On the stabilization by fixation of configurational states in beef heart mitochondria

Wakabayashi, Takashi; Hatase, Osamu; Allman, D.W.; Smoly, Jennie M.; Green, David E.

doi:10.1007/bf01517190

Cited by 20 publications

(2 citation statements)

References 18 publications

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“…The significance of our observations of increased numbers of condensed and tubular mitochondria in cells fixed 30 seconds after electric shock becomes clearer when these observations are compared with those of mitochondria fixed in various metabolic states (Green, 1974;Homburger et al, 1976;Munn, 1974;Wakabayashi et al, 1970;Williams et al, 1970). According to these studies, the cristae of cardiac mitochondria are invaginations of the mitochondrial inner membrane into the matrix space and have the shape of hot-water bottles opening into this space.…”

Section: Ultrastructural Changes Following 80 V/cm Shocksmentioning

confidence: 56%

Ultrastructural injury to chick myocardial cells in vitro following "electric countershock".

Jones¹,

Proskauer²,

Paull³

et al. 1980

Circulation Research

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We studied the structural alterations that follow the application of currents similar to those used in clinical electric countershock procedures in cultured chick myocardial cells. Myocardial cells 48 hours in culture were subjected to electric field stimulation. The cells then were fixed for electron-microscope examination 30 seconds postshock. The ultrastructural alterations that appeared after an 80 V/cm shock included the appearance of >25% of the mitochondria per cell in the "condensed" configuration and mitochondria with swirled or tubular cristae. Large-amplitude swelling of the mitochondria and swollen endoplasmic reticulum also were observed in a few cells. The alterations that appeared after a 200 V/cm shock included contracture and disorganization of the myofibrils, large-amplitude swelling and loss of cristae in the mitochondria, swollen endoplasmic reticulum and nuclear envelope, and intracellular edema. The degree of ultrastructural change was dependent on the intensity of the shock. These structural alterations are consistent with an osmotic imbalance which occurs during a shock-induced prolonged depolarization of the cell membrane (Jones et al., 1978a), possibly due to a transient dielectric breakdown during the shock, and may underlie the arrhythmias and necrosis which often occur after high-intensity clinical and experimental eountershock procedures in vivo.

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Section: Ultrastructural Changes Following 80 V/cm Shocksmentioning

confidence: 56%

Ultrastructural injury to chick myocardial cells in vitro following "electric countershock".

Jones¹,

Proskauer²,

Paull³

et al. 1980

Circulation Research

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show abstract

“…For thin-section electron microscopy, polymerized tubulins were sedimented at 70,000 g for 60 min at 25"C, fixed in glutaraldehyde, postfixed in 0~0 4 , and embedded in Epon 812 according to the method of Wakabayashi et al (1970). The sections were examined with a Hitachi HU-12A electron microscope.…”

Section: Ultrastructurementioning

confidence: 99%

Stimulation of Tubulin‐Dependent ATPase Activity in Microtubule Proteins from Porcine Brain by Taxol

Fujii

Kondo

Kumasaka

et al. 1983

Journal of Neurochemistry

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Taxol, an antimitotic agent that induces microtubule assembly, stimulated tubulin-dependent Mg2+-ATPase activity of microtubule-associated proteins (MAPs). A concentration-dependent increase in the rate of ATP hydrolysis was observed. Taxol acted through its binding to the tubulin molecule on MAP ATPase, and maximal stimulation, which was found at approximately equal concentrations of taxol and tubulin, reached about 140% of the original level in the absence of taxol. Taxol enhanced ATP hydrolysis by a mixture of MAPs and tubulin, and this continued at a steady linear rate even when the polymerization had approached a plateau. In the presence of taxol, a large portion of ATPase activity and protein was recovered in the pellet after centrifugation at 70,000 g for 60 min at 25 degrees C. Both colchicine and podophyllotoxin inhibited taxol-stimulated ATPase activity via the same mechanism by which they inhibited taxol-induced microtubule polymerization. The stimulation by taxol was not found in the presence of Ca2+ alone but required Mg2+. We conclude that tubulin effectively stimulates Mg2+-ATPase activity of MAPs under conditions that induce tubulin polymerization.

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Energy Metabolism : Methods in Isolated Smooth Muscle and Methods at Cellular and Subcellular Levels

1975

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On the stabilization by fixation of configurational states in beef heart mitochondria

Cited by 20 publications

References 18 publications

Ultrastructural injury to chick myocardial cells in vitro following "electric countershock".

Ultrastructural injury to chick myocardial cells in vitro following "electric countershock".

Stimulation of Tubulin‐Dependent ATPase Activity in Microtubule Proteins from Porcine Brain by Taxol

Energy Metabolism : Methods in Isolated Smooth Muscle and Methods at Cellular and Subcellular Levels

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