Solanum nigrum L.
| 1. NAME |
| 1.1 Scientific name |
| 1.2 Family |
| 1.3 Common name(s) |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 2.5 Poisonous parts |
| 2.6 Main toxins |
| 3. CHARACTERISTICS |
| 3.1 Description of the plant |
| 3.1.1 Special identification features |
| 3.1.2 Habitat |
| 3.1.3 Distribution |
| 3.2 Poisonous parts of the plant |
| 3.3 The toxin(s) |
| 3.3.1 Name(s) |
| 3.3.2 Description, chemical structure, stability |
| 3.3.3 Other physico-chemical characteristics |
| 3.4 Other chemical contents of the plant |
| 4. USES/CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.2 High risk circumstances |
| 4.3 High risk geographical areas |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Animal data |
| 7.2.3 Relevant in vitro data |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 CNS |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Relevant laboratory analyses and other investigations |
| 10.2.1 Sample collection |
| 10.2.2 Biomedical analysis |
| 10.2.3 Toxicological/toxinological analysis |
| 10.2.4 Other investigations |
| 10.3 Life supportive procedures and symptomatic treatment |
| 10.4 Decontamination |
| 10.5 Elimination |
| 10.6 Antidote/antitoxin treatment |
| 10.6.1 Adults |
| 10.6.2 Children |
| 10.7 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 11.2 Internally extracted data on cases |
| 11.3 Internal cases |
| 12. ADDITIONAL INFORMATION |
| 12.1 Availability of antidotes/antitoxins |
| 12.2 Specific preventive measures |
| 12.3 Other |
| 13. REFERENCES |
| 13.1 Clinical and toxicological |
| 13.2 Botanical |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
POISONOUS PLANTS
1. NAME
1.1 Scientific name
Solanum nigrum L. and Solanum americanum Miller
1.2 Family
Solanaceae (Potato family)
1.3 Common name(s)
Aguaragua
Aguaraquia
Black or common nightshade
Caraxixa
Caraxixu
Erva moura
Erva-de-bicho
Guaraquinha (Brazil)
Hierba mora (Spain, Argentina, Uruguay)
Maria-preta
Morelle noir (France)
Nightshade
Pimenta-de-cachorro
Pimenta-de-galinha
Pimenta-de-rato
Poison berry (USA, UK)
Sué
2. SUMMARY
2.1 Main risks and target organs
Poisoning occurs mainly from ingestion of plant, especially
the unripened fruits.
The main target organs are the cardiovascular and central
nervous system, and the gastrointestinal tract.
The main signs and symptoms are cardiovascular (tachycardia,
arrhythmia and hypotension) on the central nervous system
(delirium, psychomotor, agitation, paralysis, coma and
convulsion) and gastrointestinal (nausea, vomiting, diarrhea).
2.2 Summary of clinical effects
The initial symptoms of poisoning are gastrointestinal,
occurring within six hours of ingestion, manifested as nausea,
vomiting and diarrhoea, followed by cardiovascular and CNS
symptomology. Dehydration and electrolyte imbalance from
prolonged vomiting and diarrhoea may result.
If the patient survives after 24 hours, the prognosis is
favorable. Death may occur from cardiac arrhythmia and
circulatory and respiratory failure.
2.3 Diagnosis
Diagnosis is based on the above mentioned clinical signs and
symptoms and knowledge on the ingestion of the plant (e.g.
berries).
Solanine can be identified in gastric contents or in the
suspected plant (e.g. chromatography).
A sample of the plant should be obtained for botanical and
pharmacognostic identification.
2.4 First-aid measures and management principles
No specific antidote is available. Treatment is mainly
symptomatic and supportive:
- Gastric lavage or induced emesis.
- Fluid and electrolyte replacement.
- Cardiovascular support, including vasopressors if
necessary.
- Respiratory support.
- Diazepam for control of convulsions.
2.5 Poisonous parts
Solanine, a glyco-alkaloid, is found throughout the plant.
The highest concentrations are found in the unripened fruit.
2.6 Main toxins
Solanine
Other glyco-alkaloids also present: chaconine and solasodine.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
Annual branched herb up to 90 cm high, with dull dark
green leaves, juicy, ovate or lanceolate, toothless to
slightly toothed on the margins. Flowers are small and
white with a short-pedicellate and five widely spread
petals. Fruits are small, black when ripe, glossy and
in an umbel (S. americanum) or dull and in a raceme (S.
nigrum).
