Tgl/Jam : 22 September 2021 / 11.30 - 14.

00
Dosen : Drh Diah Nugrahani Pristihadi,
MSi
Kelompok : 4

CYANIDE POISONING

By

1. Kushaleni Bala B04188010

2. Nicole Sin Shuk Ching B04188012

3. Izzah Izzati Filzah B04188014

4. Shieh Zhi Yang B04188018

5. Rachel Leong Yi Zhen B04188020

DEPARTEMEN ANATOMI, FISIOLOGI DAN FARMAKOLOGI

FAKULTAS KEDOKTERAN HEWAN IPB
INSTITUT PERTANIAN BOGOR
BOGOR
2021
 INTRODUCTION

Cyanide is a toxic substance that can be deadly. The effects of cyanide are
very fast and can cause death within minutes. Cyanide can be produced by
bacteria, fungi and algae. Cyanide in low doses can be found in nature and in food
products. Cyanide is also found in cigarettes, motor vehicle fumes, and foodstuffs
such as spinach, bamboo, peanuts, tapioca flour and cassava. In addition, it can
also be found in some synthetic products. Cyanide is widely used in many
industries, especially in the manufacture of salts such as sodium, potassium or
calcium cyanide.
Cyanide undergoes a biochemical process that can bind and inactivate
certain enzymes, resulting in death or onset of histotoxic anoxia that is due to
cyanide molecules binding to the active site of cytochrome oxidase enzymes that
will result in the cessation of metabolism cells aerobically. This process is able to
interrupt the neuronal transmission within minutes. Cyanide can be removed
through certain processes before the molecules manage to enter the cell.
Symptoms caused by cyanide include headache, nausea, vomiting, shortness of
breath, chest palpitations, and excessive sweating until the patient is unconscious
and if not treated immediately, will result in death.

LITERATURE REVIEW

Cassava (Manihot esculenta), an edible tuberous root. It is a woody shrub

native to South America of the spurge family, Euphorbiaceae. Although a
perennial plant, cassava is extensively cultivated as an annual crop in tropical and
subtropical regions for its edible starchy tuberous root, a major source of
carbohydrates. It is often made into flour and contains cyanogenic glycosides,
which can result in fatal cyanide poisoning if not properly detoxified by soaking,
drying, and scraping before being consumed. Acute cyanide poisoning, often with
fatal consequences, can occur after eating a large amount of cassava. (Alitubeera
et al. 2019)
An antidote is a drug, chelating substance, or a chemical that counteracts
(neutralizes) the effects of another drug or a poison. Sodium nitrite is an inorganic
compound with the chemical formula NaNO2. It is a white to slightly yellowish
crystalline powder that is very soluble in water. Sodium thiosulfate is an inorganic
compound with the formula Na₂S₂O₃xH₂O. Typically it is available as the white or
colorless pentahydrate, Na₂S₂O₃·5H₂O. The solid is an efflorescent crystalline
substance that dissolves well in water. (Barbera et al. 2012) Sodium nitrite and
sodium thiosulfate administered by intramuscular injection are effective against
severe cyanide poisoning. (Bebarta et al. 2017) Sodium nitrite induces
methemoglobin in red blood cells, which combines with cyanide, thus releasing
cytochrome oxidase enzyme. Sodium thiosulfate donates a sulfur atom necessary
for the transformation of cyanide to thiocyanate by rhodanese, thus increasing the
activity of the endogenous detoxification system.

AIM

The aim of this practice is to learn the clinical signs of cyanide poisoning
and the effects of the antidotes sodium nitrite (NaNO2) and sodium thiosulfate
(Na2S2O3) on rabbits; to identify cyanide in plants using picrate paper and to
identify solutions of NaCN and KCN.

METHOD

Tools and Materials

Test tubes, test cube cork, test tube holder, glass dropper, mortar, pinset,
syringes, water bath. Cassava Leaves, NaCN 1%, HCl 5%, NaOH 50%, FeSO4
10%, FeCl3 10%, NaNO2 1%, Na2S2O3, aquadest, picrate paper.

Procedure

a. Identification of cyanide in plants

The first test tube is labelled as a negative control and it is filled with 3ml
of aquadest, the second test tube is labelled as positive control which is filled with
2-3 ml of NaCN 1% and 5 drops of HCl 5%. The cassava leaves are grinded and
smashed using the mortar, then the pieces of cassava leaves are inserted into the
third test tube. One piece of picrate paper is inserted into each tube with half of it
left hanging out from the test tube cork. The test tubes are then placed in the water
bath. The colour change of the picrate paper is observed.

b. Identification of cyanide in animal samples

NaCN 1%, 1ml of NaOH 50%, 3 drops of FeSO4 10% and 3 drops of
FeCl3 10% are added into a test tube. The test tube is heated in a water bath. Then
concentrated HCl is added after the test tube is cooled.

c. Clinical signs of cyanide poisoning in rabbits and its antidote

 The lab rabbit is weighed on a weighing scale. NaNO2 1% and Na2S2O3
5%, 2.5ml each are prepared in two separate syringes. NaCN 1% is given to the
rabbit per oral using syringe with the dose of 5-10 mg/kg body weight. The
clinical signs of the rabbit are observed. The antidotes are administered via the
vena auricularis of the rabbit. The first dose given is NaNO2 1%, while the second
is Na2S2O3 5%.

