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 Post subject: Re: Ядовитые животные и растения
PostPosted: 23 Aug 2011 15:35 
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Антон wrote:
Всё-таки ,семейство молочайные,а не бобовые :)

Почему-то в США его относят к бобовым.

Это же американцы :) . Два разных мира.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 23 Aug 2011 17:08 
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ОСОБЕННОСТИ СТРОЕНИЯ И ФАРМАКОКИНЕТИКА РИЦИНА


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03.00.04. - биохимия
Диссертация на соискание ученой степени
кандидата биологических

Chelnokova O.V. Konformacionnye izmeneniya rastitel#nyh toksinov v hode vnutrikletochnogo transporta. (kand., 2002).pdf [864.62 KiB]
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 Post subject: Re: Ядовитые животные и растения
PostPosted: 06 Sep 2011 17:29 
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Вот еще немного фотографий клещевины. Такие "цветочки" растут поблизости от института.
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 Post subject: Re: Ядовитые животные и растения
PostPosted: 13 Sep 2011 23:19 
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Разрезал плод клещевины. В средине оказалось три штучки недозрелых семян, которые действительно напоминают бобы.
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 Post subject: Re: Ядовитые животные и растения
PostPosted: 14 Sep 2011 19:24 
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Клещевина: плоды и семена.
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Не знаю, как насчет клещей, но по моему зрелые семена напоминают бобы фасоли. В каждой коробочке по три зерна.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 15 Sep 2011 02:25 
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Клеща они точно напоминают, по крайней мере собачьего (насосавшегося крови) даже окрас почти такой же, только без пятен.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 16 Sep 2011 04:52 
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Vladimir wrote:
Клещевина: плоды и семена...
Не знаю, как насчет клещей, но по моему зрелые семена напоминают бобы фасоли. В каждой коробочке по три зерна.

И как они на вкус?


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 Post subject: Re: Ядовитые животные и растения
PostPosted: 16 Sep 2011 12:52 
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Моня Квасов wrote:
Vladimir wrote:
Клещевина: плоды и семена...
Не знаю, как насчет клещей, но по моему зрелые семена напоминают бобы фасоли. В каждой коробочке по три зерна.

И как они на вкус?

Что-то не тянет пробовать: даже если забыть о рицине, есть перспектива несколько часов просидеть в туалете.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 16 Sep 2011 13:01 
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А понадкусать та выплюнуть? :)
Шееле же как-то описал вкус синильной кислоты.


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 Post subject: Re: Ядовитые животные и растения
PostPosted: 16 Sep 2011 13:04 
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O'Bu wrote:
А понадкусать та выплюнуть? :)
Шееле же как-то описал вкус синильной кислоты.

Если бы следовал примеру Шееле, мне бы оставалось жить 9 лет. А так много еще хочется сделать :)
Впрочем, возможно попробую (только не подать бы дурной пример).

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 17 Sep 2011 01:02 
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O'Bu wrote:
А понадкусать та выплюнуть? :)
Шееле же как-то описал вкус синильной кислоты.

На вкус они напоминают сырые семена подсолнуха, но более жирные. Если семена недозрелые, то они немного горчат. Разжевать одно семечко не опасно. А вот если употребить граммов 100-200, есть риск отравится (в крайнем случае часа четыре провести в туалете). В любом случае такая затея - вариант русской рулетки.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 17 Sep 2011 07:07 
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А если их сварить или прожарить? По идее, термическая обработка должна изменить свойства ядовитого белка.