3.1.2 Habitat
Solanum americanum and Solanum nigrum are weeds of waste
land, old fields, ditches, and roadsides, fence rows, or
edges of woods and cultivated land.
3.1.3 Distribution
Solanum americanum is probably of southern Europe origin,
but is now a common weed of waste lands, and edges of
cultivated land in most parts of the world. Solanum
nigrum is established as a weed in similar habitats
(Frohne & Pfänder, 1983)
3.2 Poisonous parts of the plant
Solanine, a glyco-alkaloid, is found throughout the plant,
with the highest concentrations in the unripened berries. The
concentration of solanine increases in the leaves as the plant
matures (Cooper & Johnson, 1984). When ripe, the berries are
the least toxic part of the plant and are sometimes eaten
without ill effects (Watt & Breyer-Brandwijk, 1962).
3.3 The toxin(s)
3.3.1 Name(s)
Solanine.
3.3.2 Description, chemical structure, stability
C45 H73 N O15
NW = 868.04
Solanine is a mixture of two classes of glycosides,
solanine and chaconines. These compounds contain the
same basic alkamine aglycone, solanidine, but differ
with respect to the composition of the sugar chain.
Alpha-solanine is the main constituent.
3.3.3 Other physico-chemical characteristics
Solanine is water soluble and is destroyed by boiling
but not by baking.
Solanine is readily soluble in hot alcohol, practically
insoluble in water (25 mg/l at pH 6), ether, chloroform
(Merck, 1989).
3.4 Other chemical contents of the plant
Solanine may be separated by chromatography into six
components:
alpha, beta gamma chaconines, and
alpha, beta gamma solanines (Merck, 1989)
Solanidine (C27 H43 NO; MW = 397,62) is obtained after
hydrolysis of solanine, and is less toxic. Nitrates and
nitrites also occur in variable amounts in black nightshade
and may contribute to its toxic effects (Cooper & Johnson,
1984).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
It has limited medicinal uses: in liniments, poultices
and decoctions for external use (Martindale, 1982). It
has also been used in folkloric medicine as sedative and
anticonvulsant.
Solanine hydrochloride has been used as an agricultural
insecticide (Merck, 1989).
4.2 High risk circumstances
Accidental and intentional ingestion of parts of the plants,
especially the unripened fruits.
4.3 High risk geographical areas
World-wide, where these plants grow.
5. ROUTES OF ENTRY
5.1 Oral
Accidental or intentional ingestion of parts of the plants,
especially the unripened fruits.
5.2 Inhalation
No data available.
5.3 Dermal
No data available.
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Oral
The unhydrolyzed glyco-alkaloid (solanine) is poorly absorbed,
while alkamine (solanidine) is rapidly absorbed through the
gastrointestinal wall. Alkamine is the active principle mainly
responsible for the toxic manifestations.
6.2 Distribution by route of exposure
The alkamine reaches the target organs within 30 minutes after
ingestion. Maximum blood levels are reached after 12 hours.
Animal studies showed that solanine concentrates in tissue, in
the following order: spleen, kidney, liver, lung, heart,
brain, blood (Nishie et al, 1971).
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
No data available.
6.5 Elimination by route of exposure
Solanine elimination occurs rapidly, 78% through the urine and
faeces within 24 hours (Dalvi & Bowie, 1983).
7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
7.1 Mode of action
No data available in humans.
Animal studies comparing solanine with K-strophantidine
revealed similar effects. Exposure of neonatal rat cells to
solanine caused an initial increased contraction rate followed
by cessation (Bergers & Alink, 1980). Isolated frog muscle
showed an increased intropy. Toxic intravenous doses caused
ventricular fibrillation in rabbits. In addition, in rabbits,
toxic intra-peritoneal (I.P) doses caused mild to moderate
inhibition of both specific and non-specific cholinesterase
(Patil et al, 1972).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Solanine is extremely toxic and small amounts
may be fatal. The toxic dose in man in 2.8
mg/kg.
7.2.1.2 Children
Solanine is extremely toxic and small amounts
may be fatal.
7.2.2 Animal data
Variability in the toxic alkaloid and nitrate
concentrations of the plants in different situations
accounts for the conflicting reports of their being
harmless in some cases and harmful in others (Cooper &
Johnson, 1984).
