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Neuromuscular Physiology
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Resulting from densely packed myofibrils and other organelles, muscle fiber mitochondria are typically shorter than those of other types of cells, oblong in structure and approximately 1.5 µ in length. Mitochondria have a major function of energy production and are primarily found in cellular areas where energy supply is a primary requisite, for example, near the myofibrils. Mitochondria have a double membrane structure with the inner membrane folded into ridges termed “cristae.” This enfolding results in a large inner membrane surface area (Figure 1.3). The matrix or matrix space is contained within the cristae.
Mitochondria in Huntington’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Mitochondria, OXPHOS, and HD: Mitochondria play a crucial role in generating and delivering cellular energy currency, that is, ATP. Mitochondria have an outer mitochondrial membrane (OMM) and an inner mitochondrial membrane (IMM), which has a larger surface area and is folded to fit inside OMM creating cristae. Cristae are the seat of mitochondrial oxidative phosphorylation (OXPHOS) machinery, namely, electron transport chain (ETC) complexes I–IV, two electron carriers, and a specialized ATP synthesizing enzyme called ATP synthase. The space between the two membranes of mitochondria is called intermembrane space and the space constrained by the IMM is called matrix, which is filled with a gel-like substance. The matrix contains the mtDNA and the enzymes of the tricarboxylic acid (TCA) cycle (also known as the citric acid cycle or Krebs cycle). Due to the high energy demand and limited regenerative capability of neurons, mitochondrial dysfunction (broadly including individual enzyme complex deficiencies or fusion-fission abnormalities or disrupted movement along the cytoskeletal elements) is especially debilitating for these specialized cells.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Mitochondria in electron micrographs appear as elongated cylinders bounded by two layers of membrane, the outer and inner membranes. Together, they enclose and define two separate compartments, the matrix space and intermembrane space. The inner membrane is highly convoluted, forming many infoldings, known as cristae, projecting into the matrix space (Figure 16). According to recent studies by Candipan and Sjostrand (1984, a,b,c), however, some of the morphological features of the mitochondria, which are widely accepted as real, may be artifacts caused during preparation for electron microscopy. They suggest that (1) the inner and outer membranes are closely apposed and that there is no space within the cristae; (2) the cristae membrane is not simply an infolding of the inner membrane but differs structurally from it; (3) there is no evidence that the cristae undergo conformation changes in different metabolic states; and (4) two size classes of mitochondria, often referred to as “condensed” and “orthodox,” are preparatory artifacts.
Coenzyme Q10 protects against doxorubicin-induced cardiomyopathy via antioxidant and anti-apoptotic pathway
Published in Tissue Barriers, 2023
Dalia A. Shabaan, Nora Mostafa, Manal M. El-Desoky, Eetmad A. Arafat
Mitochondrial ultrastructural changes were apparent in most of the sections in the Dox-treated group. The changes included large-sized mitochondria with abnormal shapes, mitochondrial vacuolation, and loss of cristae. Our results were in line with those of Wenceslau et al.40 They attributed the change to the direct effect of Dox on mitochondria through increased mitochondrial oxidative stress. On the other hand, Zhang et al.41 attributed Dox-induced mitochondrial damage, defective mitochondrial biogenesis, nuclear degeneration, and p53 activation to the interference of Dox with topoisomerase. In addition, an increased mitochondrial iron level was reported after Dox treatment. The hazardous effect of an increased mitochondrial iron level was confirmed by using dexrazoxane that exports mitochondrial iron.42,43
Sericin-mediated improvement of dysmorphic cardiac mitochondria from hypercholesterolaemia is associated with maintaining mitochondrial dynamics, energy production, and mitochondrial structure
Published in Pharmaceutical Biology, 2022
Kitiya Rujimongkon, Sumate Ampawong, Duangnate Isarangkul, Onrapak Reamtong, Pornanong Aramwit
High serum cholesterol is one of the factors that leads to myocardial and cardiac mitochondrial degeneration (Ampawong et al. 2017a). Ultrastructural observations of mitochondria have revealed four mitochondrial stages from a normal to a severely degenerated structure. The normal stage involves a structure containing double membranes (inner and outer membranes) covering the intermembrane space. The inner membrane forms pore-like structures termed crista junctions in the mitochondrial matrix. The swelling stage involves the first dysmorphic structure, which includes an increased size, distensions of the intercellular matrix, and partial disappearance of cristae. The spheroid stage is characterised by the complete loss of cristae and the formation of multiple cysts in the matrix. In the final stage, the ghost stage, the membrane disappears, leaving granular and electrodense material (Mariappan et al. 2007; Ampawong et al. 2017a, 2017b). Dysmorphic cardiac mitochondria under hypercholesterolemic coupled with hyperglycaemic conditions have revealed different numbers of mitochondria between the dysmorphic and normal stages (Ampawong et al. 2017a). This evidence suggests the possibility that high serum cholesterol levels are related to the structure of cardiac mitochondria, are associated with mitochondrial dysfunction and result in organ failure, especially in the heart.
scRNA-seq reveals ATPIF1 activity in control of T cell antitumor activity
Published in OncoImmunology, 2022
Genshen Zhong, Qi Wang, Ying Wang, Ying Guo, Meiqi Xu, Yaya Guan, Xiaoying Zhang, Minna Wu, Zhishan Xu, Weidong Zhao, Hongkai Lian, Hui Wang, Jianping Ye
Our data reveal that energy metabolism was reprogrammed in CD8+ T cells of ATPIF1-KO mice for enhanced glycolysis in ATP production. Glycolysis was enhanced in CD8+ T cells of KO mice for ATP production as indicated by reduced OCR, increased ECAR, and profile of intermediate metabolites in metabolomics. In the KO cells, the ATP synthase activity is supposed to be enhanced in mitochondria in the absence of ATPIF1, which might increase ATP hydrolysis in the energy deficient conditions. However, those possibilities were disproved by our data as mitochondrial function was reduced by ATPIF1 inactivation. The mechanism underlying the KO phenotype is related a change in mitochondrial structure and mass. ATPIF1 is important in the maintenance of mitochondrial biogenesis and crista density,20,26 and ATPIF1 gene knockdown was reported to decrease the mitochondrial crista.33 Our data suggest that mitochondrial mass was decreased in the KO cells. The enhanced glycolysis is likely a consequence of mitochondrial deficiency in KO T cells. The OXPHOS deficiency is a driving force for the induction of glycolysis.34