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 Post subject: Re: Ядовитые животные и растения
PostPosted: 17 Sep 2011 12:11 
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Некоторые белковые токсины очень устойчивы, в том числе - и к термической обработке.
___________________________________________
Случайно нашел небольшой материал по рицину:
Ricinus communis L
Ricinus communis 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
Ricinus communis
1.2 Family
Euphorbiaceae (Spurge family).
1.3 Common name(s)
African coffee tree (USA)
Carrapateiro (Brazil)
Castor (Argentine)
Castor bean (USA)
Castor-oil (USA)
Higuereta (Cuba, Puerto Rico)
Koli, Pa'aila (Hawaii)
La'au-'aila (Hawaii)
Mamona (Brazil)
Mamoneiro (Brazil)
Palma de Cristo (Uruguay)
Palma-cristi (Brazil)
Ricin (France)
Ricino (Argentine)
Steadfast (USA)
Tartago (Uruguay)
2. SUMMARY
2.1 Main risks and target organs
Intense gastroenteritis and acute dehydration. Renal and
hepatic insufficiency have been reported.
2.2 Summary of clinical effects
Burning sensation of the mouth and throat occurs after chewing
the seeds. After a latent period of 3 to 6 h, nausea,
vomiting, severe stomach pains, diarrhoea, and excessive
thirst developed leading to acute dehydration, hypotension
and circulatory failure. Prostration, blurring of vision,
loss of consciousness, convulsions, haemolysis, uraemia and
liver necrosis have also occurred.
2.3 Diagnosis
Blood gases and electrolytes.

Close monitoring of renal, hepatic and haematologic systems.

A sample of the plant should be obtained for botanical and
pharmacognostic identification.
2.4 First-aid measures and management principles
Ingestion of any part of Ricinus communis is an indication for
admission to hospital for close observation.

Immediate gastric lavage or emesis should be performed.
Activated charcoal may be administered.

Correct fluid and electrolyte imbalances immediately.
2.5 Poisonous parts
All parts of the plant are poisonous, especially the seeds.
2.6 Main toxins
Ricin, a toxalbumin, is one of the most toxic substances of
plant origin.
3. CHARACTERISTICS

3.1 Description of the plant
3.1.1 Special identification features
Shrublike herb, stems 1 to 4 metres high, branched,
green to reddish or purple, leaves alternated, simple,
long-stalked, 20 to 80 cm wide and palmately lobed
with 5 to 11 long lobes which are toothed on the
margins, green or reddish. It has clusters of seed
pods, green or red, and covered with fleshy spines. The
seeds contained in the pods are 3 per capsule, about
1.5 to 2.5 cm across, elliptical glossy, black or white
or usually mottled with grey, black, brown and white.
The seeds have a pleasant taste (Lampe, 1985; Hardin,
1974; Font-Quer, 1979).
3.1.2 Habitat
Castor bean is cultivated as a decorative plant in
gardens. It is very common in South America growing
wild in uncultivated lands (Pronczuk, 1988). It is
commercially cultivated mainly in Brazil and India and
in several other countries (Ecuador, Paraguay, Tanzania,
Rumania, Ethiopia, USA, USSR, South Africa) for its
industrial and medicinal use (Lampe, 1985; Cooper, 1989).

Seeds are used to make ornamental necklaces and there
are commercially prepared packages of seeds available
in plant stores (Kinamore, 1980).
3.1.3 Distribution
Originally from tropical Africa, it is now growing in
tropical, subtropical and temperate areas.

Ricinus communis is now worldwide in distribution.
3.2 Poisonous parts of the plant
If chewed, the seeds are the most toxic part of the plant
although the leaves are also poisonous. The seeds contain 0.2
to 3% ricin (Favarel-Carriques, 1978; Schvartsman, 1979)
and one mg of pure ricin can be isolated from its grains
(Frohne, 1984).
3.3 The toxin(s)
3.3.1 Name(s)
Ricin. It must not be confused with ricine oil (Castor
oil) produced commercially as a cathartic.
3.3.2 Description, chemical structure, stability
Ricin

CAS: 9009-86-3

A glycoprotein composed of two peptide chains of
differing molecular weights attached by a disulfide
bond (Wedin, 1986).

It is destroyed by heat and light (Cooper, 1989;
Schvartsman, 1979). The toxins are dimers of 30 000 to
33 000 mol. wt. (Budavari, 1989).
3.3.3 Other physico-chemical characteristics
Ricin is crystallizable, toxic, soluble in water and
chloroform and insoluble in alcohol. Ricin resists
degradation by hydrochloric acid, pepsin, chemopepsine and papaine.



3.4 Other chemical contents of the plant
A potent allergen that has not been identified (Knight, 1979).

Castor oil contains about 80% of the trigliceride of rinoleic
acid (Martindale, 1982).

Castor bean also has an agglutinating protein composed of four
polypeptide chains which are non-toxic orally (Wedin, 1986).
This protein shows decreased agglutinating activity at low
temperatures (Cooper, 1989).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
Folk medicine: ricine oil is used as a cathartic (Font-
Quer, 1979).