RESULTS

A. Identification of CN in plants

Table 1: Identification of cyanide from plants

No. Test tube Colour change of
picrate paper

1 Aquades (Negative control) No changes

2 NaCN 1% + HCl 5%(Positive Control) Yellow to brick red

3 Tapioca Leaves Yellow to brick red

B. Identification of CN from samples of animal origin

Sodium cyanide was tested against water and the test tube with sodium
cyanide turned blue upon adding HCl however the water did not

C. Clinical symptoms of cyanide and antidote poisoning

Clinical signs of Rabbit Cyanide was given When antidote is given

Overall appearance Coordination decreased Increased coordination

(Lost its integrity, lame)

Eyes Constricted Dilated and back to

normal

Respiration Rapid, shallow Less Rapid

 DISCUSSION

The term "cyanides" refers to compounds that have the – C≡N group in
their structure. Cyanides can be found in a variety of forms in the environment
(Kuyucak and Akcil 2013). Excessive cyanide exposure can be lethal. All
terminology for the same toxic principle include cyanide, hydrocyanic acid,
hydrogen cyanide (HCN), and prussic acid . Hydrogen cyanide (HCN) was
extracted for the first time from blue dye (Prussian blue), and due to its acidic
nature, it is also known as “prussic acid” (Clarke et al. 1981). It can also be found
in gaseous HCN, water soluble potassium cyanide and sodium cyanide, poorly
water soluble mercury, copper, gold, and silver cyanide salts, and other forms .
The colorless or pale blue liquid or gas hydrogen cyanide (HCN) has a subtle
bitter almond-like odor, whereas sodium cyanide (NaCN) and potassium cyanide
(KCN) are white crystalline powders (Newhouse and Chiu 2016). Cyanogenetic
plants are those that contain hydrocyanic acid (HCN), either free or in the form of
cyanogenic glycosides, and are the most important source of cyanide poisoning in
animals. These glycosides are normally non-toxic, but when they are hydrolyzed,
they become hazardous to both animals and humans. It has been claimed that if
the plant is frozen, cut, or chewed, damaged plant cells can release enzymes in
their vacuoles, and that these enzymes and cyanoglycosides can interact to
generate cyanure. The cyanogenic chemical is found mostly as a glycoside in
about 2650 plant species. Apricot kernel, peach kernel, cassava, almond, bamboo
shoot, sorghum, Japanese apricot, flaxseed, and other fruits and vegetables have
been consumed all over the world as food or herbal medicine (Gark 2004).

The danger of poisoning reduces as the plant matures, with older plants
and leaves containing less cyanogenic glycoside. If the plants contain more than
200ppm of these glycosides, they are deemed hazardous. When cyanide enters the
body, it is rapidly absorbed and circulated, where it combines with
methemoglobin to generate cyanmethemoglobin (Patel et al. 2014). Cyanide in the
blood inactivates the cytochrome oxidase enzyme by attaching to ferric (Fe+++)
iron within the enzyme. The cytochrome oxidase enzyme normally catalyzes the
final step of oxidative phosphorylation. This task is prevented from being
completed by the enzyme-cyanide complex. As a result, the enzyme is unable to
react with oxygen, and electron transport is impeded. The patient is unable to
utilise caloric oxygen, and cellular respiration instantly ceases. Death happens as a
result of histotoxic anoxia as a result of this process (Gupta 2012). As observed in
the experiment on tapioca leaves, traces of cyanide were discovered when the
yellow picrate paper turned brick red. This explains that there is a possibility
tapioca contains cyanide, as stated in the literature. In the experiment, NaCN was
used in place of the animal product. When sodium cyanide was tested against
water, the sodium cyanide test tube turned blue when HCl was added, but the
water did not. This is due to the existence of ferric hexacyanoferrate(iii)
(Fe4(Fe(CN)6)3 in the production of Prussian Blue.
Based on the results upon administering cyanide orally to the rabbit, it
showed that the rabbit lost its integrity, became lame, eyes were constricted and
respiration was rapid and shallow. This happens because cyanide irritates the
mucosa, both in the eyes, respiratory and digestive organs, this irritation is mainly
due to the strong alkaline strength of the hydrolysis of sodium and potassium
cyanide salts. The toxic effect of cyanide is to block the uptake and use of oxygen,
resulting in low levels of oxygen in the tissues. According to the Cummings
(2004), the initial symptoms and signs that occur after inhaling NaCN or ingesting
cyanide salts are anxiety, headache, nausea, confusion, vertigo, and hyperpnea,
followed by dyspnea, cyanosis (bluing), hypotension, bradycardia, and sinus or
AV arrhythmias. node. This cyanide poison inhibits body cells from getting
oxygen so that the heart and brain are most affected.
Then, the antidote was given to the rabbit intravenously via vena
auricularis. The rabbit recovered from cyanide toxicity after the second antidote
was given. It gained by its coordination and the pupil size also back to normal.
With the administration of a combination of sodium nitrite and sodium thiosulfate,
the toxic effect of cyanide will be stopped because the most important pathway of
cyanide excretion is from the formation of thiocyanate (SCN-) which is excreted
through urine. Sodium thiosulfate will work by accelerating elimination
mechanism, while sodium nitrite will work with competitive inhibition
mechanism (Knight and Walter 2001). For this reason, sodium nitrite and sodium
thiosulfate can be used as antidotes in cases of cyanide poisoning. But keep in
mind that the dose of sodium nitrite should not be excessive because it will cause
nitrite poisoning (Djunarko 2007).

CONCLUSION

In conclusion, cyanide toxicity is rapid acting and can cause central

nervous problem and respiratory problem. However, cyanide toxicity can be
reduced with antidote given on time and accurate amount. Tapioca leaves also
might contain cyanide and causes alterations in the leave colour. Animal product
which contains cyanide turned blue when adding HCL causing the formation of
(Fe4 (Fe(CN)6) 3.

REFERENCES
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