The effect of cyanide on catalase activities in the organs of birds (Gallus Domesticus)

CHAPTER ONE
INTRODUCTION
Cyanide, long considered a toxic, deadly substance, has been used as
a poison for thousands of years. The effects of a high dose of cyanide are
quick, and death occurs within minutes. Antidotes are effective if
administered in time. Cyanide is ubiquitous. It is present in some foods, in
the products of combustion of synthetic materials, and is widely used in
industry. Much of the cyanide used is in the form of salts, such as sodium,
potassium, or calcium cyanide.
Cyanide and cyanide compounds are present in air, water, soil, and
food due to both natural and anthropogenic sources. Plants and other living
organisms produce minute quantities of cyanide (Leduc 1984; Knowles
1988; Alström and Burns 1989; Davis 1991; Eisler 1991). Cyanogenic
glycosides are widely distributed in more than 1000 species of food plants
(notably cassava, peas, beans, and kernels of almonds) (Hulbert and Oehme
1968; Buck et al. 1973; Cade and Rubira 1982; Eisler 1991). Although
cyanide is ubiquitous in the environment, the highest environmental levels
are found in the vicinity of combustion sources (automotive exhaust, fires,
1

cigarette smoke, and solid waste incineration); in wastewaters from water
treatment facilities, iron and steel plants, and organic chemicals industries;
in landfills and associated groundwater; and in areas of road salt applications
and runoff (Towill et al. 1978; Fiksel et al. 1981; ATSDR 1991). The
toxicity of cyanide will vary according to the route of exposure. Inhalation is
the most rapid route of entry and results in the rapid onset of toxic effects.
Ingestion of soluble salts results in lower absorption via the gut and a faster
detoxification. The chemical form of cyanide will also affect toxicity.
Hydrogen cyanide is the most toxic cyanide form, whereas a complex
cyanide compound such as acetonitrile requires metabolism to release free
cyanide, and thus the toxic effects may be delayed by as much as 12 h
(Ballantyne 1984).
Cyanide is a highly toxic compound that is readily absorbed
and causes death by preventing the use of oxygen by tissues
(Egekeza et al., 1980). This toxicant is widespread in the
environment. Many naturally occurring substances as well as
industrial products have been shown to contain cyanide (Egekeza
et al., 1980). More than 2,000 species of plants are also known to
2

contain cyanogenic glycosides (Vennesland et al., 1982). It has
been reported that ingestion of cyanogenic glycosides in forage
crops can result in the death of grazing animals (Keeler et al.,
1987).many studies have reported the death of birds from
cyanide poisoning through several routes, including exposure to
cyanide salts or ingestion of cyanogenic plants (Wiemeyer et al.,
1986). Cyanide is produced by certain bacteria, fungi and algae
and is found in number of foods and plants. They are also found
although in small amounts in certain seeds e.g. those of peach
and bitter almonds. It can also be found in vegetables of the
cabbage family, grains like alfalfa and sorghum, roots like
cassava, potato, radish and turning, white clover and young
bamboo shorts.
The effect of Cyanide has been carried out on various enzymes in
plants and animals. However, limited reports exist on the metabolic fate of
cyanide on Catalase activities. This study was undertaken to acess the effect
of cyanide on the activities of catalase in the organs of Gallus Domesticus.
3

Significance of Study
1. It will provide a baseline data on the toxicity response of Gallus
domesticus after exposure to cyanide.
2. It will give an idea on the level of peroxidation activities in the organs
of Gallus domesticus after cyanide intoxication.
CHAPTER TWO
4