Industry: castor oil is used as a lubricant in the
plastics, soap and paint industries. The fibrous
residue (cake) left by castor oil extraction is
detoxified by steam treatment and used as a fertilizer
(Cooper, 1989; Schvarstman, 1979).

Ricin is used as a tool in studies of cell surface
properties and experimentally used in cancer research
(Budavari, 1989).
4.2 High risk circumstances
Accidental or intentional poisoning occurs by ingestion if the
seeds are chewed (Pronczuk, 1988). Because of the hard,
water-impermeable coat, the seed is considered harmless if
swallowed whole. In some countries, the seeds are used as
beads for necklaces which could cause toxicity because the
seeds are already broken (Pronczuk, 1988; Kinamore, 1980).
Allergic reactions have been reported among workers exposd to
R. communis in commercial cultivation and gardening (Cooper,
1989; Schvartsman, 1979). Also people living in the vicinity
of castor oil factories have developed allergic reactions
(Schvartsman, 1979). Severe allergies have been reported
from handling necklaces and other trinkets made from castor
bean. Secondary intoxication can occur from harvesting or
consumption of contaminated crops (such as soy bean) (Cooper,
1984).
4.3 High risk geographical areas
Ricin is widely distributed. Poisoning cases have been known
to occur in many countries.
5. ROUTES OF ENTRY
5.1 Oral
Accidental ingestion can occur.
5.2 Inhalation
The allergen can produce asthma and rhinitis (Cooper, 1989,
Schvartsman, 1979).
5.3 Dermal
Prolonged exposures can induce dermatitis and eczemas
(Schvartsman, 1979).
5.4 Eye
Allergic conjunctivitis can occur through this route
(Schvartsman, 1979).

5.5 Parenteral
Subcutaneous administration of rincin has been reported in
experimental studies (Knight, 1979).
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
After ingestion of the chewed seeds the toxins are rapidly
absorbed through the gastrointestinal tract (Schvartsman,
1979).
6.2 Distribution by route of exposure
The fate of ricin in the human body is still not established
(Kopferschmitt, 1983).
6.3 Biological half-life by route of exposure
The biological half-life is not yet known. The plasma
elimination half-life has been estimated to be approximately
8 days (Kopferschmitt, 1983).
6.4 Metabolism
No data available.
6.5 Elimination by route of exposure
Two routes of excretion have been proposed: intestinal and
faecal (Kopferschmitt, 1983).
7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
7.1 Mode of action
Ricin binds to galactose-containing receptors on the cell
surface. This is followed by uncoupling of the peptide chains
from the ricin molecule, and the smaller chain is taken into
the cell by endocytosis. Ricin impairs chain elongation in
protein synthesis, causing cell death (Olnes, 1974).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The estimated lethal dose in man is 1 mg/kg
(Kopferschmitt, 1983). Two to four seeds may
cause severe poisoning in an adult, and 8 are
generally fatal (Wedin; 1986), Hardin, 1974).
If seeds are swallowed without chewing,
poisoning is unlikely.
7.2.1.2 Children
One to three seeds can be fatal to a child
(Weding, 1986).
7.2.2 Animal data
The fatal dose by intravenous injection of ricin in
experimental animals (mice) has been reported to be as
low as 300 nanaogram/kg (Martindale, 1982). The
ingestion of 2 g undetoxified fibrous residue of castor
oil can determine toxic effects in large animals
(Schvartsman, 1979).

Ricin - MLD ip mice: 0.001 microgram ricin nitrogen per
g body weight (Budavari, 1989). In animals, repeated
small doses result in antibody production. Pretreated
animals can withstand up to 800 times the lethal dose
(Knight, 1979).
7.2.3 Relevant in vitro data
No data available.

