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Fungi and Water
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Fungi including mushrooms, molds, and yeasts are eukaryotic organisms as vegetable or animal species, but are classified as a separate kingdom because fungal cell walls contain rigid chitin and glucans that are not found in animal, vegetal, or bacterial species (1–8). Eukaryotic cells are cells that contain a nucleus and other organelles enclosed within membranes. In other words, the fungal kingdom comprises a hyper diverse clade of heterotrophic eukaryotes characterized by the presence of a chitinous cell wall, the loss of phagotrophic capabilities, and cell organizations that range from completely unicellular monopolar organisms to highly complex syncytial filaments (containing several nuclei) that may form macroscopic structures (8). Mushrooms like morels, button mushroom, and puffballs are macroscopic multicellular fungi, while molds are a large group of microscopic multicellular fungi. Molds are characterized by filamentous forms named hyphae. Many fungi occur not as hyphae but as unicellular forms called yeasts, which are invisible to the naked eye and reproduce by budding (2–4).
Mitochondria and Embryo Viability
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Irene Corachan Garcia, Laura Iñiguez Quiles, Antonio Diez-Juan
Mitochondria play a critical role in the generation of metabolic energy in eukaryotic cells, using oxidative phosphorylation to derive energy (ATP) from carbohydrates and fatty acids. Mitochondria contain their own DNA, which encodes tRNAs, rRNAs, and some mitochondrial proteins (1). Ranging in size from 0.5 to 1.0 μm in diameter (2), these unique organelles have a double-membrane system consisting of inner and outer membranes separated by an intermembrane space (1). The outer mitochondrial membrane encloses the matrix (internal space) and contains a large number of proteins that form channels allowing small molecules to pass. The inner mitochondrial membrane, which is folded into structures (cristae) that increase the surface area, is less permeable, blocking the movement of ions and other small molecules. Both the inner and outer membranes contain specific transport proteins that can move molecules by a passive or active transport (2) (Figure 15.1).
Mitochondrial Dysfunction in Chronic Disease
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Christopher Newell, Heather Leduc-Pessah, Aneal Khan, Jane Shearer
Present in almost all eukaryotic cells, the mitochondrion is the organelle responsible for aerobic energy production via cellular respiration. Proper mitochondrial function is vital for metabolic homeostasis of the human body, whereas dysfunctional mitochondria, characterized by loss in the efficiency of the electron transport system and therefore a reduction in energy synthesis, has been linked to the ageing process (12) and a multitude of chronic disease states. These include neurodegenerative diseases (62), cardiovascular diseases (113), diabetes (112), cancers (109), musculoskeletal diseases (96), and gastrointestinal disorders (40), among others. Exercise is a well-known intervention proven to maintain mitochondrial function and density. This chapter highlights our current understanding of how mitochondria are affected by both exercise and chronic disease. There are also primary mitochondrial diseases that are a group of rare diseases which can be caused by mutations to either mitochondrial or nuclear DNA (mtDNA or nDNA) (106); however, these are beyond the scope of this chapter.
Syntaphilin mediates axonal growth and synaptic changes through regulation of mitochondrial transport: a potential pharmacological target for neurodegenerative diseases
Published in Journal of Drug Targeting, 2023
Qing-Yun Wu, Hui-Lin Liu, Hai-Yan Wang, Kai-Bin Hu, Ping Liao, Sen Li, Zai-Yun Long, Xiu-Min Lu, Yong-Tang Wang
Physiological activities such as the generation of nerve impulses, the formation of synapses, and the transmission of nerve signalling are all heavily energy-consuming processes. Mitochondria, the organelles found in eukaryotic cells, are responsible for converting stored energy from organic matter into adenosine triphosphate (ATP). They play a critical role in cellular energy metabolism and produce 90% of the ATP required for cellular metabolism [1]. The brain relies heavily on mitochondria to produce most of the ATP needed for its functions and energy metabolism [2], and synapses are the main site of energy expenditure [3]. As the primary energy source for neurons, mitochondria are crucial for maintaining synaptic activities, including synaptic assembly, action potential and synaptic potential production, and synaptic vesicle (SV) transport and recycling [4]. Axonal mitochondrial deficiency affects synaptic transmission, and defective mitochondrial transport and energy deficiency are associated with the failure of axonal regeneration after injury and the pathogenesis of multiple neurological diseases [5–7]. Mitochondrial motility is also affected by stress or damage to its integrity. Consequently, ensuring mitochondrial health and motor function is essential for axonal growth, maintenance of synaptic energy balance, and synaptic function.