LITERATURE REVIEW
WHAT ARE CYANIDES
Cyanide is any chemical compound that contains the cyano
group (C≡N) which consists of a carbon atom triple bound to a
nitrogen atom. Inorganic cyanides are generally salts of the anion
CN-(Greenwood and Earushaw, 1997). The organic salts of
cyanide are called nitrites. All of the salts and organic cyanide
are made from the parent compound called hydrogen cyanide,
hydrocyanic acid or prussic acid.
HCN is a highly valuable precursor to many chemical
compounds ranging from polymers to pharmaceuticals. This is a
simple compound that only contains hydrogen, carbon and
nitrogen.
Cyanide occurs naturally, they are found in spoiled
cabbage, mustard cauliflower and other member of Brassica
family. Some fruits like cherries, apples and bitter almonds
5

contain a tiny amount of cyanohydrins that degrade to release
hydrocyanide.
HISTORY OF CYANIDE
The early origin of cyanides begins with an experiment
performed by J.C. Dippel and H. Diesbach in 1704 in Berlin. In
the simple way they heated dried blood with potash (potassium
carbonate) and green vitraiol (Iron sulfate) that produced an
intensely blue pigment called blue Berlin in Germany or Prussian
blue in English.
In 1782, a Swedish chemist by name schecle heated the
pigment with diluted sulfuric acid and he got a combustible gas
that formed acid when dissolved in water that he called “Berlin
Blue Acid” or we call recently the gas with hydrogen cyanide.
The name “Cyanide” was in use from the Greek word of
“Kyamos” that represent blue.
In 1811, a French chemist Gay Lussac succeeded in
determining the hydrogen cyanide composition as already
6

mentioned, the molecule contains one atom each of hydrogen,
carbon and nitrogen.
In World War 1, the French were the only advocates of
using cyanide. Since hydrogen cyanide is higher than air and
subject to variation with the wind, the agent proved to be
difficult to be delivered effectively enough to gain the
concentration needed to affect the enemy. To reduce the
volatility and permit greater delivery potential to the enemy, the
French devised cyanogens chloride which basically chlorine gas
to hydrogen cyanide at O0
C. This irritating peppery and lethal gas
had limited use on the battle field after being introduced in
September 1916. In 1916, the Austrians chose to experiment with
hydrogen cyanide mixed with bromide instead of chloride. This
agent seems difficult to handle and corroded the storage tanks so
they abandoned this agent.
More recent history indicates that Iraq may have used
cyanide against the Kurds, the Iranians and a Syrian Village in
7

1981. The Aum Shinriko in Japan left potassium cyanide and
dilute sulfuric acid in the restrooms of the same subway two
weeks After they had killed 12 people and 5,500 with a sarin
nerve gas attack in 1995. The materials were discovered before
they could be employed. Tylenol capsules deliberately
contaminated with cyanide were responsible for seven deaths in
1982.
Though uncommon, most information about cyanide
poisoning comes from the civilian sector since hundreds of
thousands of pound of cyanide salts and organic cyanides are
produced and used in industries every year.
In February 2000, a mine accident in baia mare Romania
released 100,000cubic meters of cyanide contaminated water into
the Tizna River system and eventually the Danube which caused
a large fish and plant kill in Romania, Yugoslavia and Hungary
and closed the public drinking system for an extended period of
time to over 2 million people. Local authorities called it one of
8

the worse environmental catastrophes since Chernobyl (United
Nations Economic commission for Europe, 2000).
TYPES OF CYANIDE
The common types of cyanide are:
1. Sodium cyanide
2. Calcium cyanide
3. Potassium cyanide which are white solids and have a bitter
almond like odour in damp air.
Hydrogen cyanide is a colourless gas form of cyanide
which also has a faint bitter almond like odour that some people
are unable to detect due to genetic trait.
PHYSICAL AND CHEMICAL PROPERTIES OF SODIUM
CYANIDE
Sodium cyanide is also known as cyanide of sodium
hydrocyanic acid sodium salt. It is a white powder or solution in
water. Liquid cyanide contains 30% cyanide while solid cyanide
is 98% pure in Australia. It is principally used in Australia in
9

gold mining industry to extract gold from gold bearing ore using
the carbon in leach and carbon in pulp processes with 98% of
Australia’s gold production dependent on it.
Sodium cyanide is also used in nickel production as an
arsenic suppressant. A small amount of sodium cyanide is also
used in electroplating and metal cleaning baths, metal hardening
and insecticides.
10

