Cynide Toxicity

CYANIDE TOXICITY
INTRODUCTION:
C yanid e or Hyd rogen cyani de poisoni ng in an imal s occu rs generally du e toi ng estion of cyan og enic p lan ts( cyan og en et ic g lycosid es) .
WHAT ARE CYANOGE NIC PLANTS?
Th esearep lant s whi ch yeild s h yd rog en cyan id e up on acidi c or enzymat ic h ydrolysis d u rin g di gestion.Cyan id e(h yd rog en cyanid e) is th emost r ap id lyact in g and d ead ly toxicant th at aff ect all mammals.Ex:Sorg hu m,b itter almon d ,cotton seed cake,cherry plant ,sud an gr ass.
CHEMICAL FORMULA AND STRUCHTURE

OF CYANIDE MOLECULE:
PROPERTIES:
Hydrogen cyanide(HCN) is a colourless,readily

volatile gas having charachteristic odour of bitter
almond.
A solution of HCN in water is called as Hydrocyanic

acid or prussic acid.
Cyanogenetic glycosides are formed from nitrates

and anminoacids as part of plant metabolism.
Cyanogenetic glycosides present in epidermal cells

of plant and their mesenchymal cells(leaf tissue)
contains beta glycosidase enzyme which enables
hydrocyanic acid production in plants.
Plant cells can be ruptured in leaves by

cutting,chewing by the animal,wilting
freezing,draught,trampling,crushing and
also by conditions in the rumen also
favours the degradetion of glycoside to free
hydrogen cyanide.
This conversion is mainly because of rumen

microbial enzymes, which metabolizes
cyanogenetic glycosides.
DIFFERENT PLANTS WITH THEIR CYANOGENIC

GLYCOSIDES:
BITTER ALMOND AMYGDALINE-250mg of HCN

per 100g.
SORGHUM PLANT-DHURRIN
250mg HCN
per 100g.
LINSEED(FLAX) - LINAMARIN 10 to 300 mg

HCN /100g
WILD CHERRY - TRIGLOCHININ-200mg HCN
per 100mg
BITTER ALMOND
SORGHUM PLANT
CASSAVA
COTTON SEED CAKE
WILD CHERRY
SUDAN GRASS
BAMBOO YOUNG SHOOTS:
ACACIA
ROSEWOOD
MAIZE PLANT
BRACKENFERN
INDIAN GRASS
JHONSON GRASS
LOTUS LEAF
LINSEED CAKE
LD-50 VALUES OF CYANOGENIC GLYCOSIDES

IN CATTLE ,HORSE AND SHEEP:
Amygdalin- 0.5mg/ kg body weight
Dhurrin- 1mg/ kg body weight
Linamarin-2.4mg/ kg body weight
Triglochinin-2.8mg/kg body weight
Other sources of cyanide poisoning include

cyanide containing fumigants,rodenticides
and drugs like nitropusside.
Polyurethene,polyamide,wool and silk

produces cyanide upon burning.The
combustion gas released during this process
leads to heavy morbidity and mortality by
smoke inhalation.
FACTORS AFFECTING POISONING

1.
Species:Ruminants are more susceptible to cyanide

poisoning than other animals due to ruminal
acidity(6.5-7),higher water content and rumen
microbial enzymes.Among the ruminants cattle are
more suceptible than sheep.
2.
Plant factors: Grain sorghums are more toxic than

forage sorghums or sudan grass.
Leaves contains (upper leaves) HCN than stem,stalk
and lower,older leaves.
.
Young rapidly growing and new shoots
of plants has more HCN.
.
Cyanide content usually decreases after
pollination.
.
Plants containing more amount of beta
glycosidase enzyme releases more of HCN.
3. Injury to plant: Injury due to wilting,frostbite,cutting

etc.,ruptures plant cells so they easily release more
amount of HCN.Dead plants have less prussic acid.
4. Weather: Drought-stricken stunted plants contain
high concentration of cyanogenic glycosides
because they failed to get mature and contains
mostly leaves which are high in HCN.
5.Method of feeding: Indiscriminate grazing is the most
dangerous method of feeding because cattle prefer
to graze leaves and young shoots which tend to be
high in HCN.
6. Time of cutting/grazing: Cyanogenetic glycoside

