Anthracycline-induced histamine release from rat mast cells

Riegel, E. A.; Kaliner, Michael; El-Hage, Antoine N.; Ferrans, Víctor J.; Kawanami, Oichi; Herman, Eugene H.

doi:10.1007/bf01965922

Cited by 11 publications

(3 citation statements)

References 22 publications

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“…In studies performed by other authors (Riegel et al, 1982), on the contrary, adriamycin did not produce significant histamine release on purified or unpurified rat mast cells in vitro, but caused a dose-related histamine release in vivo after i.p. injection.…”

Section: Discussionmentioning

confidence: 61%

Inhibitors of adriamycin-induced histamine release in vitro limit adriamycin cardiotoxicity in vivo

Fb¹,

Decorti²,

Candussio³

et al. 1986

Br J Cancer

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The activity of theophylline and disodium cromoglycate was tested on adriamycin-induced histamine release in vitro and on adriamycin cardiotoxicity in vivo. Both substances significantly inhibited the release of histamine induced by 100 micrograms ml-1 of adriamycin on rat peritoneal cells and produced significant protection against adriamycin-mediated acute and chronic cardiotoxicity in mice. N-acetylcysteine, a free radical scavenger, successfully used in the prevention of the cardiomyopathy, was also found to be an inhibitor of histamine release induced by adriamycin and compound 48/80 on rat peritoneal cells. This study further supports the hypothesis that the release of histamine may be involved in the pathogenesis of anthracycline cardiotoxicity. Images Figure 5 Figure 6 Figure 7 Figure 8

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Section: Discussionmentioning

confidence: 61%

Inhibitors of adriamycin-induced histamine release in vitro limit adriamycin cardiotoxicity in vivo

Fb¹,

Decorti²,

Candussio³

et al. 1986

Br J Cancer

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“…Doxorubicin and other anthracyclines are very powerful in causing release of histamine from mast cells. They are comparable in action to the standard mast cell-degranulating agent, 48/80 (32,146). This histamine-releasing action is probably responsible for the acute cutaneous reactions (162), and possibly for the acute arrhythmias that sometimes occur following clinical doxorubicin administration (176).…”

Section: Release Of Cardiotoxic Humoral Mediatormentioning

confidence: 99%

Toxic Mechanisms of the Heart: A Review*

Combs

Acosta

1990

Toxicol Pathol

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Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.

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“…Like the majority of secretagogues acting through non antigenic pathways, cytostatic drugs seem to directly activate G proteins [4,5], although adriamycine elicits a response not mediated by those G proteins sensible to pertussis toxin, benzalkonium chloride and cholera toxin [6]. Intracellular but not extracellular calcium is required for the secretion induced by cytostatics [7,8].…”

Section: Introductionmentioning

confidence: 96%

Mitoxantrone induces nonimmunological histamine release from rat mast cells

Estévez¹,

Vieytes²,

Botana³

1996

Inflamm Res

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The antineoplastic drug mitoxantrone (MTX) elicits a fast noncytotoxic and nonimmunological histamine release from peritoneal and pleural rat mast cells. The non specific phosphodiesterase inhibitor isobuthyl-methylxantine (1 mM) decreases the potency of MTX. Theophylline (10 mM) decreases both the potency and the efficacy of MTX-induced histamine secretion. The protein kinase C (PKC) activator, tetradecanoyl-phorbol-13-acetate (50 ng/mL), enhances the effect of MTX, whereas the non specific PKC inhibitor trifluoperazine (10 microM) exerts no effect. Histamine release was also unaffected by substances acting on G-proteins, namely pertussis toxin (200 ng/mL), cholera toxin (300 mg/mL) and benzalkonium chloride (10 micrograms/ mL). The inhibition of protein phosphatases 1 and 2A by okadaic acid (1 microM) does not modify the response. The results indicate that mitoxantrone elicits the exocytosis in mast cells by a mechanism similar to the parent compound adriamycine, but different to the polyamine compound 48/80.

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Anthracycline-induced histamine release from rat mast cells

Cited by 11 publications

References 22 publications

Inhibitors of adriamycin-induced histamine release in vitro limit adriamycin cardiotoxicity in vivo

Inhibitors of adriamycin-induced histamine release in vitro limit adriamycin cardiotoxicity in vivo

Toxic Mechanisms of the Heart: A Review*

Mitoxantrone induces nonimmunological histamine release from rat mast cells

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