Physical state White deliquescent solid
Melting point 5630
c
Boiling point 14960
c
Specific gravity 1.6
Solubility in water Soluble
PH String alkaline (aqueous solution)
Vapour density 1.7
Stability Stable under ordinary condition
Table 1, Physical and chemical properties of sodium
cyanide
PHYSICAL AND CHEMICAL PROPERTIES OF
POTASSIUM CYANIDE (KCN)
Potassium cyanide (KCN) is an organic compound with the
formular KCN. It is a colourless crystalline compound similar in
appearance to sugar. It is highly soluble in water. Most
potassium cyanide (KCN) is used in gold mining, organic
11

synthesis and electroplating. Smaller applications include
jewelry for chemical gilding and burring (Andreas et al.,
2006).KCN is highly toxic.
Molecule formula KCN
Molar mass 65.12g/mol
Appearance white crystalline solid
Melting point 634.50
c
Boiling point 16250
c
Solubility in water 71.6g/100ml (1500
c)
100g/100ml(100c)
Solubility in methanol 4.9g/100ml (200
c)
Solubility in glycerol Soluble
PHYSICAL AND CHEMICAL PROPERTIES OF
HYDROGEN CYANIDE
Hydrogen cyanide is known to be parent compound of
which all salts and organic cyanides are formed with a chemical
formula of HCN.
12

Molecule weight 27.03
Boiling point (at 760mmHg) 260
c (790
F)
Specific gravity 0.7 at 200
c (680
F)
Vapour density 0.94
Melting point 1340
c (7.880
F)
Vapour pressure 200
c (680
F)
Solubility Miscible with water and alcohol
and slightly soluble in ether
Hydrogen cyanide is a colourless, extremely poisonous and
highly volatile liquid that boils slightly above room temperature
at 260
c (78.80
F). HCN has a faint bitter, almond like odour that
some people are unable to detect due to genetic trait.
SOURCES OF CYANIDE
Cyanides are produced by certain bacteria, fungi and algae
and are found in a number of food and plants. Cyanides are
found, although in small amounts in certain seeds and stones e.g.
those of apple, mango peach and bitter almonds. In plants,
13

cyanides are usually bound to sugar molecules in form of
cyanogenic glycocides and defend the plant against herbivores.
Cassava roots (also called manioc), an important potato like food
grown in tropical countries (and the base from which tapioca is
made) also contain cyanogenic glycoside, (Vetter, 2000; Jone,
1998).
Hydrogen cyanide is produced by the combustion or
pyrolysis of certain materials under oxygen deficient conditions.
For example, it can be detected in the exhaust of internal
combustion engines and tobacco smoke. Certain plastic
especially those derived from acrybritrile, release hydrogen
cyanide when heated or burnt.
CYANIDE TOXICITY
Many types of cyanide are highly toxic, and cyanide
poisoning occurs when a living organism is exposed to a
compound that produces cyanide ions when dissolved in water.
Common poisonous cyanide compound include:
14

a) Hydrogen cyanide gas and the crystalline solids.
b) Potassium cyanide
c) Sodium cyanide
The cyanide ion halts cellular respiration by inhibiting an
enzyme in mitochondria called cytochrom C oxidase.
MECHANISM OF ACTION OF CYANIDE TOXICITY
The cyanide anion is an inhibitor of the enzyme cytochrome
C oxidase in the fourth complex of the electron transport chain
(found in the membrane of the mitochondria of eukaryotic cells).
It attaches to the Iron within this protein, it binding of cyanide to
this cytochrome prevents transports of electron from cytochrome
C oxidase to oxygen. As a result, the electron transport chain is
disrupted, meaning that the cell can no longer aerobically
produce ATP for energy.
Tissues that depend highly on aerobic respiration such as
the central nervous system and the heart are particularly
affected, (Carlsson et al., 2001).
15

