitochondria inner membrane into planar lipid bilayer