Cynaogenic Plants

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o INTRODUCTION

Cyanide is one of the most rapidly actingand deadly toxicant that affects allmammals.

Cyanogenetic glycosides are presentnaturally in nearly 1000 species ofplants, which yields HCN upon acidic orenzymatic hydrolysis.


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PROPERTIES

•

HCN is a colorless readily "olatile gas withcharacteristic odour of bitter almond.• • # solution of HCN in water is called prussic acid.

• The cyanogenetic glycosides are formed from nitriteand amino acids as a part of normal plant metabolism.

• #ny e"ent that causes plant cell to rupture allowingcyanogenetic compounds and the $%&lucosidase tocombine will produce HCN.


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SOURCES O( )CN*

• $itter almond and white cherry containscyanogenetic glycoside amygdaline.

• 'orghum, millet, (owar, sudan grass containsdhurrin.

• )inseed, "el"et grass and wild clo"er containlinamarin.

• *ther sources li!e lotus,maize,peach,cyanidecontaining fertilizers,electroplating and (ewellerymanufacturing, + ay film reco"ery and laboratorychemicals .


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• Method of feeding- &razing may be the most dangerous method offeeding.

• Time of cutting or grazing- HCN content are usually high during morning.

• se of fertilizer and pesticide- Hea"y use of nitrite fertilizers inhosphorous deficient soil increase HCN concentration.

• Soil composition- High content of nitrogen and low phosphorous is

fa"orable for high HCN content.• Processing of material- rying or ma!ing of silage reduces HCN content.

• !astric p"- #cidic gastric pH decreases release of HCN and hencecyanide toxicity.

• 2## ppm "$% in fresh plants .#2'( or 2## mg)*g in plant isconsidered the standard +lo,est le el for "$% a/o e ,hich poisoning in0 1# min can /e e pected if plant is palata/le &3 *g eaten(.


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-EC)ANIS- O( ACTION$yanide has strong affinity for tri alent iron of the

cytochrome o idase molecule and acts /y inhi/iting itsenzyme acti ity and hence cellular respiration.

CYTOC)RO-E O+IDASEIt s a last enzyme in the respiratory electron transport

system in mitochondria.

It recei es an electron from each of four cytochromec molecules4 and transfers them to one o ygen molecule4con erting molecular o ygen to t,o molecules of ,ater.


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• ;ut ,hen cyanide com/ines ,ith tri alent iron ofcytochrome o idase and forms a sta/le comple calledcyanocytochromeo idase.

• This comple do not allo, con ersion of tri alent ironof cytochrome o idase to di alent iron ofcytochromeo idase and further com/ination of o ygenand su/se


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• In the mitochondria cyanide radicalcom/ined ,ith iron of cytochrome o idase

and inhi/its >T$.• %ormally ? 2 com/ined ,ith di alent cyt a1@@ and o idises it to cyt a1@@@ 4 ,hich isrecon erted to cyt a1@@ for the cycle tocontinue.

• $yanide com/ined ,ith cyt a1@@@ it forms asta/le comple called cyan-cytochromeo idase.

• This comple inhi/its >T$ system and hencerespiration leading to cell death.


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• CLINICAL SIGNS

• er acute and acute toxicity%-n peracute animal die within few

minutes.• -n acute cases clinical signs may occur within 1 % 20 min to few hours.

• 'igns include laboured breathing, restlessness ,dyspnoea ,sali"ation,excess lacrimation, mydriasis "oiding of urine and feaces ,gum scleraand mucous membrane are bright red and become cyanotic terminally.

• eath occur during se"ere asphyxial con"ulsion due to respiratoryparalysis.

• Chronic toxicity% Consumption of cyanide in lower concentraton forlonger period produce a neurotoxic syndrome similar to lathyrism.

•

)ow doses of cyanide are also goitrogenic in humans and animals.


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POST MORTEM FINDINGS

In acute or peracute to icity /lood may /e cherry redinitially /ut may /ecome dar* red /ecause as ? 2 ofarterial /lood cannot /e used.

umen may /e distended ,ith gas and odor of /itteralmond may /e detected after its opening.

!I tract and lungs may ha e congestion and petechialhemorrhages .


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DIAGNOSIS

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Acute onset /right red mucous mem/rane and /lood odour of"$% are indicati e of cyanide poisoning.

DI((ERENTIAL DIAGNOSIS

$ar/on mono ide – color of /lood is /right red /ut death is notso acute.

"ydrogen sulphide- causes rapid death /ut /lood and tissues aredar* /ro,n in color and smell of "2S comes.

%itrite and nitrate – $olor of /lood is /ro,n red.

rea to icity- Signs include colic 4 ner ous and /eha ioralchanges.


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• TREAT-ENT

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'odium nitrite%• -s used as an antidote for cyanide in con(unction with sodium

thiosulphate

• Cattle and sheep dosage%20mg3!g slow i" as 14 soln. followed bysodium thiosulphate 5 00mg3!g slow i" as 2 4 soln6

• og and cat % 2 mg3!g slow i" as 14 soln followed by sodiumthiosulphate 51.2 g3!g i" as 2 4 soln6

• Horse % 70 mg3!g slow i" as 14 soln followed by sodiumthiosulphate 580 9 :0 mg3!g slow i" as 204 soln6


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-EC)ANIS- O( ACTION


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• 'odium thiosulphate%

• *ften administered after systemic administration of sodium nitratebut alone is an effecti"e antidote to cyanide poisoning.

• -t hastens detoxification of cyanide by pro"iding an exogenous sourceof sulphur to the enzyme rhodanese .

• osage

• Cattle and sheep% 00 mg3!g as 204 soln ; 80 g per cow or 7 g persheep *.

• ogs and cats %1.2 g 3!g slow i" 2 4 soln.

• Horse %80 9 :0 mg3!g slow i" 204 soln.


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C!.alt /r%/arati!n

*ral prep of 4 soln ofcobaltous chloride 5 10mg3!g6 or large dose of"it $12 a may be usedacute cyanide poisoning.


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• PROGNOSIS Bdepends on the time of institution of therapy .

PREVENTION:• on

Cynaogenic Plants

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