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Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
In chronic cell injury, many cellular cytoplasmic organelles show abnormalities. A variety of inflammatory factors induces dramatic changes involving the formation of a larger number of smaller mitochondria under some conditions and of a fewer number but larger mitochondria in others. Large mitochondria show irregular shape with disorganized cristae and paracrystalline inclusions in the inner compartment. The cause of megamitochondria production has been attributed to aging,433 vitamin deficiency (vitamin E, riboflavin, thiamine),283,447,521 essential fatty acid deficiency,23 choline,443 copper and iron deficiency,90,516 alcoholism, and kidney hypertrophy.230 The exact significance of these changes is not known, although in certain cases mitochondrial metabolism is reduced, whereas megamitochondria show normal function in some instances.
Modifying macronutrients is superior to microbiome transplantation in treating nonalcoholic fatty liver disease
Published in Gut Microbes, 2020
Fontini Tania Mitsinikos, Denise Chac, Nicholas Schillingford, R. William DePaolo
H&E stained slides were evaluated for the percentage of hepatic steatosis, portal inflammation, lobular inflammation and hepatocyte ballooning. These slides were also assessed for the presence or absence of Mallory-Denk bodies, megamitochondria, lipogranuloma and glycogenated nuclei. The NAFLD activity score (NAS) was scored on cumulative scoring of steatosis, lobular activity and hepatocyte ballooning with maximum score of “8”.43,44 Steatosis was scored between “0” and “3” with less than 5% steatosis scored “0”, 5–55% scored “1”, 33–65% scored “2”, and greater than 66% scored “3”. Lobular activity was scored between “0” and “3” with no lobular necroinflammatory infiltrates given a score of “0”, 1–2 foci scored “1”, 2–4 foci scored “2” and more than 4 foci scored “3”. No hepatocyte ballooning scored “0”, occasional presence scored “1”, many presences scored of “2” was issued. Fibrosis was graded on Masson trichrome stains and scored from “0” to “4”. No fibrosis scored “0”, presence of either perisinusoidal or periportal fibrosis scored “1”, presence of both scored “2”, presence of bridging fibrosis scored “3” and frank cirrhosis scored “4”.
Alcoholic steatohepatitis (ASH) and alcoholic hepatitis (AH): cascade of events, clinical aspects, and pharmacotherapy options
Published in Expert Opinion on Pharmacotherapy, 2018
ASH is characterized by hepatic injury accompanying steatosis [13,14]. Hepatocyte ballooning as the most frequent sign of cellular injury, shown by markedly swollen hepatocytes with rarified cytoplasm, clumping of intermediate filaments and loss of staining for cytokeratin 8 and 18 [14,15], progression markers of human liver disease [16]. Whereas lytic necrosis is most frequent in ASH, apoptosis is rare [14,17]. Known as Councilman bodies or acidophil bodies, apoptotic hepatocytes show cell shrinkage, chromatin condensation, as well as nuclear and cellular fragmentation [14]. Mallory-Denk bodies (MDB) are clumps or skeins of eosinophilic ropy material in the cytoplasma of the hepatocyte, preferentially in the perinuclear region. Misfolded and aggregated keratin filaments accumulate to form MDB [14,15]. Lobular inflammation often consists of neutrophils, surrounding ballooned hepatocytes and appearing as so-called satellites [14]. Portal inflammation is variable and consists of lymphocytes, plasma cells, eosinophils, and even mast cells, rarely accompanied by ductular reaction and periportal fibrosis [14,15]. Other histological features include glycogenated nuclei, megamitochondria, hemosiderin deposition, and cholestasis [13–15].
The role of mitochondrial dysfunction in cardiovascular disease: a brief review
Published in Annals of Medicine, 2018
Dimitry A. Chistiakov, Tatiana P. Shkurat, Alexandra A. Melnichenko, Andrey V. Grechko, Alexander N. Orekhov
Cardiac pathologies are generally associated with structural changes of mitochondria in the tissue, including formation of giant mitochondria (megamitochondria) that have a size up to 30 μm [10]. Giant mitochondria are generated by fusion of adjacent organelles due to overexpression of fusion proteins, such as mitofusin 1 (Mfn1) and Mfn2 [11] or by enlargement of an individual mitochondria. Megamitochondria are usually dysfunctional and eliminated through the mechanism of mitophagy [9]. Other pathological changes in mitochondrial shape involve loss or reorientation of cristae, formation of intramitochondrial rods and crystalloids mainly composed by creatine kinase crystals [12].