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Oleander is generally considered unsafe for internal use. Extracts from oleander have been used as rat poison, insecticide and fish poison and are toxic to humans. Accidental deaths and suicides have occurred after taking oleander by mouth. The cause of death is probably related to oleander?s effects on the heart. Possible benefits must be weighed carefully with the risk of toxicity.
When using oleander, some people may experience stomach discomfort, including pain, anorexia, diarrhea, vomiting or nausea. Liver and kidney damage has also been reported. Oleander may have significant adverse effects on the heart, resulting in complete heart block, extremely slow heart rhythms, irregular rhythms or rapid, pounding heartbeat. Potassium levels in the body may become dangerously high with oleander. Depression, difficulty breathing, vision abnormalities and ringing in the ears have also occurred. Other side effects may include nerve pain, weakness and fatigue, irritability, altered level of consciousness, dizziness, seizures, headaches, sweating and neck stiffness. Skin irritation may occur after contact with sap from freshly cut oleander leaves. These adverse effects may be the result of oleander allergies. It is possible that plants grown in the same soil as oleander plants or in soil exposed to oleander may contain trace amounts of oleander.
Interactions With Drugs
Oleander has similar cardiac glycoside properties to digoxin (Lanoxin), and the adverse effects of oleander on the heart are likely to be increased if it is taken with digoxin or digitoxin. Many drugs interact with digoxin, and because of the similarities between oleander and digoxin, these drugs may also increase the toxicity of oleander. Examples include erythromycin, tetracycline, quinine, laxatives, antiarrhythmic agents and diuretics. Oleander toxicity may also be increased if used with drugs that lower potassium levels, such as some diuretics or laxatives.
Interactions With Herbs And Dietary Supplements
Oleander may have an increased risk of toxic effects if used with other herbs that possess glycoside properties, such as foxglove. Additionally, these toxic effects may be increased if used with other supplements that affect the heart, such as calcium; those that cause potassium loss, such as licorice (Glycyrrhiza glabra); or herbs with laxative properties, such as senna; or herbs with diuretic (urine-producing) properties, such as horsetail.
Biochem Pharmacol. 2003 Dec 1;66(11):2223-39.
Oleandrin suppresses activation of nuclear transcription factor-kappa B and activator protein-1 and potentiates apoptosis induced by ceramide.
Sreenivasan Y, Sarkar A, Manna SK.
Laboratory of Immunology, Centre for DNA Fingerprinting & Diagnostics, Nacharam, Hyderabad 500 076, India.
Ceramide (N-acetyl-D-sphingosine), a second messenger for cell signaling induces transcription factors, like nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) and is involved in inflammation and apoptosis. Agents that can suppress these transcription factors may be able to block tumorigenesis and inflammation. Oleandrin (trans-3,4',5-trihydroxystilbene), a polyphenolic cardiac glycoside derived from the leaves of Nerium oleander, has been used in the treatment of cardiac abnormalities in Russia and China for years. We investigated the effect of oleandrin on NF-kappa B and AP-1 activation and apoptosis induced by ceramide. Oleandrin blocked ceramide-induced NF-kappa B activation. Oleandrin-mediated suppression of NF-kappa B was not restricted to human epithelial cells; it was also observed in human lymphoid, insect, and murine macrophage cells. The suppression of NF-kappa B coincided with suppression of AP-1. Ceramide-induced reactive intermediates generation, lipid peroxidation, cytotoxicity, caspase activation, and DNA fragmentation were potentiated by oleandrin. Oleandrin did not show its activity in primary cells. Oleandrin's anticarcinogenic, anti-inflammatory, and growth-modulatory effects may thus be partially ascribed to the inhibition of activation of NF-kappa B and AP-1 and potentiation of apoptosis.
Toxicol Appl Pharmacol. 2004 Mar 15;195(3):361-9. Related Articles, Links
Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced tumor promotion markers in CD-1 mouse skin by oleandrin.
Afaq F, Saleem M, Aziz MH, Mukhtar H.
Department of Dermatology, Medical Sciences Centre, University of Wisconsin, Madison, WI 53706, USA.