7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
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)
Ricin can be measured by radioimmunassay. Anti-
ricin antibodies can be labelled
with isotopic iodine (I 125) (Kopferschmitt,
1983).
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
Cases of ricin poisoning been described in which
the serum concentration is 1.5 nanogram/l but there
is no correlation between serum levels and evolution
of the clinical signs (Kopferschmitt, 1983).
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
If chewed, the seeds are toxic; the leaves are less
toxic. Ricin causes a burning sensation of the mouth
and throat (Schvartsman, 1979). After a latent period
of 3 to 6 h (or sometimes several days), nausea,
vomiting, severe stomach pains, diarrhoea (sometimes
bloody), excessive thirst, and acute dehydration
develop. Prostration, blurring of vision, mydriasis,
fever, necrosis of the liver, spleen and lymphatic
system, nephritis, proteinuria, uremia, red cell
hemolysis, loss of consciousness and convulsions occur
(Arena, 1981; Hardin, 1974; Jouglard, 1977; Kinamore,
1980; Kopferschmitt, 1983; Pronczuk, 1988; Wedin,
1986).
9.1.2 Inhalation
The allergen can produce asthma and rhinitis.
9.1.3 Skin exposure
The allergen can produce dermatitis and eczema
9.1.4 Eye contact
The allergen can produce conjunctivitis.
9.1.5 Parenteral exposure
A case of subcutaneous injection which in a few hours
developed circulatory failure, hypothermia and high
leucocyte count leading to death, was reported Knight,
1979).
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
The allergen can produce asthma and rhinitis
(Schvartsman, 1979).
9.2.3 Skin exposure
Prolonged contact can produce allergic dermatitis and
eczema (Schvartsman, 1979).
9.2.4 Eye contact
Allergic conjunctivitis (Schvartsman, 1979).
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Nausea and burning sensation of the mouth and throat appear
immediately after ingestion of the chewed seed (Schvartsman,
1979). Intense vomiting and profuse watery or bloody
diarrhoea appear 3 to 6 h later. In some cases, symptoms may
be delayed for up to 15 h after ingestion (Schvartsman, 1979).

Other effects are secondary to extensive fluid and
electrolyte depletion. Death can occur through dehydration
and electrolyte imbalance within a few hours. Convulsions
may precede death (Pronczuk, 1988; Knight, 1979). However,
death due to uraemia may occur within 12 days. The prognosis
epends on the promptness of treatment and the number of seeds
chewed and ingested.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Hypotension is frequently observed due to fluid
depletion. Tachycardia and ECG changes have been
described (Wedin, 1986).
9.4.2 Respiratory
Bronchial asthma and allergic rhinitis (Cooper, 1989;
Schvartsman, 1979).
9.4.3 Neurological
9.4.3.1 CNS
Vertigo, mydriasis, somnolence, stupor, and
coma. Convulsion may precede death
(Kopferschmitt, 1983; Knight, 1979, Wedin,
1986).
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Muscular weakness and cramps are observed.
9.4.4 Gastrointestinal
Burning sensation of the mouth and throat almost
immediately after ingestion. Nausea, vomiting and
intense watery or bloody diarrhoea, stomach-ache follow
(Hardin, 1974; Jouglard, 1977; Arena, 1981;
Kopferschmitt, 1983; Wedin, 1986, Pronczuk, 1988).
9.4.5 Hepatic
Liver necrosis with elevation of SGPT, SGOT and and LDH
have been described (Kinamore, 1980).
9.4.6 Urinary
9.4.6.1 Renal
Proteinuria and nephritis with elevation of BUN
and poor urinary output have been reported
(Wedin, 1986).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Prolonged contact can produce dermatitis and eczema
(Schvartsman, 1979).
9.4.9 Eye, ears, nose, throat: local effects
Eyes: Allergic conjunctivitis and rhinitis (Schvartsman,
1979).

Throat: Burning sensation is the first symptom of this
poisoning (Schvartsman, 1979).
9.4.10 Haematological
Hyperplastic myelosis initially occurs followed by

haemolytic anaemia, neutropenia and eosinophilia
(Schvartsman, 1979).
9.4.11 Immunological
(see 9.4.13 - Allergic reactions).
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
9.4.12.2 Fluid and electrolyte disturbances
Severe dehyradation with various degrees of
hypokalaemia and hyponatraemia.
9.4.12.3 Others
9.4.13 Allergic reactions
Occur mostly among gardners; workers exposed to
agricultural cultivation of castor bean; and mill
workers exposed to ricine oil.