content usaually high in plants during morning
and low in afternoon and evening.So avoid
grazing cattle during morning.
7.Processing of materials: Drying or making of
silage reduces HCN content in plants.Hay stored
for about 2-3 months gradually losses its HCN
content due to the volatilization of HCN.
8.Soil composition: High contents of nitrogen and
low phophorous favourable for high HCN in
plants.
9.Gastric pH: Acidic pH reduces release of HCN and

incidence of cyanide toxicity. Although gastric
acid facilitates the release of HCN by hydrolysing
cyanogenetic glycosides, yet at the same time it
destroys plant enzyme responsible for release of
HCN. So, humans.dogs,horses and pigs are less
susceptible for HCN poisoning because of their
highly acidic stomach.
10.Rumen content: Chances of HCN release is
more in full stomach animal compared to empty
stomach animal due to presence of more
enzymes in ingested plant.
TOXICITY:
Toxicity of cyanide varies with type of salt,
species,speed of ingestion and indivisual animal
tolerence.
HCN or its alkaline salts are highly toxic having
oral LD50 of 0.5-3.0mg/kg in most of the animals.
A plant containing morethan 20mg HCN/100g
is considered as toxic to animals.
Numerous forms of cyanide exist,including

gaseous HCN ,water soluble Na and K cyanide
salts and Hg,Cu, Au and Ag cyanide salts are
poorly water soluble.
Salts of cyanic acid (cyanates) are more
while salts of thiocyanic
acid(thiocyanate,rhodanide) have less
toxicity.Potassium ferricyanate and ferrocyanide
are practically non-toxic.
TOXICO-KINETICS:
Hydrogen cyanide rapidly released by the

cyanogenic glycosides upon chewing,rumen and
intestinal microflora.This is due to damage
caused to the plantcells,allows enzyme and
cyanogenic glycosides to come into contact to
release HCN.
Upon
HCN release, it is rapidly absorbed by GIT

and in various organs in the body,and lungs by
inhalation route.
The
cyanide rapidly metabolised in the liver.The

principal excretory product produced is
THIOCYANATE.Production of thiocyanate is
catalysed by the enzyme RHODANESE which
is commonly occurs in mammalian tissue.
Other
minor routes of metabolism are

production of thiazoline oxidative pathway leads
to production of CO2 and formate.Some amount
of HCN is also eliminated by expiration giving
charachteristic bitter almond smell to the
exhailed air.
PRODUCTION OF THIOCYANATE BY
RHODANESE:
MECHANISM OF
TOXICITY:
The toxic effects of cyanide is due to its affinity to

the metalloporphyrin containing enzymes more
susceptible towards cytochrome oxidase enzyme.
Cyanide has strong affinity for TRIVALENT IRON

of the CYTOCHROME OXIDASE (cyt).HCN
molecule acts by inhibiting its activity and hence
cellular respiration.
In mitochondria, the CN- radical combines with

ferric ions of cyt and inhibits electron transport
system (ETC).
Cyt
is phyciologically responcible for transfer of

oxygen and its utilization at cellular level.
Normally
oxygen combines with cyta3++ and

oxidises it to cyta3+++ which is reconverted to
cyta3++ for cycle to continue.
But this not happens when cyanide radical binds

to cyt, which results in the formation of cyancytochrome oxidase complex.
This does not allow converstion of cyta3+++ to

cyta3++ .And further combination of oxygen and
SHAEMATIC REPRESENTION OF CYANIDE

TOXICITY:
This results in blockade of ETS, hence respiration and

cells die due to lack of oxygen.All tissues are
susceptible, but death is primarily due to BRAIN
TISSUE ANOXIA.
As arterial blood is not utilised ,venous blood retains

the bright colour of oxyhaemoglobin.
Cyanide radicle inhibits several other enzymes.It also

reacts with the methhaemoglobin to produce
cyanmethheamoglobin.
DEATH OF PAERT OF BRIAN DUE TO TISSUE

ANOXIA
CLINICAL SIGNS:
1.PERACUTE TOXICITY:
In this condition animal may found dead or death

occurs in few hours.
2.ACUTE TOXICITY:
The clinical course of toxicity depends on

concentration of cyanide ingested by the animal and
rate,duration of consumption.
Acute poisoning occurs due to consumption of large

amount of toxin in shorter duration.
Signs include restlessness,laboured

breathing,stumbling gait,dyspnoea and
tachycardia.
Salivation, lacrymation,mydriasis,voiding of urine

and feaces are seen.
Mucous membrane, gum,sclera become cyanotic.