Oleandrin, derived from the leaves of Nerium oleander, has been shown to possess anti-inflammatory and tumor cell growth-inhibitory effects. Here, we provide evidence that oleandrin could possess anti-tumor promoting effects. We determined the effect of topical application of oleandrin to CD-1 mice against l2-O-tetradecanoylphorbol-13-acetate (TPA), a widely studied skin tumor promoter, -induced conventional and novel markers of skin tumor promotion. Topical application of oleandrin (2 mg per mouse) 30 min before TPA (3.2 nmol per mouse) application onto the skin afforded significant inhibition, in a time-dependent manner, against TPA-mediated increase in cutaneous edema and hyperplasia, epidermal ornithine decarboxylase (ODC) activity and ODC and cyclooxgenase-2 (COX-2) protein expression. In search for novel markers of skin tumor promotion, we found that TPA application to mouse skin resulted, as an early event, in an increased expression of phosphatidyinositol 3-kinase (PI3K), phosphorylation of Akt at threonine308 and activation of nuclear factor kappa B (NF-kappaB). Topical application of oleandrin before TPA application to mouse skin resulted in significant reduction in TPA-induced expression of PI3K and phosphorylation of Akt, and inhibition of NF-kappaB activation. NF-kappaB is a eukaryotic transcription factor that is critically involved in regulating the expression of specific genes that participate in inflammation, apoptosis and cell proliferation. Employing Western blot analysis, we found that oleandrin application to mouse skin resulted in inhibition of TPA-induced activation of NF-kappaB, IKKalpha and phosphorylation and degradation of IkappaBalpha. Our data suggest that oleandrin could be a useful anti-tumor promoting agent because it inhibits several biomarkers of TPA-induced tumor promotion in an in vivo animal model. One might envision the use of chemopreventive agents such as oleandrin in an emollient or patch for chemoprevention or treatment of skin cancer.
Afr Health Sci. 2003 Aug;3(2):77-86. Related Articles, Links
The cardiotonic effect of the crude ethanolic extract of Nerium oleander in the isolated guinea pig hearts.
Adome RO, Gachihi JW, Onegi B, Tamale J, Apio SO.
Department of Pharmacy, Makerere University, P.O. Box 7072 Kampala, Uganda, email@example.com
Cardiovascular diseases are increasingly becoming one of the leading diseases causing morbidity and mortality in Uganda. Ethnographic evidence suggests that these diseases are often first managed by indigenous and related herbs before patients are referred for allopathic forms of management. One such herb of interest is Nerium oleander. Therefore the crude ethanolic extracts of the dried leaves of this herb were tested against the following parameters in the isolated guinea pig hearts: force of contraction, heart rate and cardiac flow. The extracts brought about dose-dependent increases in all these parameters from their baseline readings. Compared with graded doses of digoxin the effects closely mirrored the activities in a dose dependent manner. At the mechanism of action level, it would appear the extract works in the same as digoxin since their dose-contraction-reponse curves are parallel. This finding would tend to provide a strong rationale for the herb's traditional use in cardiovascular illness. KEY WORDS: contraction, cardiac flow, heart rate, Nerium oleander, extract, and digoxin
Ann Fr Anesth Reanim. 2005 Jun;24(6):640-2. Related Articles, Links
[Nerium oleander self poisoning treated with digoxin-specific antibodies]
Bourgeois B, Incagnoli P, Hanna J, Tirard V.
Samu de Grenoble, CHU de Grenoble, BP 207, 38043 Grenoble, France. BBourgeois@chu-grenoble.fr
A chronically depressed 44-year-old man was rescued by the French medicalised ambulance service four hours after the ingestion of Nerium oleander leaves in a suicide attempt. Cardiotoxicity was evidenced by the presence of bradycardia with mental confusion and vomiting. The patient was empirically treated in the prehospital phase with a single dose of digoxin-specific Fab antibody fragments (Digidot). In spite of this treatment, the patient presented a new episode of important bradycardia (25 b/minute). Thereafter, the patient's rhythm stabilized and neurological signs and vomiting resolved. The patient recovered uneventfully and was discharged from the intensive care unit two days later.
Pacing Clin Electrophysiol. 2004 Dec;27(12):1686-8. Related Articles, Links
A rare cause of complete heart block after transdermal botanical treatment for psoriasis.
Wojtyna W, Enseleit F.
Kantonsspital Glarus, Department of Internal Medicine, Glarus, Switzerland.
We report the case of a 59-year-old man with a new 3 degrees AV block with a history of psoriasis. After implantation of a definitive DDDR pacemaker, the patient reported a transdermal self-medication with an extract of Nerium oleander for the treatment of his psoriasis. The pharmacological, epidemiological, and clinical features are discussed in brief.
J Environ Biol. 2002 Jul;23(3):231-7. Related Articles, Links
Toxicity of Nerium oleander leaf extract in mice.
Haeba MH, Mohamed AI, Mehdi AW, Nair GA.
Department of Zoology, Faculty of Science, University of Garyounis, Post Box: 9480, Benghazi, Libya.
Non-lethal dose of 70% ethanol extract of the Nerium oleander dry leaves (1000 mg/kg body weight) was subcutaneously injected into male and female mice once a week for 9 weeks (total 10 doses). One day after the last injection, final body weight gain (relative percentage to the initial body weight) had a tendency, in both males and females, towards depression suggesting a metabolic insult at other sites than those involved in myocardial function. Multiple exposure of the mice to the specified dose failed to express a significant influence on blood parameters (WBC, RBC, Hb, HCT, PLT) as well as myocardium. On the other hand, a lethal dose (4000 mg/kg body weight) was capable of inducing progressive changes in myocardial electrical activity ending up in cardiac arrest. The electrocardiogram abnormalities could be brought about by the expected Na+, K(+)-ATPase inhibition by the cardiac glycosides (cardenolides) content of the lethal dose.