Mitochondrial swelling

Recent studies by Crompton et al. have shown that oxidant stress may open a Ca-sensitive, non-selective pore in the inner mitochondrial membrane that is blocked by cyclosporin A (Crompton, 1990 Crompton and Costi, 1990). This pore opening results in massive mitochondrial swelling, dissipation of the transmembrane proton gradient and disruption of mitochondrial energy production (Crompton et al., 1992). Since mitochondria may play a role as a slow, high-capacity cytosolic calcium buffer (Isenberg et al., 1993), disruption of mitochondrial function may also contribute to calcium overload and cell injury. 

Rat (Sprague-Dawley) 6 wk Cardio ad lib (W) 873 M (myofibrillar fragmentation, mitochondrial swelling) Asokan 1974 PbAc... 

After administration of mercuric chloride to adult rat kidneys, several changes were found, for example, pars recta of the proximal tubular segment showing fragmentation and disruption of the plasma membrane, basophilic staining, vesiculation and disruption of endoplasmic reticulum and other cytoplasmic membranes, mitochondrial swelling, loss of mitochondrial dense granules and condensation of nuclear chromatin [223-225]. 

Necrosis A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH]... 

Darios, F., et ah. Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-dependent cell death. Hum Mol Genet, 2003, 12(5), 517-26. 

Numerous ultrastructural studies have noted lung mitochondrial swelling and degenerative changes after ozone exposure. 

Mitochondrial swelling occurs in vitro in association with lipid peroxidation of the mitochondrial membrane. However, the biochemical concomitants of ozone-induced damage to lung mitochondria have not been extensively studied. 

Degeneration Mitochondrial permeability transition with membrane depolarization, cytochrome c release, and mitochondrial swelling and fragmentation activation of caspases and cell death pathway, endonuclease fragmentation of DNA with chromatin and nuclear condensation phosphatidyserine exposure on cell surface cytoskeletal disruption with membrane blebbing... 

Megamitochondria were induced in male Wistar rats placed for three or seven days on a diet containing 1% hydrazine (Wakabayashi et al., 1987). From biochemical analysis, the authors concluded that the formation of megamitochondria was due to fusion of adjacent mitochondria rather than to mitochondrial swelling. 

The mechanism of mitochondrial swelling in animal cells has been examined intensively (36). This phenomenon is less well documented for algal cells. 

Examination of the root apex showed much the same effects as reported above (Fig. 15.6a-d). The calyptra was a particularly sensitive tissue, showing dramatic mitochondrial swelling at all dilutions tested (Fig. 15.6b-d). A conspicuous effect of the treatment with the RO fraction on the root apex was the inhibition of amyloplast development as statoliths in the columella cells of the calyptra (Fig. 15.6b-c). The almost complete lack of starch and of lipid-associated microbodies in... 

Figure 17.7. Two types of mitochondrial membrane permeabilization. Upper Bax/Bak pore leads to release of intermembrane space proteins, but the inner membrane is intact. Lower PTP (permeability transition pore) opening destroys the impermeability of the inner mitochondrial membrane (IMM). The pore opening causes influx of solutes and water into the matrix resulting in swelling. The mitochondrial swelling ruptures outer mitochondrial membrane (OMM). CypD, cyclophilin D.

It has been shown that the oxidation of choline by isolated rat liver mitochondria is biphasic (269). The initial phase of choline oxidation is slow and coupled to the uptake of inorganic phosphate. The ensuing phase is 3-5 times faster and not coupled to phosphorylation. The slow phase can be extended in the presence of Mg-+ and ADP or ATP. These compounds are considered to control the permeability of mitochondria to choline (270). Calcium ions and conditions which result in mitochondrial swelling and membrane disruption have been shown to increase choline oxidation (266, 271). 

Ferrans et al. (1969) noted ultrastructural changes in myofibrils, including mitochondrial swelling and disorganization. Catecholamines also produce changes in the activity of oxidative enzymes. The decline in the activity progresses to the point where necrosis is evident. Ancillary effects include loss of myocardial potassium and an increase in interstitial fluid. Intracellular calcium overload also develops as noted by Fleckenstein et al. (1974). It has been hypothesized that necrosis due to catecholamine overload may be caused by a defect in energy supply needed for the maintenance of cellular processes. 

Ultrastructural changes of proximal tubular cells occur as early as 1 hour after cephaloridine administration to rabbits and are characterized by loss of brush border, less elongated mitochondria and disappearance of structures associated with endocytosis. Later ultrastructural changes include disorganization of lateral interdigitations of plasma cell membrane and mitochondrial swelling [28,29]. 

Renal biopsies in chronic lead nephropathy show nonspecific tubular atrophy and interstitial fibrosis with minimal inflammatory response as well as mitochondrial swelling, loss of cristae, and increased lysosomal dense bodies within proximal tubule cells [4,18]. (Figure 1)... 

Cellular shrinkage Sarcolemmal blebbing Chromatin condensation Redistribution of membrane phospholipids DMA fragmentation Cellular swelling Sarcolemmal blebbing Chromatin clumping Mitochondrial swelling... 

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