Omentin-1 promotes mitochondrial biogenesis via PGC1α-AMPK pathway in chondrocytes
Published in Archives of Physiology and Biochemistry, 2023
Zhigang Li, Yao Zhang, Fengde Tian, Zihua Wang, Haiyang Song, Haojie Chen, Baolin Wu
The mitochondrion is the "powerhouse" in eukaryotic cells. Mitochondrial biogenesis is the process of increasing cellular metabolic capacity, featured with the synthesis of enzymes for both glycolysis and oxidative phosphorylation (Jornayvaz and Shulman 2010). An efficient mitochondrial biogenesis needs the import of nuclear protein as well as mitochondrial replication, mitochondrial fusion and fission (Nunnari and Suomalainen 2012). Mitochondria in mammalian cells contain more than 1500 proteins, but only 13 proteins are coded in mitochondrial DNA, a majority of them are synthesised from nuclear DNA coding genes. Various mitochondrial molecular markers are used to study the mitochondrial regulation in eukaryotes. Translocase of the outer membrane (TOM) complex is a membrane-bound translocator vital to import mitochondrial precursors, and TOM complex includes several subunits including TOM20, TOM40 and TOM70 and is secured by TOM5, TOM6, TOM7, etc. (Ahting et al.1999). Several subunits of mitochondrial ATP synthases are also used as the markers of functional mitochondria, including ATPA, ATP5C1, ATPD and other subunits. The electron transport chain (ETC) located within the mitochondrial inner membrane composes of four protein complexes. Succinate dehydrogenase complex iron-sulfur subunit B (SDHB) links the pathways of Krebs cycle and oxidative phosphorylation. Mitochondrial DNA encoded subunits (MTCO1, MTCO2, MTCO3) are important subunits of complex IV (Zhao et al.2019).
Protective role of PERK-eIF2α-ATF4 pathway in chronic renal failure induced injury of rat hippocampal neurons
Published in International Journal of Neuroscience, 2023
Qi Chen, Jingjing Min, Ming Zhu, Zhanqin Shi, Pingping Chen, Lingyan Ren, Xiaoyi Wang
The endoplasmic reticulum is one of the most important organelles in eukaryotic cells. It is not only the site for protein translation and synthesis as well as calcium ion storage, but also a participant in the transmission and processing of various cell signals. In addition, one of the major functions of the endoplasmic reticulum is to serve as a site for synthesizing secretory and integral membrane proteins.5,6 When cells are stimulated by hypoxia, an imbalance of calcium ions or a change in their concentration occurs in the internal environment, accompanied with the accumulation of some unfolded proteins in the endoplasmic reticulum, resulting in an imbalance between the structure and function of the endoplasmic reticulum. At this time, the corresponding signal pathway is activated to further trigger the endoplasmic reticulum stress (ERS) response.7 Unfolded protein response activation can be triggered in the following three ways: (1) inhibition of protein translation to prevent the production of more folded proteins; (2) induction of the folding of unfolded proteins by the endoplasmic reticulum chaperone; (3) activation of endoplasmic reticulum associated degradation pathways to remove unfolded proteins accumulated in the endoplasmic reticulum.8 However, under prolonged or severe stress, the unfolded protein response initiates programmed cell death.