Finally tissue dies by depletion of oxygen.
Muscle
tremors,fasciculations,regurgitation pf
rumen contents,clonic convulsions,bloat occurs.
MYDRIASIS
Finally death occurs due to severe asphyxial

convulsions due to RESPIRATORY
PARALYSIS.
Ultimately
breathing stops.This whole

syndrome does not exceeds 30-45
minutes.Most of the animals showing signs
for 2 hours after ingestion of cyanide toxin,
usually survives.
CHRONIC TOXICITY:
Consumption of lower concentration of
cyanide for a long period may produce
nuerotoxic syndrome and goitre
POSTMORTEM FINDINGS:
In acute and peracute cases blood may be bright

CHERRY RED colour initially.
Mucous membranes are pink initially,then

become cyanotic when respiration ceases.
Rumen may be distended with gas,which

produces bitter almond smell upon
opening,congestion,
Some haemorrhages seen in GIT,lungs.AGONAL
HEMORRHAGES SEEN IN HEART,froath is seen in
respiratory passages.
CHERRY RED LIVER PIECES
HEMORRHAGES ON HEART
CHERRY RED APPEARANCE OF SKIN

DURING CYANIDE TOXICITY IN HUMANS
DIAGNOSIS:
The acute onset,bright red mucous membrane and

blood,odour of HCN is indicative of cyanide poisoning.
By demonstration of HCN in rumen

contents,heparinised whole blood,liver and muscles.
Rumen contents and liver showing >10ppm and

1.4ppm
HCN respectively indicative of cyanide poisoning.
PICRIC ACID PAPER TEST METHOD:
HCN SPOT TEST:

PRINCIPLE: In acidic medium HCN get
released by the feed and reacts with the picric

acid pre-treated whatmann paper No.42
changing its yellow colour to red colour,
indicating the presence of HCN in suspected
feed sample.
PROCEDURE: 1 ml of sulphuric acid+0.5 ml of

chloroform +suspected feed sample.keep picric
acid pre-treated paper at the top of test
tube.Observe for the red discolouration of
paper.
DIFFERENTIAL DIAGNOSIS:
1.Carbon monoxide toxicity: Bright red coloured blood
but no acute death.
2.Hydrogen sulphide toxicity:Blood and tissue are
dark brown in colour and smell of hydrogen sulphide
comes from tissues.
3.Nitrate and Nitrite toxicity: Causes rapid death but
colour of blood is brown red.
4.Urea toxicity: Causes rapid death but main signs are
colic,nervous and behavioural changes.Rumen gives off
odour of ammonia.
TREATMENT AND
MANAGEMENT:
The major objective of treatment is to re-establish oxygen

transport to cellular level.
1.SODIUM NITRITE: It is used as ANTIDOTE for the cyanide

poisoning ,conjunction with sodium thiosulphate.It converts
hemoglobin(Fe++ ) to methemoglobin
(Fe+++ )by process of oxidation.
Methemoglobin reacts with cyanide of cyt to produce
cyanmethemoglobin.This process reactivates the inactivated
cyt enzyme.
The cyanmethemoglobin takes sulphur in presence of
rhodanese enzyme from the donor sodium thiosulphate
( Na2 SO3 ) and forms sodium thiocyanate(NaSCN) which is
non-toxic and eliminated through URINE.
Sodium nitrite is toxic substance due to its potential

to produce methemoglobinaemia,so its dose
should be carefully regulated.
DOSAGE:
Cattle and sheep: 20mg/kg,slow I/V as 1% solution

followed by sodium thiosulphate (500mg/kg,slow I/V as 25%
solution).
DOGS AND CATS: 25 mg/kg,slow I/V as 1%solution followed
sodium thiosulphate (1.25g/kg,I/V as 25% solution).
HORSES:16mg/kg,slow I/V as 1% solution followed by
sodium thiosulphate(30-40 mg/kg,slow I/V as 20% solution).
MECHANISM OF ACTION OF
ANTIDOTE :
HbO2
NO
2Met Hb
CN
CNMetHb
HCN
CN
S2O3
SCN+ SO 3
RHODANESE
URINE
2.SODIUM THIOSULPHATE: It is administered after