TYPES OF TOXICITY
There are two types of cyanide toxicity namely.
a) Acute toxicity
b) Chronic toxicity
ACUTE TOXICITY
Inhalation of high concentrations of cyanide causes a coma
milk seizures, apnea and cardiac arrest with death following in a
matter of minutes. At lower doses, loss of consciousness may be
preceded by general weakness, giddiness, headaches, vertigo,
confusion and perceived difficulty in breathing.
At the first stages of unconsciousness, breathing is often
sufficient or even rapid, although the stage of the victim
progresses towards a deep coma sometimes accompanied by
pulmonary edema and finally cardiac arrest. Skin colour goes
16

pink from cyanide hemoglobin complexes. A fatal dose for
humans can be as low as 1.5/kg body weight.
Cyanide toxicity can occur following the ingestion of
amygdaline (found in almonds and apricot kernels and marketed
as an alternative cancer cure). Prolonged administration of
nitroprusside and after exposure to gasses produced by the
combustion of synthetic materials (Baselt 2008, Frison, 2006).
Exposure to lower than lethal amounts of cyanide but still much
higher than safe levels will arise blurred vision followed by a
feeling of coldness rushing through the blood and tightness in the
chest. This is followed by severe shortness of breath and
hyperventilation for up to 30 seconds (provided the person has
run from the site of exposure) along with a near or total syncope.
Feeling of well being will return in about a minute if the
individual has moved to fresh air.
CHRONIC TOXICITY
17

Exposure to lower levels of cyanide over a long period of
(e.g. after use of cassava roots as a primary food source in
tropical Africa) results in increased blood cyanide level which
can results in weakness and variety of symptoms including
permanent paralysis. Cyanide does not accumulate or
biomagnify, so chronic exposure to sub lethal concentrations of
cyanide does not appear to results in acute toxicity. However,
chronic cyanide toxicity has been observed in individuals whose
diet include significant amounts of cyanogenic plant such as
cassava. Chronic cyanide exposure is linked to demydination
lesions of the optic nerve atoxia, hyperrtonia, leber’s optic
atrophy, goiters and depressed thyroid functions.
Although chronic cyanide intoxication exists, cyanide has a
low chronic toxicity. Repeated sublethal does of cyanide seldom
result in cumulative adverse effects. Many species can tolerate
cyanide in substantial yet sublethal intermittent doses for a long
period of time. There is no evidence that chronic cyanide
18

exposure has teratogenic mutagenic or carcinogenic effects
(Leuschner et al., 1983).
ENVIRONMENTAL AND HEALTH EFFECT OF CYANIDE
EFFECT ON WILDLIFE
Although cyanide reacts readily in the environment and
degrades or form complexes and salts of varying stabilities, it is
toxic to many living organism at very low concentration.
EFFECTS ON MAMMALS
Cyanide toxicity to mammals is relatively common due to
the large number of cyanogenic forage plants such as sorphum,
Sudan grasses and corn. Concentrations of cyanide in these
plants are typically highest in the spring during blooming. Dry
growing conditions enhances the accumulation of cyanogenic
glycosides in certain plants as well as increase the use of these
plants as forage.
19

Reported Oral LD50 for mammals range from 2.1
milligrams per kilogram of body weight (coyote) to 6.0-10-0
milligrams per kilogram of body weight (laboratory while rats).
Symptoms of acute poisoning usually occur within ten minutes of
ingestion, including initial excitability with muscle tremors,
salivation, lacrimation, defecation, urination, labored breathing
followed by muscular in co-ordination, gasping and convulsions.
In general, cyanide sensitivity for common livestock decrease
from cattle to sheep to horses, pigs, deer and elk appear to be
relatively resistant.
Although present in the environment and available in many
plant species, cyanide toxicity is not widespread done to member
of significant factors, cyanide has low persistence in the
environment and is not accumulated or stored in any mammal
studied. There is no reported biomagnifications of cyanide in the
food chain.
EFFECTS ON AQUATIC ORGANISMS
20

