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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