Severe allergies have been reported from wearing or
handling necklaces or other trinkets made from castor
bean. The allergens can produce bronchial asthama,
allergic rhinitis, dermatitis, eczema, eosinophilia,
conjunctivitis, and anaphylactic shock (Schvartsman,
1979; Knight, 1979; Cooper, 1989). Other agricultural
products such as coffee and soya bean contaminated
with ricin can produce allergic reactions among exposed
workers.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Ricin crosses the placenta and is excreted in breast
milk.
9.5 Others
9.6 Summary
10. MANAGEMENT
10.1 General principles
Any person ingesting any part of Ricinus communis should be
hospitalized for close observation. Treatment is mainly
symptomatic with gastric decontamination and correction
of fluid and electrolyte disturbances (Lampe, 1985; Pronczuk,
1988; Wedin, 1986; Kopferschmitt, 1983).
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Blood and urine for biomedical analysis.

Gastric contents for identification of the plant.

The plant should be obtained for botanical and
pharmacognostic studies.
10.2.2 Biomedical analysis
Electrolytes and blood gases.

Monitoring of renal, hepatic functions, haematology
and blood clotting.
10.2.3 Toxicological/toxinological analysis
Ricin has been measured in plasma and urine by means
of radioimmunassay with antiricin antibodies
labelled with iodine 125 (Kopferschmitt, 1983).
10.2.4 Other investigations

10.3 Life supportive procedures and symptomatic treatment
Symptomatic treatment: correction of fluid and electrolyte
disturbances. Antispasmodics may be needed for colic.

In case of bronchial asthma, oxygen, epinephrine or
aminophylline, and corticosteroids may be necessary.

Antihistamines or corticosteroids may be beneficial in
treating skin lesions.

Renal insufficiency may require haemodialysis. However,
ricin is not dializable (Kopferschmitt, 1983).
10.4 Decontamination
Induce emesis or perform gastric lavage immediately.
Activated charcoal may be administered. Cathartics are
contraindicated (Wedin, 1986).
10.5 Elimination
Forced alkaline diuresis has not been proved to be effective
(Arena, 1981; Oladosu, 1979; Kopferschmitt, 1983)
10.6 Antidote/antitoxin treatment
10.6.1 Adults
10.6.2 Children
10.7 Management discussion
The effectiveness of forced diuresis has not been proved.

Ricin is not dialyzable.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Wedin et al. (1986) reported two cases with intense vomiting,
diarrhoea, dehydration and transient elevation of serum
creatinine. There was no clinical or laboratory evidence
of liver necrosis or dysfunction. One case had slight
abnormalities of haematological values either due to
dehydration or haemolysis. Both patients recovered
uneventfully with symptomatic treatment.

Kopfershmitt et al. (1983) described the case of a 21-year-
old man who ingested 31 castor beans. Soon after ingestion
he developed vomiting and profuse diarrhoea with marked
dehydration, circulatory collapse and elevated BUN. His
ricin plasma level reached up to 1.5 nanogram/l; urinary
excretion began after 3 days at a rate of 0.72 nanogram/24
h. Recovery was rapid with fluid administration.
11.2 Internally extracted data on cases
Ingestion of seeds of Ricinus communis is a common cause of
consultation at CIAT (Montevideo). Most are admitted with
vomiting, diarrhoea and abdominal pain, but they never
develop the severe dehydration and other complications
described in the literature.

Early treatment was effective in preventing the appearance
of symptoms (Pronczuk, 1988).
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
Arena JM (1981) Plants that poison. Emergency Medicine,
June, 15: 22-.57.

Budavari S (ed) (1989). The Merck Index: an encyclopedia of
chemicals, drugs and biologicals. 11th ed. Rahway, New
Jersey. Merck & Co. Inc.

Cooper WC (1989) Castor oil. Encyclopaedia of Occupational
Health and Safety, IWO. Vol 1: 38-39.

Favarel-Carrigues JC, Castaig Y, Obikpi-Benissan G, Gabinski
C (1978) Les intoxications d'origine végétal dans le sud-
ouest. Bordeaux Médicale, 28(11): 1617-1621.

Font Quer P (1979) Plantas medicinales. Ed. Labor.
Barcelona.

Hardin JN & Arena JM (1974) Human poisoning from native and
cultivated plants. 2nd Ed. Duke University Press, Durham,
North Carolina.

Jouglard J (1977) Intoxication d'origine végétale.
Encyclopédie Médico-Chirurgicale. Intoxications 16065 A
10.