Toxicity of solanine in different species (LD50 in
mg/kg) is: 590 mg/kg in the rat (oral), 20 to 30 mg/kg
in the rabbit (intraperitoneally), 32 to 42 mg/kg in the
mouse (intraperitoneally), and 18.8 mg/kg in the ckick
embryo (Dalvi & Bowie, 1983).
In vivo: in rabbits, the intra-peritoneal
administration caused mild to moderate inhibition of
specific and non-specific cholinesterases (Patil et al.,
1972). Intravenously, it caused ventricular
fibrillation (Nishie et al, 1971).
In sick animals, blood-tinged serum and edema is seen
around the kidneys, and blood dots if the animal lives
for several days. Histological lesions in the kidneys
consisted on: tubular toxic necrosis, focal hemorrhages
and edema. Lesions in the digestive tract are:
hemorrhagic gastritis and enteritis with ulcers (Scineca
& Oehme, 1985).
7.2.3 Relevant in vitro data
Neonatal rat cells exposed to solanine show initial
increased contraction rate followed by cessation
(Bergers & Alink, 1980). Isolated frog muscle showed an
increased intropy (Nishie et al., 1971).
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
Possible teratogenic effect has been reported, associated to
solanine-containing potatoes (Solanum tuberoseum), but not to
solanum nigrum. Many workers investigated whether solanidan
alkaloids might be teratogenic, and although some effects were
reported in chick embryos and hamsters, most workers found not
terata in rats, rabbits and mice (Keeler & Tu, 1983).
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
The active principles affect mainly the heart, the
central nervous system and the gastrointestinal tract.
Symptoms may appear rapidly: nausea, vomiting,
abdominal pains, diarrhoea, headache, mydriasis, flushed
and warm skin, delirium, psychomotor agitation, coma,
paralysis, circulatory and respiratory depression, loss
of sensation and even death.
Unripe, green fruits should always be considered
poisonous.
9.1.2 Inhalation
No data available.
9.1.3 Skin exposure
No data available.
9.1.4 Eye contact
No data available.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
The course of poisoning is rapid: symptoms appear soon after
ingestion of the unripened fruits. Symptomatology is rarely
delayed beyond six hours. In severe poisoning, death usually
occurs within 24 hours.
Death may occur from cardiac arrhythmias and from respiratory
failure.
If the patient survives after 24 hours, the prognosis is
favorable due to the rapid elimination of the toxin through
faeces and urine.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Tachycardia and cardiac arrhythmia occur, followed by
circulatory depression.
9.4.2 Respiratory
Respiration depression may occur.
9.4.3 Neurological
9.4.3.1 CNS
Altered mental status manifested as drowsiness,
headache, hallucinations, delirium, psychomotor
agitation or restlessness, coma and death.
9.4.3.2 Peripheral nervous system
Paralysis may occur.
9.4.3.3 Autonomic nervous system
Skin is warm and flushed. Initial tachycardia
can occur.
9.4.3.4 Skeletal and smooth muscle
9.4.4 Gastrointestinal
Nausea, vomiting, diarrhoea, abdominal pains.
9.4.5 Hepatic
No data available.
9.4.6 Urinary
9.4.6.1 Renal
Dysuria or oliguria may occur.
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Flushed and warm skin.
9.4.9 Eye, ears, nose, throat: local effects
Eyes: mydriasis.
9.4.10 Haematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Acidosis may occur.
9.4.12.2 Fluid and electrolyte disturbances
Hypokalemia and dehydration may be observed.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Suggestive evidence of placental passage with reports
of possible teratogenicity.
Breast milk: No data available.
9.5 Others
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Treatment is mainly symptomatic and supportive:
- Gastric lavage or induced emesis (if the patient is
seen early and has not vomited spontaneously).
- Correction of fluid and electrolyte disturbances.
- Respiratory support.
- Cardiovascular monitoring with circulatory support.
Vasopressor drugs may be administered if necessary.
In cases of seizures, diazepam should be given.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
- Blood and urine for biomedical analyses.
- Gastric contents for identification of plant
parts and active principles or of solanine
(e.g. chromatography).
- A plant sample should be obtained for botanical
and pharmacognostic studies.
10.2.2 Biomedical analysis
- Electrolytes and blood gases.
- E.C.G. monitoring.
- Routine blood studies and urinalysis.
10.2.3 Toxicological/toxinological analysis
Identification of solanine and other alkaloids in the
sample of the plant specimen or remainder from the
gastric lavage.
