Disease relevance of Mitochondrial Swelling

• Neuroprotective effects of propofol in models of cerebral ischemia: inhibition of mitochondrial swelling as a possible mechanism [1].
• Reye's syndrome: mitochondrial swelling and Ca2+ release induced by Reye's plasma, allantoin, and salicylate [2].
• Correlation of mitochondrial swelling after capsaicin treatment and substance P and somatostatin immunoreactivity in small neurons of dorsal root ganglion in the rat [3].
• On the 7th and 15th days, damage in thin and thick myelinated axons, endoneural edema and mitochondrial swelling were less severe in the trapidil group histopathologically [4].
• SZ-induced hyperglycemia was noted at 36 and 48 hours after the treatment, but the hepatic changes including lipid peroxidation, mitochondrial swelling, peroxisome proliferation and inhibition of hepatocyte proliferation occurred before the elevation of the serum glucose levels [5].

Psychiatry related information on Mitochondrial Swelling

• Transgenic mouse strains overexpressing wild-type human SOD1 (Tg-SOD1) were shown to have mitochondrial swelling, vacuolization, or learning and memory deficits and are widely used for biochemical, genetic, and cognitive studies; this, along with the advent of advanced proteomic methods, made us investigate protein expression in hippocampus [6].

High impact information on Mitochondrial Swelling

• Alternatively, receptor tyrosine kinase or certain G protein-coupled receptor activation elicits cell protection (without mitochondrial swelling or durable memory) by inhibiting GSK-3beta, via protein kinase B/Akt and mTOR/p70(s6k) pathways, PKC pathways, or protein kinase A pathways [7].
• Cell damage to mTALs included mitochondrial swelling, nuclear pyknosis, and cytoplasmic disruption with superimposed calcification; these changes were most severe in the deepest areas of the outer medulla, away from vasa recta in zones remote from oxygen supply [8].
• Mice treated with buthionine sulfoximine, an inhibitor of glutathione synthesis, showed striking alterations of morphology of lung type 2 cell lamellar bodies (swelling and disintegration) and mitochondria (degeneration) and of lung capillary endothelial cells (mitochondrial swelling) [9].
• However, granzyme C did cause rapid mitochondrial swelling and depolarization in intact cells or in isolated mitochondria, and this mitochondrial damage was not prevented by cyclosporin A pretreatment [10].
• Interestingly, Parkin acted by delaying mitochondrial swelling and subsequent cytochrome c release and caspase-3 activation observed in ceramide-mediated cell death [11].

Chemical compound and disease context of Mitochondrial Swelling

• Diazoxide prevents mitochondrial swelling and Ca2+ accumulation in CA1 pyramidal cells after cerebral ischemia in newborn pigs [12].

Biological context of Mitochondrial Swelling

• Thymocyte apoptosis is characterized by an early dissipation of the mitochondrial transmembrane potential, with transient mitochondrial swelling and a subsequent loss of plasma membrane potential (DeltaP sip) related to the loss of cytosolic K+, cellular shrinkage, and DNA fragmentation [13].
• Loss of NF-kappaB-mediated transactivation resulted in downregulation of bcl-2 mRNA and protein expression, leading to mitochondrial swelling and release of cytochrome c. The apoptotic process involved activation of both caspase 9 and caspase 8 [14].
• Furthermore, IP rats had preserved cardiac function (heart rate, rate pressure product, coronary flow and aortic flow) and myocardial ATP (P<0.03), decreased tissue water content (73.2 vs. 90.6%), increased expression of Bcl-2, and less mitochondrial swelling, cytochrome C release and apoptosis (2.6 vs. 12.4%) when compared to sham-operated rats [15].
• Protection of oxidative phosphorylation by bencyclane against the damaging effect of mitochondrial swelling [16].
• The rate of oxygen consumption in State 3 and State 4, the transmembrane potential (deltapsi), mitochondrial swelling, and the polyethylene-glycol mediated recontraction were used to follow opening of the YMUC [17].

Anatomical context of Mitochondrial Swelling

• These included inhibition of reduced nicotinamide adenine dinucleotide and succinoxidase activities, as previously demonstrated, and mitochondrial swelling, which suggested interaction of CMNQ with the inner mitochondrial membrane [18].
• The addition of Ca(2+) to isolated rat heart mitochondria resulted in a profound decrease in their NAD(+) content, which followed mitochondrial swelling [19].
• These data indicate that the mitochondrial ROS are critical in initiating mitochondrial inner membrane permeabilization, which leads to mitochondrial swelling, cytochrome c release to the cytosol, and apoptotic death during PDT with Pc 4 [20].
• In particular, we observed that melatonin effectively prevented exogenously applied H2O2-induced mitochondrial swelling in rat brain astrocytes at an early time point (within 10 min) and subsequently reduced apoptotic cell death (150 min later) [21].
• Transmission electron microscopy showed that 22,26-azasterol induced marked morphological changes, including mitochondrial swelling, invaginations of the inner mitochondrial membrane, and the appearance of large bodies containing concentric membranes [22].

Associations of Mitochondrial Swelling with chemical compounds

• Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk [23].
• Incubation of energized mitochondria with succinate in the presence of Ca(2+) and diclofenac resulted in mitochondrial swelling, leakage of accumulated Ca(2+), membrane depolarization, and oxidation of nicotinamide adenine dinucleotide phosphate and protein thiol [24].
• Ca(2+) efflux was associated with contraction, but not with mitochondrial swelling [25].
• In contrast, Mphi infected with Mtb in presence of the mitochondrial calcium uniporter inhibitor ruthenium red showed increased mitochondrial swelling and cytochrome c release and decreased MPT and antimycobacterial activity [26].
• ATP also induced mitochondrial swelling in potassium glutamate, chloride, and acetate but not in phosphate solutions [27].

Gene context of Mitochondrial Swelling

• We purified mitochondria from livers of the Bcl-2 transgenics and measured PTP directly by the mitochondrial swelling assay [28].
• Electron microscopic observation indicated that IFN-alpha prevented the induction of mitochondrial swelling by ASA [29].
• Deltapsi(m) disruption is associated with mitochondrial swelling and cytochrome c leakage [30].
• Interestingly, we also found that specific inhibitors of ANT such as MT-21 and atractyloside could induce cytochrome c release without mitochondrial swelling and that this event was highly dependent on the presence of Mg(2+) [31].
• In any case (low or high phosphate concentration) exogenous catalase prevented mitochondrial swelling, suggesting that reactive oxygen species (ROS) participate in these mechanisms [32].

Analytical, diagnostic and therapeutic context of Mitochondrial Swelling

• Electron microscopy after ALA + R, ALA + R + IR and R + IR treatments showed early mitochondrial swelling that was more pronounced in the ALA + R + IR group [33].
• With immunoelectron microscopy, the expression of c-Fos/c-Jun and HSP70 was observed in the neurons which retained neuronal integrity except for mitochondrial swelling and polyribosomal disaggregation [34].
• Within 6-12 hr a single intravenous injection of 40 mg/kg paraquat dichloride caused selective mitochondrial swelling and loss of intramitochondrial granules within 24 hr in alveolar Type II cells [35].

References