Mitochondria swelling

Mitochondrial ATPase inhibition. Smoke extract, in the mouse brain mitochondria culture in the presence or absence of vitamin C for 60 minutes, inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. The effect of extract on mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. The extract treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane was preserved. Nicotine produced no significant damage . Mitogenic activity. Water extract of the dried leaf, administered to mice at a concentration of 0.05%, was active on lymphocytes from mesenteric lymph node and lymphocytes B and T. Intracellular Ca level was unchanged. The extract was active on... 

Fig. 10.11. The effect of osmolarity on the apparent number of GDP binding sites in brown adipose tissue mitochondria. The number of GDP-binding sites was measured in mitochondria from control and cold-exposed (24 h at 4°C) rats as earlier described (Sundin and Cannon [37]), but in media with the indicated concentrations of sucrose. Note that, if iso-osmotic sucrose is used (250 mM), a low GDP binding can be observed, especially in control rats. This may be related to the condensation phenomenon discussed in section 2.4. However, if 100 mM sucrose is used, the mitochondria swell, and the full number of binding sites is determined. (Our unpublished observations.)...

Apoptosis is delayed and may be maximal at 24-48 h after an insult. However, apoptotic cells can be seen even within 6 h of an insult, but are not common. Apoptosis involves condensation of the nucleus. Condensation of the cytoplasm occurs with large vacuole formation. Some mitochondria may condense. Very uncommonly, some mitochondria swell in apoptosis. The cell splits up into membrane-bound apoptotic bodies that can be seen in the limit areas surrounding the core of an infarction. Apoptosis is a programmed form of cell death that occurs following a small but sufficient amount of damage to a cell. This initiates a program that eventually kills the cell. 

Pronounced mitochondria swelling with loss of cristae, development of amorphous matrix densities, and breaks in the sarcolemma are seen in irreversibly injured myocytes. Increased mitochondrial size is an early indication of ischemia. In hearts with 3-15 min of ischemia, morphologic injury is reversible, yet some mitochondria remain swollen even at 20 min of reperfusion. Therefore, a majority of the mitochondria in the ischemic myocardium is expected to be edematous at 30 min of reperfusion. However, early CSIL treatment of ischemic hearts (I and 5 min) results in normal mitochondrial size, smaller than that of CSIL-treated hearts at later times (35). Cessation of mitochondrial electron transport has been observed 2 s after the onset of global ischemia in isolated rat hearts (36). The results of mitochondrial size determination are compatible with the delay in the recovery of function with later administration of CSIL. Thus, mitochondrial ultra-structural data agree with the functional and histochemical data. Preservation of cell membrane integrity after CSIL intervention results in a faster recovery of function and a reduction in infarct size. Whether this is associated with prevention of the influx of extracellular Ca that is associated with ischemia and reperfusion is not assessed in our studies. However, uncontrolled influx of Ca into the cytosol occurs after reperfusion and results in rigor (37, 38). 

Administration of cephaloridine induces mitochondria elongation followed by mitochondria swelling [28, 29] which lead to mitochondrial dysfunction. Cephaloridine and other P-lactams decreased mitochondrial respiration significantly, suggesting a loss of mitochondrial integrity [35,56]. It has been suggested that mito-... 

A metal ion not infrequently implicated in superoxide-associated damage to cells is Fe ". It is known that Fe can form complexes with superoxide, thereby leading to the formation of peroxide or even possibly OH-radicals, which are highly damaging. It is also feasible that damage can result from the interaction of superoxide with other metal ions. Isolated mitochondria swell rapidly when incubated in the presence of Ca. Such cells can be protected for long periods by 10% dimethylsulfoxide, an agent which readily destroys peroxide. Suspensions of liver cells tolerate ischemic... 

Fig. 229. Annulate lamellae and damaged mitochondria (swelling and cristolysis) in a repetitively reoxygenated pineal cell (block 1211) from a rat (No. 7) treated for 7 consecutive days with intraperitoneal injection of 1.5 ml Tyrode s solution per kg body weight x day. On the last 4 days of experimentation the animal was exposed to an atmosphere containing only 5 % oxygen for 30 min. Half an hour after the last exposure under pentobarbital anaesthesia (30 mg/kg), the animal was perfused from the abdominal aorta with 2.5 % glutaral-dehyde in 0.1 M sodium cacodylate buffer (pH 7.4). Postfixa-tion with 1 % osmium tetroxide in sodium cacodylate buffer. Embedded in Epon 812 and sectioned at 50 nm. Lead citrate and uranyl acetate. Plate 3395...

Electrolyte movements in general, but calcium movements in particular, are important in mitochondrial physiology. (The movement of electrolytes in and out of mitochondria will be discussed in another chapter.) However, parathormone s effect on calcium movements in kidney and liver mitochondria is relevant to the possible mode of action of the hormone on the kidney. Parathormone has a complex effect on isolated liver and kidney mitochondria. Not only does the hormone stimulate calcium release from mitochondria, but this effect on the divalent cation is associated with all sorts of changes in the electrolyte composition of the mitochondria, and with altering mitochondrial metabolism. When incubated with the hormone, the mitochondria swell and take up potassium, ATP is hydrolyzed, and the ATP-Pj exchange is blocked. 

Metabolism Changes in tissue fatty acid composition Cholesterol in plasma i Cholesterol in liver adrenals skin f Mitochondria swelling and uncoupling of oxidative phosphorylation Liver triacylglycerol output ... 

To explain these two stages in mitochondrial swelling, it has been proposed that the mitochondrion can be described as a structure made of two concentric compartments. Without thyroxine or another swelling agent, only the outside compartment is permeable to sucrose, but when thyroxine is added to the medium, the second compartment also becomes permeable to sucrose. During swelling, the NAD bound to the mitochondrial structure is progressively lost, and oxidation is uncoupled from phosphorylation. 

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