10.2.4 Other investigations
No data available.
10.3 Life supportive procedures and symptomatic treatment
Patients should be admitted to hospital for observation for
at least 24 hours.
Symptomatic and general supportive therapy is essential.
Fluid and electrolyte status should be carefully checked in
patients and corrected if necessary with I.V. fluids.
Cardiac monitoring and E.C.G. are indispensable for
detection of arrhythmias and their symptomatic treatment.
Control body temperature through physical methods.
Maintain respiratory function: endotracheal intubation if
respiratory depression appears.
Diazepam is indicated to control convulsions.
10.4 Decontamination
Induce emesis or perform gastric lavage, if the patient is
seen less than four to eight hours after ingestion, has not
vomited and no contraindications exist.
Administer activated charcoal.
Cathartics are contraindicated.
10.5 Elimination
No data available.
10.6 Antidote/antitoxin treatment
10.6.1 Adults
No antidote available.
10.6.2 Children
No antidote available.
10.7 Management discussion
Symptomatic and supportive treatment should never be delayed
by decontamination measures.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A 10-year-old girl was brought to the hospital with loss of
consciousness of unknown origin. The mother denied any
possibility of poisoning. The child's sister later
confessed that, on the previous day, the patient had eaten
15 to 20 black berries. The plant, when examined, turned out
to be black nightshade. The child's mental status alternated
between sleepiness and restlessness. Later, it was found out
that due to severe headache, the child herself took four to
six sleeping tablets (Polster, 1953).
11.2 Internally extracted data on cases
No cases registered at the poisons centre.
11.3 Internal cases
To be added by the poisons centre.
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes/antitoxins
No antidotes are available.
12.2 Specific preventive measures
Usual preventive measures for avoiding ingestion of berries
by small children.
12.3 Other
No data available.
13. REFERENCES
13.1 Clinical and toxicological
Bergers WA; Alink GM (1980) Toxic effects of glyco-
alkaloids solanine and tomatine on cultured neonatal rat
heart cells. Toxicology letters 6:29-32.
Cooper MR; Johnson AW, (1984). Poisonous Plants in Britain
and other effects on Animals and Man. Ministry of
Agriculture, Fisheries and Food, Ref. Book n° 161, London
pp 219-220.
Hardin JN; Arena, JM (1974), Human poisoning from native and
cultivated plants. 2nd ed. Duke University Press, Durham,
North Carolina.
Keeler RF (1978). Alkaloid teratogens from lupines, Conium,
Veratrum and related genera. Lu: Effects of Poisonous
Plants on Livestock. Ed. RF Keeler, KR Van Kampen, LF
James. Academic Press, New York & London, pp 397-408.
Keeler RF; Tu AT, (1983). Handbook of Natural Toxins. Vol.
1, Plant and Fungal Toxins. New York, pp 176.
Merck Index (1989) Ed. S. Budavari, 11th Ed., NJ, USA.
pp:1371. Watt JM; Breyer-Brandwijk MG (1962). The
Medicinal and Poisonous Plants of Southern and Eastern
Africa E & S, Livingston Ltd., Edinburgh and London, UK, pp
996-1000.
Schvartsman, S (1979), Plantas venenosas. Sarvier, Sao
Paulo.
Scineca JM, Oehme FW (1985). Post-mortem guide to common
poisonous plants to livestock. Vet. Hum. Toxicol 27(3)197.
Soler & Battle, E (1947), Medicamenta. Editorial Labor,
Buenos Aires.
13.2 Botanical
Frohne D & Pfänder HS (1983) A colour atlas of Poisonous
Plants. Wolfe Puld. Ltd., London.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Dr Héctor Armando Mosto
Hospital de Clinicas "Jose de San Martin"
Facultad de Medicina
Universidad de Buenos Aires
Cordoba 2351
Buenos Aires
Argentina
Tel: 54-1-9621280
Fax: 54-1-3318605
Date: March 1989
Co-author: Professor Julia Higa de Landoni
Jefa Seccion Toxicologia
Hospital de Clinicas "Jose de San Martin"
Facultad de Medicina
Universidad de Buenos Aires
Cordoba 2351
Buenos Aires
Argentina
Tel: 54-1-9621280
Fax: 54-1-3318605
Peer review: Strasbourg, April 1990
Review: IPCS, July 1991 and May 1994