Fish and aquatic invertebrates are particularly sensitive to
cyanide exposure. Concentrations of free cyanide in the aquatic
environment ranging from 5.0 to 7.2 microorganisms per liter
reduce swimming performance and inhibit reproduction in many
species of fish.
Invertebrates experiences adverse non-lethal effect at 18 to
43 microorganism per liter free cyanide and lethal effects a 30 to
100 microorganism per liter (although concentrations in the
range of 3 to 7 microorganisms per liter caused death in the
amphipod (Gammarus Pulex). Algae and macrophytes can
tolerate much high environmental concentrations of free cyanide
than fish and invertebrates and do not exhibit adverse effects on
plants. However, differing sensitivities to cyanide can result in
changes to plant community structure with cyanide exposure
leaving the plant community dominated by less sensitive species.
21

The toxicity of cyanide to aquatic life is probably caused
by hydrogen cyanide that has ionized, dissociated or
photochemical decomposed from compounds containing cyanide.
EFFECTS ON BRIDS
Reported Oral LD50 for birds range from 0.8 milligrams
per kilogram of body weight (American racing pigeon) to 11.1
milligram per kilogram of body weight (Domestic chicken).
Symptoms including panting, eye blinking, salivation and
lethargy appear within one half to five minutes after ingestion in
more sensitive species and up to ten minutes after ingestion by
more resistant species. Exposure to high dose resulted in deep
laboured breathing followed by gasping and shallow intermittent
breathing in all species.
Mortality topically occurred in 15 to 30 minutes. However,
birds that survived for one hour frequently recovered possibly
22

due to the rapid metabolism of cyanide to thiocyanate and its
subsequent excretion. Ingestion of WAD (Weak acid dissociable)
cyanide solutions by birds may drink water containing WAD
cyanide that is not immediately fatal, but which breaks down in
the acidic conditions to be toxic. Sublethal effects of cyanide
exposure to birds such as an increase in their susceptibility to
predators have not been fully investigated and reported.
CYANIDE DETOXIFICATION
Detoxification is the physiological or medicinal revival of
toxic substance form a living organism, additionally
detoxification can also be refer to as the period of withdrawal
during which an organism returns to homeostasis after long term
use of an addictive substance.
In conventional medicine, detoxification can be achieved
by decontamination of poison ingestion and the use of antidotes
as well as techniques such as dialysis and chelation therapy.
23

The United States standard cyanide antidote kit first uses as
mall inhaled dose of amyl nitrite, followed by intravenous
sodium nitrite, followed by intravenous sodium thiuosulfate.
Hydroxocabalamni is newly approved in the US and is available
in cyanokit antidote kits. Alternative methods of treating cyanide
intoxication are used in other countries.
MODE OF ACTION
Nitrites and Sodium Thiosulfate: The nitrites oxidize some of
the hemoglobin’s iron from the terms state to the ferric state,
converting the hemoglobin into methemoglobin cannot carry
oxygen and methemoglobinemia needs to be treated in turn with
methylene blue.
Cyanide preferentially bonds to methemoglobin rather than
the cytochrome oxidase, converting nuthemoglobin into
cyanimethemoglobin. In the last step, the intravenous sixfrim
thiosulfate converts the cyanmethemoglobin to thiocyanate,
24

sulfite and hemoglobin. The thiocyanate is then excreted in the
urine.
HYDROXOCOBALAMIN
Hydroxocobalamin, a form of vitamin B12 made by bacteria.
Hydroxocobalamin works both within the intravascular space and
within the cells to combat cyanide intoxication. This versatility
contrast with methenoglobin which acts only within the vascular
space as an antidote.
Administration of sodium thiosulfate improved the ability
of the hydroxocobalamin to detoxify cyanide poisoning. This
treatment is considered so effective and in nacreous that it is
administered routinely in Paris to victims of smoke inhalation to
detoxify any cyanide intoxication. However, it is relatively
expensive and not universally available.
THIOCYANATE
Thiocyanate also known as rhodanide is the anion (SCN), it
is the conjugate base of thiocyanic acid. Common derivatives
25

