cynide toxicity

7/23/2019 Cynide toxicity

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CYANIDE TOXICITY



INTRODUCTION:

CyanideorHydrogencyanidepoi soning in animalsoccurs generally duetoingestionofcyanogenic plants(cyanogeneticgl ycosides).

WHAT ARE CYANOGENICPLANTS? Theseareplantswhich yeildshydrogen cyanideupon acidicorenzymat ichydrol ysisduring digestion.Cyanide(hydrogen cyanide) isthemost rapidlyactingand deadly toxicant thataect allmammals.Ex: orghum!"itteral mond!cottonseedca#e! cherryplant!sudan grass.



CHEMICAL FORMULA AND STRUCHTUREOF CYANIDE MOLECULE:



PROPERTIES:

Hydrogen cyanide(HC$) is a colourless!readily%olatile gas ha%ing charachteristic odour of "itteralmond.

& solution of HC$ in water is called as Hydrocyanicacid or prussic acid.

Cyanogenetic glycosides are formed from nitratesand anminoacids as part of plant meta"olism.

Cyanogenetic glycosides present in epidermal cellsof plant and their mesenchymal cells(leaf tissue)contains "eta glycosidase enzyme which ena"leshydrocyanic acid production in plants.



TTE* &+,-$ –AMYGDALINE/012mg of HC$ per 322g.

-*4H5, '+&$T/DHURRIN - 012mg HC$

per 322g.

+$EE(6+&7) / LINAMARIN – 32 to 822 mg

HC$ 9322g

+ CHE**; / TRIGLOCHININ-022mg HC$

per 322mg

DIFFERENT PLANTS WITH THEIR CYANOGENICGLYCOSIDES:



TTE* &+,-$ -*4H5, '+&$T



C&&<& C-TT-$ EE C&=E



+ CHE**; 5&$ 4*&



&,-- ;-5$4 H--T:



&C&C& *-E--



,&>E '+&$T *&C=E$6E*$



$&$ 4*& ?H-$-$ 4*&



+-T5 +E&6 +$EE C&=E



Amygdal!- "#$mg% &g '(dy )*g+,

D+..!- /mg% &g '(dy )*g+,

L!ama.!-0#1mg% &g '(dy )*g+,

T.gl(2+!!-0#3mg%&g '(dy )*g+,

LD-$" 4ALUES OF CYANOGENIC GLYCOSIDESIN CATTLE 5HORSE AND SHEEP:



-ther sources of cyanide poisoning includecyanide containing fumigants!rodenticidesand drugs li#e nitropusside.

'olyurethene!polyamide!wool and sil#produces cyanide upon "urning.The

com"ustion gas released during this processleads to hea%y mor"idity and mortality "ysmo#e inhalation.



/# S6*2*7:*uminants are more suscepti"le to cyanidepoisoning than other animals due to ruminal

acidity(@.1/A)!higher water content and rumenmicro"ial enzymes.&mong the ruminants cattle aremore sucepti"le than sheep.

0# Pla!, 8a2,(.7: 4rain sorghums are more toxic thanforage sorghums or sudan grass.. +ea%es contains (upper lea%es) HC$ than stem!stal#

and lower!older lea%es.. ;oung rapidly growing and new shoots

of plants has more HC$.•. Cyanide content usually decreases after

pollination.•. 'lants containing more amount of "eta

glycosidase enzyme releases more of HC$.

FACTORS AFFECTING POISONING



8. nBury to plant: nBury due to wilting!frost"ite!cuttingetc.!ruptures plant cells so they easily release more

amount of HC$.ead plants ha%e less prussic acid.

. eather: rought/stric#en stunted plants containhigh concentration of cyanogenic glycosides

"ecause they failed to get mature and containsmostly lea%es which are high in HC$.

1.,ethod of feeding: ndiscriminate grazing is the most

dangerous method of feeding "ecause cattle preferto graze lea%es and young shoots which tend to "ehigh in HC$.



@. Time of cutting9grazing: Cyanogenetic glycosidecontent usaually high in plants during morningand low in afternoon and e%ening.o a%oidgrazing cattle during morning.

A.'rocessing of materials: rying or ma#ing ofsilage reduces HC$ content in plants.Hay storedfor a"out 0/8 months gradually losses its HC$content due to the %olatilization of HC$.

D.oil composition: High contents of nitrogen andlow phophorous fa%oura"le for high HC$ inplants.



.4astric pH: &cidic pH reduces release of HC$ andincidence of cyanide toxicity. &lthough gastricacid facilitates the release of HC$ "y hydrolysingcyanogenetic glycosides! yet at the same time itdestroys plant enzyme responsi"le for release ofHC$. o! humans.dogs!horses and pigs are lesssuscepti"le for HC$ poisoning "ecause of theirhighly acidic stomach.

32.*umen content: Chances of HC$ release ismore in full stomach animal compared to emptystomach animal due to presence of moreenzymes in ingested plant.



T-7CT;:

Toxicity of cyanide %aries with type of salt!species!speed of ingestion and indi%isual animal

tolerence.

