Vesicular Changes Research Articles

Cytoplasmic constriction and vesiculation after axotomy in the squid giant axon

The squid giant axon responded to a transection injury by producing a gradient of cytoplasmic and vesicular changes at the cut end. At the immediate opening of the cut axon the cytoplasm was fragmented and dispersed and the vesicles in this region were in rapid Brownian movement. Approximately 0.1 mm further in, at the site of maximal axonal constriction, the axoplasm was condensed into a compact, constricted mass containing many large vesicles. The axoplasm was normal a few millimetres beyond this constricted, vesiculated end. It appears that transection triggered the transformation of normal axoplasm into a tightly constricted, highly vesiculated structure. This modified axoplasm at the cut end may slow the spread of damage and degeneration by preventing the bulk outflow of axoplasm, by slowing down the loss of intracellular molecules and by slowing down the influx of destructive extracellular ions (like calcium and chloride).

Vesicular changes in the myopathies of AIDS. Ultrastructural observations and their relationship to zidovudine treatment.

Six patients with AIDS and AIDS related complex (ARC) who developed neuromuscular symptoms associated with vesicular changes in muscle fibres are reported. Two patients in the advanced stages of AIDS, who did not receive zidovudine, developed proximal limb weakness and wasting: both had a necrotising myopathy with an unusual segmental vesicular change of myofibres. There were numerous vesicles 0.1 to 2 microns in diameter produced by dilatations of the sarcoplasmic reticulum in fibres depleted of myofibrils. Four patients developed a myopathy while receiving zidovudine for AIDS. One of these had an inflammatory myopathy which showed the development of vesicular change due to enlargement and electron lucency of mitochondria. The three other patients with ARC developed muscle pains or weakness and elevated serum CK while on zidovudine. These patients also showed vesicular changes due to enlargement and electron lucency of mitochondria associated with disruption of sarcomeres and the presence of cytoplasmic bodies. The muscular symptoms resolved when ziduvodine was stopped and repeat biopsy in one case revealed no abnormalities.

Alterations of oligodendrocytes and demyelination in the spinal cord of patients with mitochondrial encephalomyopathy

The spinal cords of 2 autopsied patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) were examined. Histologically, the spinal cords showed a spongy state due to the presence of distended myelinated fibers with enlarged periaxonal spaces. Ultrastructurally, the affected fibers showed extensive microvacuolation of the inner myelin sheath with occasional vesicular changes. The presence of macrophages near the degenerated myelin was a frequent finding. The stripping of myelin lamellae by macrophage was observed, with frequent appearance of denuded axons. Furthermore, prominent morphological changes were observed in oligodendrocytes. These findings indicate that demyelination, probably secondary to the degeneration of oligodendrocytes, occurs in the spinal cord of MELAS.

The mechanism of liposomal damage by taurocholate

The stability of small unilamellar vesicles formed by egg-yolk phosphatidylcholine (PC) has been examined in the presence of sodium taurocholate. The permeability of the vesicular membrane changes as the total taurocholate concentration increases, until a transformation from mixed bile salt/PC vesicles to mixed micelles occurs. Based on experiments in which the bile salt-induced release of either hydrophilic (carboxyfluorescein) or hydrophobic (Bromothymol blue) probes was studied, and on fluorescence polarization of the probe 1,6-diphenyl-1,3,5-hexatriene and turbidity measurements, a two-step process for the initial stage of liposomal damage by taurocholate is postulated.

Osmotic water permeabilities of brush border and basolateral membrane vesicles from rat renal cortex and small intestine.

The osmotic water permeability Pf of brush border (BBM) and basolateral (BLM) membrane vesicles from rat small intestine and renal cortex was studied by means of stopped-flow spectrophotometry. Scattered light intensity was used to follow vesicular volume changes upon osmotic perturbation with hypertonic mannitol solutions. A theoretical analysis of the relationship of scattered light intensity and vesicular volume justified a simple exponential approximation of the change in scattered light intensity. The rate constants extracted from fits to an exponential function were proportional to the final medium osmolarity as predicted by theory. For intestinal membranes, computer analysis of optical responses fitted well with a single-exponential treatment. For renal membranes a double-exponential treatment was needed, implying two distinct vesicle populations. Pf values for BBM and BLM preparations of small intestine were equal and amount to 60 microns/sec. For renal preparations, Pf values amount to 600 microns/sec for the fast component, BBM as well as BLM, and to 50 (BBM) and 99 (BLM) microns/sec for the slow component. The apparent activation energy for water permeation in intestinal membranes was 13.3 +/- 0.6 and in renal membranes 1.0 +/- 0.3 kCal/mole, between 25 and 35 degrees C. The mercurial sulfhydryl reagent pCMBS inhibited completely and reversibly the high Pf value in renal brush border preparations. These observations suggest that in intestinal membranes water moves through the lipid matrix but that in renal plasma membranes water channels may be involved. From the high Pf values of renal membrane vesicles a transcellular water permeability for proximal tubules can be calculated which amounts to approximately 1 cm/sec. This value allows for an entirely transcellular route for water flow during volume reabsorption.