include the colourless salts potassium thiocyanate and sodium
thiocyanate. Organic compounds containing the functional group
SCN are also called thiocyanates.
Thiocyanate is analogous to the cyanate ion, where in
oxygen is replaced by sulfur. Thiocyanate used to be known as
rhodanide (from a Greek work for rose) because of the red colour
of its complexes with iron. Thiocyanate is produced by the
reaction of elemental sulfur or thiosulfate with cyanide.
8CN-
+ S8 8SCN-
CN-
+ S2O3
2-
SCN-
+ SO3
2-
The second reaction is catalyzed by the enzyme
sulfotransferase known as rhodanase and may be relevant to
detoxification of cyanide in the body.
S = C = N S – C ≡ N
Thiocyanate is known to be an important part in the
biosynthesis of hypothiocyanite by a lactoperoxidase. Thus the
26

complete absence of thiocyanate or redacted thiocyanate in the
human body can lead to diseases like cystic fibrosis. Thiocyanate
is of high importance in the human host reference system.
Thiocyanate is a metabolite of sodium nitroprussise after
rhodanase catalyses its reaction with thiosulfate.
Basic Processes Involved in the Metabolism of Cyanide (ATSDR, 1997)
27

CYANIDE ANTIDOTES
Management of cyanide poisoning in both children and
adults entails removal of the victim from the source of cyanide in
inhalation exposure, gastric decontamination with aspiration of
gastric contents and administration of activated charcoal in the
event of poisoning by ingestion. (If care for the victim begins
soon after ingestion). Ensuring supportive care include 100%
oxygen, cardiopulmonary resuscitation if necessary and an
appropriate antidote (megerbane et al., 2003).
Because cyanide toxicity can culminate quickly in death,
rapid intervention is crucial and is usually undertaken on the
basis of a presumptive diagnosis before confirmatory blood
cyanide concentrations are available.
The cyanide antidote kit is the only cyanide antidote
currently commercially available in the United States, although
other antidotes are available in other countries. (Dart and
Bogdan, 2004). The antidote kit is composed of amyl, nitrite,
28

sodium nitrite and sodium thiosulfate. Amyl nitrite contained in
ampoules intended to be crushed and the contents inhaled are
administered to stabilize the victim before intravenous
administration of sodium nitrite and sodium thiosulfate.
The nitrite moieties from amyl nitrite ad sodium nitrite
oxidase heamoglobin to create methemoglobin which competes
with cytochrome oxidase for the cyanide ion, binding of cyanide
to methemoglobin frees the cytochrome necessary for aerobic
cellular respiration. The extent of methemoglobinania required to
achieve the desired therapeutic benefit is uncertain, a prudent
strategy is to use lowest amount of methemoglobinania that
reverse the cyanide (Pearce et al., 2003). Another mechanism by
which nitrites might achieved their therapeutic benefits involves
induced alteration in the nitric oxide redox path way. (Johnson et
al., 1998). Sodium thiosulfate serves as a sulphur donor that
increases the rate of rhodanase catalyzed transformation of
cyanide to much less toxic thiocyanate.
29

MEDICAL USES OF CYANIDE
The cyanide compound sodium nitroprusside is used mainly
in clinical chemistry to measure urine keline bodies mainly as a
follow up to diabetic patients.
On occasion, it is used in emergency medical situations to
produce a rapid decrease in blood pressure in humans. It is also
used as a vasodilator in vascular research. The cobalt in artificial
vitamin B12 contains a cyanide ligand as an artifact of the
purification process. This must be removed by the body before
the vitamin molecule can be activated for biochemical use.
During World War I, copper cyanide compound was briefly
used by Japanese physicians for the treatment of tuberculosis and
leprosy.
CATALASE AS AN ENZYME
Catalase was first noticed in 1811 when Louis Jacques Thénard, who
discovered H2O2 (hydrogen peroxide), suggested its breakdown is caused by
an unknown substance. Catalase is a common enzyme found in nearly all
30

