Studies on the Role of Potassium Ions in the Lethal Toxicity of Streptolysin O

Halbert, Seymour P.; Dahle, E. Jill; Keatinge, S.; Bircher, R.

doi:10.1016/b978-0-08-010811-7.50024-1

Cited by 3 publications

(4 citation statements)

References 14 publications

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“…The same preparations were used in earlier studies on the cardiotoxicity of this substance in vivo (6,19). These fractions were contaminated with a maximum of 1.5% DPNase 1 on the basis of the purest fractions of that enzyme presently available.…”

Section: Methodsmentioning

confidence: 99%

The Toxicity of Streptolysin O for Beating Mammalian Heart Cells in Tissue Culture

Thompson

Halbert

Smith

1970

The Journal of Experimental Medicine

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Pulsating mammalian myocardial cells were found to be highly susceptible in tissue culture to rapid destruction by streptolysin O. Cessation of beating occurred almost immediately, followed within minutes by multiple cell membrane bleb formation. Parallel with these changes, the cytoplasm became intensely granular and the nuclear membrane apparently thickened when viewed by phase microscopy. At the ultrastructural level, the cell membrane blebs were found to contain relatively small numbers of granular fragments. The endoplasmic reticulum of damaged heart cells was quite swollen, and its contents were considerably condensed. The myofibers were not strikingly altered, but cytoplasmic and mitochondria vacuoles were rather abundant. Cardiac endothelial, kidney epithelial, and fibroblast cells were also susceptible to lysis by this toxin, but the reactions occurred more slowly or bleb formation was less evident. An antiserotonin drug known to be protective against streptolysin-O in vivo (UML-491), did not protect against killing of cardiac cells at the tissue culture level. Serotonin could not be detected in the culture fluid after lysis of cardiac cells by streptolysin O.

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Section: Methodsmentioning

confidence: 99%

The Toxicity of Streptolysin O for Beating Mammalian Heart Cells in Tissue Culture

Thompson

Halbert

Smith

1970

The Journal of Experimental Medicine

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“…~ These preparations were made according to methods previously described (8)(9)(10)(11)(12) and had been used in other studies (4)(5)(6). The Group A toxin consisted entirely of protein and had a titer of 160,000 hemolytic units (HU) per milligram of dry weight; the Group C material, which was 67% protein, had a tlter of 40,000 HU/mg.…”

Section: Methodsmentioning

confidence: 99%

“…In subsequent studies, Halbert et al (6) considered the likelihood that the in vivo cardiovascular changes observed were consequent to an elevated plasma potassium concentration resulting from intravascular hemolysis. They found sufficient discrepancies, however, in the relationships among hemolysis, potassium levels, and electrocardiographic changes to render inadequate this mechanism as being responsible for the rapid lethality of the toxin.…”

mentioning

confidence: 99%

“…The present work (see also reference 7) endeavors to extend the in vitro studies (1,2) and to investigate the provocative in vivo electrocardiographic findings (3)(4)(5)(6) by an analysis of the electrophysiological, pharmacological, and mechanical changes occurring in the isolated whole heart and separate cardiac tissues of the guinea pig pursuant to their challenge with streptolysin O.…”

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confidence: 99%

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An Analysis of the Toxic Actions of Purified Streptolysin O on the Isolated Heart and Separate Cardiac Tissues of the Guinea Pig

Reitz

Prager

Feigen

1968

The Journal of Experimental Medicine

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The cardiotoxidty of streptolysin O was first demonstrated by Bemheimer and Cantoni (1) who induced systolic contracture in the frog heart perfused with the toxin. Subsequently, Kellner et al. (2) showed that permanent and irreversible standstill, accompanied by a profound but transitory reduction in coronary flow, resulted from the exposure of the isolated hearts of guinea pigs, rabbits, and rats to small amounts of the toxin. Halpem and Rahman (3) found that the electrocardiograms of mice given large lethal doses of toxin exhibited immediate and intense bradycardia followed, in some cases, by temporary arrest; progressive atrioventricular dissociation implicated the conductile tissue. Electrocardiograms, obtained by Halbert, Bircher, and Dahle (4) from rabbits given lethal and sublethal doses of highly purified streptolysin O, were characterized by conduction defects and ventricular automatism. Intravenous injection of several multiples of the Ires0 was followed within 3-4 sec by a rapid transition from normal sinus rhythm to ventricular arrhythmia, ventricular fibrillation, and standstill. Frequently, smaller lethal doses and sublethal doses immediately produced a pronounced but transient sinus bradycardia, followed by temporary or permanent recovery. The transient nature of this bradycardia, along with the extremely rapid effects of the toxin in vivo, suggested that its toxicity might result from the release of vasoactive substances rather than from the direct action of the protein itself. Accordingly, Halbert et al. (5) studied the effectiveness of various pharmacological blocking agents in protecting against the putative physiologically active agent(s) responsible for the intravenous effects of streptolysin O. Although the several agents which exhibited protection were serotonin antagonists, there was little correlation between this property and protection. In addition, serotonin was not very toxic to rabbits and mice, so it appeared unlikely that the acute toxicity of streptolysin O could be accounted for entirely by the release of this amine.

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Tetanolysin: In-Vivo Effects in Animals

Duffin

1971

Journal of Infectious Diseases

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Studies on the Role of Potassium Ions in the Lethal Toxicity of Streptolysin O

Cited by 3 publications

References 14 publications

The Toxicity of Streptolysin O for Beating Mammalian Heart Cells in Tissue Culture

The Toxicity of Streptolysin O for Beating Mammalian Heart Cells in Tissue Culture

An Analysis of the Toxic Actions of Purified Streptolysin O on the Isolated Heart and Separate Cardiac Tissues of the Guinea Pig

Tetanolysin: In-Vivo Effects in Animals

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