Properties of a Mg2+-dependent, and Ca2+-inhibited ATPase localized in the brush border of the surface epithelial syncytium of a parasitic flatworm

The brush border membrane of the surface epithelial syncytium of the parasitic flatworm, Hymenolepis diminuta, was isolated by saponin treatment, and the ATPase activity was determined. The ATPase activity was insensitive to ouabain, SCN−, HCO3−, ethanol, and, although slightly inhibited by high oligomycin concentrations, was inhibited by ethacrynic acid. Reaction mixtures made increasingly hypertonic with mannitol resulted in vesicular changes in the microvilli and decreased ATPase activity. Although treatment of the brush border fraction with deoxycholate increased ATPase activity, the dependence of activity on the osmotic pressure of the reaction mixture persisted in the solubilized membrane preparations. ATPase activity was dependent upon Mg2+ and Na+ + K+ concentration. It is suggested that the ATPase in the flatworm surface membrane is involved in volume regulation in hypotonic media.

Chronic effects of ethanol under partial inhibition of catalase activity in the rat heart: Light and electron microscopic observations

In order to test the hypothesis that cardiac catalase plays a protective role in the pathogenesis of alcoholic cardiomyopathy, ethanol, comprising 36% of dietary calories, was administered to the rats for 5 weeks under inhibited cardiac catalase activity. Rats were treated with 3-amino-1,2,4-triazole (AT), a specific enzyme inhibitor, or iso-osmotic saline as control. During ethanol feeding, cardiac catalase activity was significantly inhibited at 24 h after AT, 25.6 ± 4.7 IU/mg protein, compared to rats given isoosmotic saline, 51.0 ± 9.1 IU/mg protein ( s.d.m.) ( P < 0.001). Under light microscopy, observed were intrasarcoplasmic vacuolization and occasional foci of necrosis and fibrosis. Ultrastructural abnormalities included very extensive vesicular changes in the myocardial cells, abnormally increased interstitial fibrosis, dilatation of tubular structures of sarcoplasmic reticulum, increased numbers of lysosomes, dehiscence of intercalated disc and various mitochondrial alterations including amorphous inclusion body. None of the rats given ethanol + saline, pair-fed diet + AT or saline showed comparable changes. Thus, cardiac catalase is considered to play a metabolic and protective role in the rat myocardium chronically exposed to ethanol.

Qualitative and quantitative changes in the ultrastructure of the dogheart after temporary ischaemia and coronary reperfusion

A total ischaemia of one area of the myocardium was produced by ligature of a coronary artery in dogs. After 30 min, 1 hr, 2 hrs, and 4 hrs the ligature was loosened and the artery was for 1--2 hrs reperfused up to 4--7 days. At the end of the ischaemia and after reperfusion the ultrastructure of the myocardium was qualitatively and morphometrically investigated. The findings concerned: loss of glycogen (partly glycogen accumulation), mitochondrial swellings and fusions and development of megamitochondria, loss of cristae, rupture of the mitochondrial outer membranes, relaxation or supercontraction of the myofibrils, vesicular and vacuolar changes of the sarcoplasmic reticulum, oedema of the sarcoplasm, rupture of the sarcolemma. No significant differences of the quantitative parameters could be observed during the ischaemia from 30 min to 4 hrs: myofibrils 53.65--59.74%, mitochondria 26.51--33.59%, sarcoplasm 8.22--11.86%, sarcoplasmic reticulum 1.41--2.63%, lipofuscin 0.05--0.87%, lipids 0.01--0.10%. In comparing the data of the single animals we could determine significant differences between some parameters at the ends of the ischaemic phase and of the reperfusion phase, but as far as the findings are concerned both increases and decreases could be observed. The investigations show that the limit of the reversibility of damages in myocardial cells is about 45 min; in special cases a longer survival time may be taken into account. Reperfusion has different, though not always positive, effects.