Fate of incorporated sperm mitochondria, flagellum and perinuclear structures
Frank J. Longo in Fertilization, 2020
Structural alterations of the sperm mitochondria have been observed in various mammalian species, including swelling and loss of cristae processes believed to be indicative of degeneration. In most animals, incorporation of the sperm nucleus is accompanied by the entry of the sperm mitochondria and components of the sperm flagellum, the axonemal complex. Hence, in this case the sperm mitochondria are incorporated into the egg. The release of the mitochondria may be necessary for fertilization because of steric factors, so allowing the sperm to pass through the chorion, i.e. it may provide the push for sperm incorporation. In the mouse sperm mitochondria begin to degenerate during the early stages of fertilization, whereas in the rat changes are noted until cleavage. In the sea urchin Arbacia changes observed in sperm mitochondria during fertilization are not consistent. Recognizable sperm mitochondria have been observed juxtaposed to the first mitotic apparatus approximately 60 min following insemination.
Ultrastructural Abnormalities of the Heart During Diabetes
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla in Heart Dysfunction in Diabetes, 2019
Mitochondrial abnormalities are the most common ultrastructural disturbance reported in the heart during diabetes. Ultrastructural derangement in the myocardium does not always accompany diabetes mellitus. Several factors have been identified in the diabetic state which affect the development of ultrastructural irregularities in the heart. One of the more closely examined factors which influence the progression of ultrastructural damage in the heart is the length of time that the animal is exposed to diabetes. The severity of the diabetes may represent a plausible explanation for the presence or absence of ultrastructural changes in the heart during diabetes. A relationship of the ultrastructural abnormalities in the heart during diabetes to cardiac functional depression has been challenged by one study; however, the existence of such damage does provide clear, undeniable evidence that the heart is undergoing a process of pathological regression. Sarcomere disorganization, myofibrillar loss, and mitochondrial swelling and clearing are among of the more common ultrastructural lesions reported.
Genetic Contributions to Mitochondrial Traits
J. Timothy Lightfoot, Monica J. Hubal, Stephen M. Roth in Routledge Handbook of Sport and Exercise Systems Genetics, 2019
Mitochondrial biogenesis is the process of increasing mitochondrial mass in response to physiological stimuli such as growth or exercise. This is a complex process that involves mitochondrial fusion and fission and mtDNA replication. The classical role of mitochondria is energy metabolism, where reducing equivalents from carbohydrate fat, and to some extent amino acids, can be used to generate ATP in the presence of oxygen. Mitochondria are also involved in a variety of other physiological and pathophysiologic processes including oxidative stress, inflammasome activation, telomere maintenance, and activation of apoptosis. The most dramatic influence of mtDNA variants upon exercise capacity are the deleterious effects of specific mutations. The lower VO 2 max was thought to be related to the known lower oxidative stress and ATP generation efficiency of mitochondrial of haplogroup. A big issue when looking at mtDNA haplogroups is that within a given country the enrichment of the haplogroups will be somewhat homogenous based upon evolutionary migration patterns.
Analysis of Mitochondrial Network Morphology in Cultured Myoblasts from Patients with Mitochondrial Disorders
Published in Ultrastructural Pathology, 2015
J. Sládková, J. Spáčilová, M. Čapek, M. Tesařová, H. Hansíková, T. Honzík, J. Martínek, J. Zámečník, O. Kostková, J. Zeman
Mitochondrial morphology was studied in cultivated myoblasts obtained from patients with mitochondrial disorders, including CPEO, MELAS and TMEM70 deficiency. Mitochondrial networks and ultrastructure were visualized by fluorescence microscopy and transmission electron microscopy, respectively. A heterogeneous picture of abnormally sized and shaped mitochondria with fragmentation, shortening, and aberrant cristae, lower density of mitochondria and an increased number of “megamitochondria” were found in patient myoblasts. Morphometric Fiji analyses revealed different mitochondrial network properties in myoblasts from patients and controls. The small number of cultivated myoblasts required for semiautomatic morphometric image analysis makes this tool useful for estimating mitochondrial disturbances in patients with mitochondrial disorders.
Mitochondrial oxidative stress and dysfunction induced by isoniazid: study on isolated rat liver and brain mitochondria
Published in Drug and Chemical Toxicology, 2016
Morteza Ahadpour, Mohammad Reza Eskandari, Vida Mashayekhi, Kamaleddin Haj Mohammad Ebrahim Tehrani, Iman Jafarian, Parvaneh Naserzadeh, Mir-Jamal Hosseini
Isoniazid (INH or isonicotinic hydrazide) is used for the treatment and prophylaxis of tuberculosis. Liver and brain are two important target organs in INH toxicity. However, the exact mechanisms behind the INH hepatotoxicity or neurotoxicity have not yet been completely understood. Considering the mitochondria as one of the possible molecular targets for INH toxicity, the aim of this study was to evaluate the mechanisms of INH mitochondrial toxicity on isolated mitochondria. Mitochondria were isolated by differential ultracentrifugation from male Sprague–Dawley rats and incubated with different concentrations of INH (25–2000 μM) for the investigation of mitochondrial parameters. The results indicated that INH could interact with mitochondrial respiratory chain and inhibit its activity. Our results showed an elevation in mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation and mitochondrial membrane potential collapse after exposure of isolated liver mitochondria in INH. However, different results were obtained in brain mitochondria. Noteworthy, significant glutathione oxidation, adenosine triphosphate (ATP) depletion and lipid peroxidation were observed in higher concentration of INH, as compared to liver mitochondria. In conclusion, our results suggest that INH may initiate its toxicity in liver mitochondria through interaction with electron transfer chain, lipid peroxidation, mitochondrial membrane potential decline and cytochrome c expulsion which ultimately lead to cell death signaling.
Mitochondrial DNA in Tumors
Published in Toxicology Mechanisms and Methods, 2004
Anna Lorenc, Jaroslaw Bryk, Ewa Bartnik
Mitochondria, cellular powerhouses, play a central role in apoptosis. In addition, they are suspected to contribute to aging. There is also increasing evidence that abnormalities in mitochondrial function help cancer development. Changes in mitochondrial transcription and oxidative phosphorylation pathways are observed in many types of cancer. Somatic mutations and quantitative changes in mitochondrial DNA were found in tumors, suggesting that alterations in mitochondrial DNA and the resulting respiratory deficiency play a role in carcinogenesis. It was postulated they could be useful as cancer markers. Mitochondria with abnormal functions are suitable targets for anticancer drugs.
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