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Biochemical and Metabolic Limitations to Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Another aspect of the efficiency of mitochondria to utilize oxygen is how the complexes of the electron transport chain themselves are organized. The structure and formation of the electron transport chain, located on the inner mitochondrial membrane, are extremely plastic and change rapidly in response to stimuli and stress. In some cases, the members of the electron transport chain can fuse to form what are known as “super-complexes.” Although this field of study is relatively new and technological challenges remain when characterizing super-complex formation, it appears that these formations may play a key role in exercise performance. For example, the formation of super-assembled complexes is increased after aerobic training (19). In this study, aerobic training promoted the redistribution of complex I from super-complex I+III2 to super-complex I+III2+IVn. Additionally, aerobic training preferentially favoured the re-distribution of complex III and complex IV to functional super-complex species, such as super-complex I+III2+IVn. This shift reinforces the plasticity of the inner mitochondrial membrane and the formation of electron transport complexes. Additionally, this supports the assertion that mitochondrial function and structure are crucial components of the ability to utilize and extract oxygen during intense exercise.
The Cell Membrane in the Steady State
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
A uniporter is a transmembrane protein that facilitates diffusion of a substance down a concentration gradient, without ATP hydrolysis, but at a rate that can be far higher than that of passive diffusion for that substance, the energy being derived from the concentration gradient of the transported substance. Glucose and amino acids are transported across the plasma membrane in this manner, the concentration gradient being established in these cases because these substances are used up in cell metabolism. The inner mitochondrial membrane has an efficient Ca2+ uniporter that allows a fast uptake of Ca2+ by mitochondria. This type of movement is referred to sometimes as facilitated transport, or facilitated diffusion. In a uniporter, a specific protein transports a particular substance by undergoing a conformational change, much like that illustrated in Figure 2.5 for the Na+-K+ pump but without ATP hydrolysis.
Carnitine-acylcarnitine translocase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Cardiomyopathy may be manifested by premature ventricular contractions, ventricular tachycardia, or hypotension [1], and bradycardia due to auriculoventricular block [3]. In one patient [1], the electrocardiogram showed ventricular hypertrophy and in another [3], a left bundle branch block. Echocardiogram showed reduced ejection fraction. Intracardiac conduction defects were seen in twin siblings who died after an episode days after onset at two months [12]. Over a period of 25 years, in 107 newborns, cardiac arrhythmia and conduction defects were the main presentations in patients with fatty acid oxidation defects [2]. Conduction disorders and atrial tachycardias were observed in patients with defects of long-chain fatty acid transport across the inner mitochondrial membrane (carnitine palmitoyl transferase type II deficiency [Chapter 38] and CACT deficiency) and in patients with trifunctional protein deficiency (Chapter 41). Arrhythmias have been attributed to the accumulation of intermediary metabolites of fatty acids, such as long-chain acylcarnitines [13].
Toxic effects and molecular mechanism of doxorubicin on different organs – an update
Published in Toxin Reviews, 2022
Kaviyarasi Renu, Lakshmi Prasanna Pureti, Balachandar Vellingiri, Abilash Valsala Gopalakrishnan
Cardiomyocytes possess a higher number of mitochondria when compared to other tissues. The elated ROS levels result in an inconvenience in the electron transport chain, thereby disrupting ATP production (Goffart et al.2004). The inner mitochondrial membrane possesses a component called cardiolipin, which is involved in lipid metabolism. Due to the net anionic charge present on the cardiolipin and the net cationic charge present on the doxorubicin, an irreversible complex is formed between cardiolipin and doxorubicin (Parker et al.2001). As cardiolipin is already bound with doxorubicin, it is unavailable for the complex II and complex IV enzymes that regulate the electron transport chain, resulting in a disturbance in the oxidative phosphorylation process eventually heading toward cardiotoxicity (Goormaghtigh et al.1980).
Targeting mitochondria in dermatological therapy: beyond oxidative damage and skin aging
Published in Expert Opinion on Therapeutic Targets, 2022
Tongyu C Wikramanayake, Jérémy Chéret, Alec Sevilla, Mark Birch-Machin, Ralf Paus
Before going into details, it may be useful to recapitulate some essentials of mitochondrial biology. Reminiscent of their endosymbiont past, mitochondria are surrounded by two phospholipidic membranes, the outer mitochondrial membrane (OMM) and the inner mitochondrial membrane (IMM), which divide the organelle into two compartments, the matrix and the intermembrane space (IMS) [212] (see Figure 2 for details). Mitochondria contain their own DNA (mtDNA) and translation system. The location of mtDNA in the matrix, in close proximity to the ETC, a major source of reactive oxygen species (ROS), makes it particularly vulnerable to oxidation, resulting in mtDNA mutations that could contribute to the pathogenesis of cancer, diabetes and aging [213]. Mutations in mtDNA are functionally recessive – a biochemical phenotype is only observed when the levels of mutated mtDNA reach a critical threshold, and the proportion of mutated versus wild-type mtDNA has a strong impact on the severity of the pathological phenotypes. Coenzyme Q (CoQ10), a ROS scavenger, and mitochondrial sirtuins (SIRT3 and SIRT4) have been implicated in maintaining mitochondrial health [109,214].
Molecular mechanisms of ethanol biotransformation: enzymes of oxidative and nonoxidative metabolic pathways in human
Published in Xenobiotica, 2020
Grażyna Kubiak-Tomaszewska, Piotr Tomaszewski, Jan Pachecka, Marta Struga, Wioletta Olejarz, Magdalena Mielczarek-Puta, Grażyna Nowicka
It is well known that ethyl esters of fatty acids can increase the fluidity of biological membranes and promote their destabilisation. This is particularly important for the inner mitochondrial membrane, as it can lead to disruption of electron flow in the respiratory chain and oxidative phosphorylation, thus reducing the energy potential of cells. It has also been demonstrated that FAEE induces an increase in Ca2+ ions concentration in pancreatic cells by inhibition of calcium ATPases SERCA (sarco/endoplasmic reticulum Ca2+-ATPase) and PCMA (plasma membrane Ca2+ ATPase) as a consequence of activation of IP3 receptors and inhibition of oxidative phosphorylation. The postulated participation of FAEEs in the pathomechanism of ethanol toxicity requires further studies (Laposata & Lange, 1986; von Bahr-Lindstrom et al., 1986) (Figure 11).