HC$ or its al#aline salts are highly toxic ha%ingoral +12 of 2.1/8.2mg9#g in most of the animals.

& plant containing morethan 02mg HC$9322gis considered as toxic to animals.



$umerous forms of cyanide exist!includinggaseous HC$ !water solu"le $a and = cyanidesalts and Hg!Cu! &u and &g cyanide salts arepoorly water solu"le.

alts of cyanic acid (cyanates) are morewhile salts of thiocyanicacid(thiocyanate!rhodanide) ha%e lesstoxicity.'otassium ferricyanate and ferrocyanideare practically non/toxic.



Hydrogen cyanide rapidly released "y thecyanogenic glycosides upon chewing!rumen andintestinal microFora.This is due to damagecaused to the plantcells!allows enzyme andcyanogenic glycosides to come into contact torelease HC$.

5pon HC$ release! it is rapidly a"sor"ed "y 4Tand in %arious organs in the "ody!and lungs "yinhalation route.

TOXICO-9INETICS:



The cyanide rapidly meta"olised in the li%er.Theprincipal excretory product produced is

THIOCYANATEG.'roduction of thiocyanate iscatalysed "y the enzyme RHODANESE; whichis commonly occurs in mammalian tissue.

-ther minor routes of meta"olism areproduction of thiazoline oxidati%e pathway leadsto production of C-0 and formate.ome amount

of HC$ is also eliminated "y expiration gi%ingcharachteristic "itter almond smell to theexhailed air.



PRODUCTION OF THIOCYANATE <YRHODANESE:



The toxic eects of cyanide is due to its anity tothe metalloporphyrin containing enzymes moresuscepti"le towards cytochrome oxidase enzyme.

Cyanide has strong anity for TRI4ALENT IRONGof the CYTOCHROME OXIDASE; =2y,>#HC$molecule acts "y inhi"iting its acti%ity and hence

cellular respiration.

n mitochondria! the C$/ radical com"ines withferric ions of cyt and inhi"its electron transport

system (ETC).

MECHANISM OFTOXICITY:



Cy, is phyciologically responci"le for transfer ofoxygen and its utilization at cellular le%el.

$ormally oxygen com"ines with 2y,a@@ and

oxidises it to 2y,a@@@ which is recon%erted to

2y,a@@

for cycle to continue.

ut this not happens when cyanide radical "inds

to 2y,! which results in the formation of cyan/cytochrome oxidase complex.

This does not allow con%erstion of 2y,a

@@@ to

2y,a@@ .&nd further com"ination of oxygen and



SHAEMATIC REPRESENTION OF CYANIDETOXICITY:



This results in "loc#ade of ETS5 hence respiration and

cells die due to lac# of oxygen.&ll tissues aresuscepti"le! "ut death is primarily due to <RAINTISSUE ANOXIA#

&s arterial "lood is not utilised !%enous "lood retainsthe "right colour of (y+a*m(gl('!#

Cyanide radicle inhi"its se%eral other enzymes.t also

reacts with the m*,++a*m(gl('! to produce2ya!m*,++*am(gl('!#



DEATH OF PAERT OF <RIAN DUE TO TISSUEANOXIA



/#PERACUTE TOXICITY: n this condition animal may found dead or death

occurs in few hours.

0#ACUTE TOXICITY: The clinical course of toxicity depends onconcentration of cyanide ingested "y the animal andrate!duration of consumption.

&cute poisoning occurs due to consumption of largeamount of toxin in shorter duration.

C+$C&+ 4$:



igns include restlessness!la"oured"reathing!stum"ling gait!dyspnoea andtachycardia.

ali%ation! lacrymation!mydriasis!%oiding of urine

and feaces are seen.

,ucous mem"rane! gum!sclera "ecome cyanotic.

6inally tissue dies "y depletion of oxygen.

,uscle tremors!fasciculations!regurgitation pfrumen contents!clonic con%ulsions!"loat occurs.



6inally death occurs due to se%ere asphyxialcon%ulsions due to RESPIRATORY

PARALYSIS#

5ltimately "reathing stops.This wholesyndrome does not exceeds 82/1 minutes.,ost of the animals showing signsfor 0 hours after ingestion of cyanide toxin!usually sur%i%es.

CHRONIC TOXICITY: Consumption of lower concentration of

cyanide for a long period may produce

!*.(,(2 7y!d.(m* and g(,.*



n acute and peracute cases "lood may "e "rightCHERRY RED colour initially.

,ucous mem"ranes are pin# initially!then

"ecome cyanotic when respiration ceases.

*umen may "e distended with gas!which

produces "itter almond smell uponopening!congestion!

ome haemorrhages seen in 4T!lungs.AGONAL HEMORRHAGES SEEN IN HEART!froath is seen in

respiratory passages.