systemic administration of sodium nitrite,but alone also
given as cyanide toxicity antidote.
It hastens de-toxification of cyanide by providing an
exogenous source of sulphur to enzyme Rhodanese.
The cyanide in presence of enzyme rhodanese takes
sulphur from sodium thiosulphate and forms sodium
thiocyanite,which is relatively non-toxic and eliminates
through urine.
DOSAGE:
CATTLE AND SHEEP: 5OO mg/kg,slow I/V as 25%
solution plus 30g/cow,6g/sheep PO.
DOGS AND CATS: 1.25g/kg.I/V as 25% solution.
HORSES: 30-40 mg/kg,slow I/V as 20% solution.
3.COBALT PREPARATIONS: cobaltous chloride at rate

of 10mg/kg given PO.
Large dose of hydroxocobalamine or aquocobalamine
may be used at the rate of 15 IU/50 KG I/M route.
4.Other measures include cooling,diluting and acidifying
the rumen contents by giving adult cattle 4L of
VINEGAR in 12-20L of cold water to slowdown the
microbial hydrolysis of cyanogenic glycosides.
PREVENTION:
1.Do not graze wilted,frosted or drought stressed plants.
2.Do not feed SORGHUM during early regrowth after
plants have been cut,when they are likely to be most
toxic.
3.Feed hungry cattle before allowing them to graze
forages which may contain high levels of HCN.
4.Thoroughly boil the linseeds to remove any HCN
content.
5.Follow fertilizer recommendations to assure adequate
soil P.Avoid high levels of soil nitrgen.
PROGNOSIS:
It depends on time of initiation of therapy.If

animal survives for a day,no further treatment is
required.

Cynide Toxicity

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What are cyanogenic plants?

What are cyanogenic plants?

What are the major cyanogenic glycosides and their cyanide content found in different plants?

What are the major cyanogenic glycosides and their cyanide content found in different plants?

CYANIDE TOXICITY

CHEMICAL FORMULA AND STRUCHTURE

Hydrogen cyanide(HCN) is a colourless,readily

A solution of HCN in water is called as Hydrocyanic

Cyanogenetic glycosides are formed from nitrates

Cyanogenetic glycosides present in epidermal cells

Plant cells can be ruptured in leaves by

This conversion is mainly because of rumen

DIFFERENT PLANTS WITH THEIR CYANOGENIC

BITTER ALMOND AMYGDALINE-250mg of HCN

LINSEED(FLAX) - LINAMARIN 10 to 300 mg

COTTON SEED CAKE

BAMBOO YOUNG SHOOTS:

LD-50 VALUES OF CYANOGENIC GLYCOSIDES

Amygdalin- 0.5mg/ kg body weight

Dhurrin- 1mg/ kg body weight

Linamarin-2.4mg/ kg body weight

Triglochinin-2.8mg/kg body weight

Other sources of cyanide poisoning include

Polyurethene,polyamide,wool and silk

FACTORS AFFECTING POISONING

Species:Ruminants are more susceptible to cyanide

Plant factors: Grain sorghums are more toxic than

3. Injury to plant: Injury due to wilting,frostbite,cutting

6. Time of cutting/grazing: Cyanogenetic glycoside

9.Gastric pH: Acidic pH reduces release of HCN and

Numerous forms of cyanide exist,including

Hydrogen cyanide rapidly released by the

HCN release, it is rapidly absorbed by GIT

cyanide rapidly metabolised in the liver.The

minor routes of metabolism are

The toxic effects of cyanide is due to its affinity to

Cyanide has strong affinity for TRIVALENT IRON

In mitochondria, the CN- radical combines with

is phyciologically responcible for transfer of

oxygen combines with cyta3++ and

But this not happens when cyanide radical binds

This does not allow converstion of cyta3+++ to

SHAEMATIC REPRESENTION OF CYANIDE

This results in blockade of ETS, hence respiration and

As arterial blood is not utilised ,venous blood retains

Cyanide radicle inhibits several other enzymes.It also

DEATH OF PAERT OF BRIAN DUE TO TISSUE

In this condition animal may found dead or death

The clinical course of toxicity depends on

Acute poisoning occurs due to consumption of large

Signs include restlessness,laboured

Salivation, lacrymation,mydriasis,voiding of urine

Mucous membrane, gum,sclera become cyanotic.

Finally death occurs due to severe asphyxial

breathing stops.This whole

In acute and peracute cases blood may be bright

Mucous membranes are pink initially,then

Rumen may be distended with gas,which