Kinamore PA, Jaeger R, Castro FJ (1980) Abrus and Ricinus
ingestion. Management of three cases. Clinical Toxicology,
17(3): 401-405.

Kopferschmitt J, Flesh F, Lugnier A, Sauder PH, Jaeger A,
Mantz JM (1983) Acute voluntary intoxication by Ricin.
Human Toxicology, 2: 239-242.

Lampe KF & McCann MA (1985) AMA Handbood of poisonous and
injurious plants. American Medical Association, Chicago,
Illinois.

Martindale. The Extra-Pharmacopoeia (1982). The
Pharmaceutical Press, 28th Ed. 695 and 1751.

Oladosu LA, Case AA (1979) Large animal hepatoxic and
nephrotoxic plants. Veterinary and Human Toxicology 21(4):
363-364.

Olnes S, Refsnes K, Piohl A (1974) Mechanism of action of
the toxic lectins abrin and ricin. Nature, 249: 627-631.

Pronczuk J, Laborde A (1988) Plantas Silvestres y de
Cultivo: riesgo de intoxicacion para el hombre.
Universidad de la Republica. Montevideo, 6f3-65.

Schvartsman S (1979) Plantas venenosas Sarvier. Sao Paulo.

92-96.

Wedin GP, Jeffrey SN, Everson GW, Krenzelok EP (1986)
Castor Bean Poisoning. American Journal of Emergency
Medicine, 4(3): 259-261.
13.2 Botanical
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Dr Mosto
Jefa Seccion Toxicologia
Hospital de Clinicas "Jose de San Martin"
Facultad de Medicina
Universidad de Buenos Aires
Cordoba 2351
Buenos Aires
Argentina
http://www.inchem.org/documents/pims/pl ... fic%20name

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 18 Sep 2011 00:49 
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Joined: 02 Sep 2011 18:27
Posts: 455
Location: Украина
КЛЕЩЕВИНА — RICINUS COMMUNIS на латыни, из семества молочайных. RICINUS - клещ в переводе. А зачем пробовать заведемо нехорошее растение на вкус?
У нас возле школы тоже растет клещевина. На мое замечание, что удалить бы ее следует, ответ - убийственный: "Ну красиво же! И еще никто не отравился!" Воистину, русская рулетка!!!


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 Post subject: Re: Ядовитые животные и растения
PostPosted: 18 Sep 2011 00:55 
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Joined: 04 Nov 2009 22:05
Posts: 62190
Location: Моя Батьківщина там, де моя лабораторія
Как компромисс можно оборвать соцветия и плоды: внешний вид почти не пострадает, но такое растение уже не будет представлять опасности.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 18 Sep 2011 06:46 
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Joined: 02 Apr 2011 23:28
Posts: 1516
Location: Украина
vitta wrote:
А зачем пробовать заведемо нехорошее растение на вкус?

Рыба фуга — деликатес, хоть тоже рулетка, только японская :be: ; может и плоды клещевины пригодны на большее, чем касторовое масло. ;)


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 Post subject: Re: Ядовитые животные и растения
PostPosted: 19 Sep 2011 18:55 
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Location: Моя Батьківщина там, де моя лабораторія
Попробовал разжевать одно семечко клещевины. Под твердой хрустящей оболочкой оказалась белая "мякоть", которая по консистенции напоминала сырые семечки подсолнуха. Какого-либо вкуса не ощутил (почувствовал только, что семечко жирное). Насчет последствий: поживем - увидим, думаю, что не будет абсолютно никаких.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 26 Dec 2011 20:51 
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Уточняю, чтобы не было недоразумений: попытки обсуждения способов суицида будут присекаться.

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 26 Dec 2011 21:48 
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Posts: 859
Location: Казахстан.
В народе клещевину называют касторка. Обладает ли касторовое масло отравляющим эффектом, как же из него извлекают ядовитый белок?

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 Post subject: Re: Ядовитые животные и растения
PostPosted: 26 Dec 2011 21:57 
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Герман инструкция здесь выложена на английском. Касторовое масло слабительное. Думаю если выпить стакан масла то "свист по всем трубам" будет не шуточный)))) С белком возится гемор он то и дело стремится к деструкции.


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