POSTMORTEM FINDINGS:



CHE**; *E +<E* 'ECE HE,-**H&4E -$ HE&*T



CHERRY RED APPEARANCE OF S9INDURING CYANIDE TOXICITY IN HUMANS



The acute onset!"right red mucous mem"rane and"lood!odour of HC$ is indicati%e of cyanide poisoning.

y demonstration of HC$ in rumencontents!heparinised whole "lood!li%er and muscles.

*umen contents and li%er showing I32ppm and3.ppm

HC$ respecti%ely indicati%e of cyanide poisoning.

DIAGNOSIS:



HCN SPOT TEST:PRINCIPLE: n acidic medium HC$ get

released "y the feed and reacts with the picricacid pre/treated whatmann paper $o.0

changing its yellow colour to red colour!indicating the presence of HC$ in suspectedfeed sample.

PROCEDURE: 3 ml of sulphuric acidJ2.1 ml ofchloroform Jsuspected feed sample.#eep picricacid pre/treated paper at the top of testtu"e.-"ser%e for the red discolouration of

paper.

PICRIC ACID PAPER TEST METHOD:



/#Ca.'(! m(!(d* ,(2,y: right red coloured "lood"ut no acute death.

0#Hyd.(g*! 7l6+d* ,(2,y:lood and tissue aredar# "rown in colour and smell of hydrogen sulphidecomes from tissues.

#N,.a,* a!d N,.,* ,(2,y: Causes rapid death "utcolour of "lood is "rown red.

1#U.*a ,(2,y: Causes rapid death "ut main signs arecolic!ner%ous and "eha%ioural changes.*umen gi%es oodour of ammonia.

66E*E$T&+ &4$-:

TREATMENT AND



The maBor o"Becti%e of treatment is to re/esta"lish oxygentransport to cellular le%el.

/#SODIUM NITRITE: t is used as &$T-TE for the cyanidepoisoning !conBunction with sodium thiosulphate.t con%ertshemoglo"in(6eJJ ) to methemoglo"in

(6eJJJ )"y process of oxidation.

,ethemoglo"in reacts with cyanide of cyt to producecyanmethemoglo"in.This process reacti%ates the inacti%ated

cyt enzyme.

The cyanmethemoglo"in ta#es sulphur in presence ofrhodanese enzyme from the donor sodium thiosulphate

( $a0 -8 ) and forms sodium thiocyanate($aC$) which is

non/toxic and eliminated through URINE#

TREATMENT ANDMANAGEMENT:



odium nitrite is toxic su"stance due to its potentialto produce m*,+*m(gl('!a*ma5so its doseshould "e carefully regulated.

DOSAGE:

Ca,,l* a!d 7+**6: 02mg9#g!slow 9< as 3K solutionfollowed "y sodium thiosulphate (122mg9#g!slow 9< as 01Ksolution).

DOGS AND CATS: 01 mg9#g!slow 9< as 3Ksolution followed

sodium thiosulphate (3.01g9#g!9< as 01K solution).

HORSES:3@mg9#g!slow 9< as 3K solution followed "ysodium thiosulphate(82/2 mg9#g!slow 9< as 02K solution).



H"-0$-

0,et H" C$ C$,etH"

HC$

C$0-8 C$J -8

*H-&$EE

5*$E

MECHANISM OF ACTION OFANTIDOTE :



0#SODIUM THIOSULPHATE: t is administered aftersystemic administration of sodium nitrite!"ut alone alsogi%en as cyanide toxicity antidote.

t hastens de/toxiMcation of cyanide "y pro%iding anexogenous source of sulphur to enzyme *hodanese.

The cyanide in presence of enzyme rhodanese ta#es

sulphur from sodium thiosulphate and forms sodiumthiocyanite!which is relati%ely non/toxic and eliminatesthrough urine.



DOSAGE:

CATTLE AND SHEEP: 1-- mg9#g!slow 9< as 01Ksolution plus 82g9cow!@g9sheep '-.

DOGS AND CATS: 3.01g9#g.9< as 01K solution.

HORSES: 82/2 mg9#g!slow 9< as 02K solution.



#CO<ALT PREPARATIONS: co"altous chloride at rateof 32mg9#g gi%en '-.

+arge dose of hydroxoco"alamine or aNuoco"alamine

may "e used at the rate of 31 5912 =4 9, route.

.-ther measures include cooling!diluting and acidifyingthe rumen contents "y gi%ing adult cattle + of

4INEGAR in 30/02+ of cold water to slowdown themicro"ial hydrolysis of cyanogenic glycosides.

PRE4ENTION



3.o not graze wilted!frosted or drought stressed plants.

0.o not feed SORGHUM during early regrowth afterplants ha%e "een cut!when they are li#ely to "e mosttoxic.

8.6eed hungry cattle "efore allowing them to grazeforages which may contain high le%els of HC$.

.Thoroughly "oil the linseeds to remo%e any HC$content.

1.6ollow fertilizer recommendations to assure adeNuatesoil O'G.&%oid high le%els of soil nitrgen.

PRE4ENTION:

PROGNOSIS



t depends on time of initiation of therapy.fanimal sur%i%es for a day!no further treatment isreNuired.

PROGNOSIS:

cynide toxicity

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