living organisms exposed to oxygen. It catalyzes the decomposition of
hydrogen peroxide to water and oxygen (Chelikani et al., 2004). It is a very
important enzyme in reproductive reactions Likewise, catalase has one of
the highest turnover numbers of all enzymes; one catalase molecule can
convert millions of molecules of hydrogen peroxide to water and oxygen
each second.(Goodsell, 2004). Catalase is a tetramer of four polypeptide
chains, each over 500 amino acids long. It contains four porphyrin heme
(iron) groups that allow the enzyme to react with the hydrogen peroxide.
The optimum pH for human catalase is approximately 7, (Maehly A and
Chance, 1954) and has a fairly broad maximum (the rate of reaction does not
change appreciably at pHs between 6.8 and 7.5). The pH optimum for other
catalases varies between 4 and 11 depending on the species with the
optimum temperature varying across species (Toner, et al, 2000).
ACTION AND FUNCTION OF CATALASE
The reaction of catalase in the decomposition of living tissue:
2 H2O2 → 2 H2O + O2
Source: Toner, et al., 2000.
31

The presence of catalase in a microbial or tissue sample can be tested
by adding a volume of hydrogen peroxide and observing the reaction. The
formation of bubbles, oxygen, indicates a positive result. This easy assay,
which can be seen with the naked eye, without the aid of instruments, is
possible because catalase has a very high specific activity, which produces a
detectable response (Boon, et al., 2007).
STRUCTURE AND MOLECULAR MECHANISM
While the complete mechanism of catalase is not currently known,[13]
the reaction is believed to occur in two stages:
H2O2 + Fe(III)-E → H2O + O=Fe(IV)-E(.+)
H2O2 + O=Fe(IV)-E(.+) → H2O + Fe(III)-E + O2
[13]
Here Fe(III)-E represents the iron center of the heme group attached
to the enzyme. Fe(IV)-E(.+) is a mesomeric form of Fe(V)-E, meaning the
iron is not completely oxidized to +V, but receives some "supporting
electrons" from the heme ligand. This heme has to be drawn then as a
32

radical cation (.+). As hydrogen peroxide enters the active site, it interacts
with the amino acids Asn147 (asparagine at position 147) and His74,
causing a proton (hydrogen ion) to transfer between the oxygen atoms. The
free oxygen atom coordinates, freeing the newly formed water molecule and
Fe(IV)=O. Fe(IV)=O reacts with a second hydrogen peroxide molecule to
reform Fe(III)-E and produce water and oxygen (Boon et al., 2000). The
reactivity of the iron center may be improved by the presence of the
phenolate ligand of Tyr357 in the fifth iron ligand, which can assist in the
oxidation of the Fe(III) to Fe(IV). The efficiency of the reaction may also be
improved by the interactions of His74 and Asn147 with reaction
intermediates (Gaetani, et al., 1996). In general, the rate of the reaction can
be determined by the Michaelis-Menten equation (Toner et al., 2000).
Catalase can also catalyze the oxidation, by hydrogen peroxide, of
various metabolites and toxins, including formaldehyde, formic acid,
phenols, acetaldehyde and alcohols. It does so according to the following
reaction:
H2O2 + H2R → 2H2O + R
33

The exact mechanism of this reaction is however not known but any heavy
metal ion (such as copper cations in copper(II) sulfate) can act as a
noncompetitive inhibitor of catalase. Also, the poison cyanide is a
competitive inhibitor of catalase, strongly binding to the heme of catalase
and stopping the enzyme's action.
CELLULAR ROLE IN METABOLISM
Hydrogen peroxide is a harmful byproduct of many normal metabolic
processes; to prevent damage to cells and tissues, it must be quickly
converted into other, less dangerous substances. To this end, catalase is
frequently used by cells to rapidly catalyze the decomposition of hydrogen
peroxide into less-reactive gaseous oxygen and water molecules (Gaetani, et
al., 1996). The true biological significance of catalase is not always
straightforward to assess: Mice genetically engineered to lack catalase are
phenotypically normal, indicating this enzyme is dispensable in animals
under some conditions (Ho, et al., 2004). A catalase deficiency may increase
the likelihood of developing type 2 diabetes. Some humans have very low
levels of catalase (acatalasia), yet show few ill effects. The predominant
34

scavengers of H2O2 in normal mammalian cells are likely peroxiredoxins
rather than catalase (Eisner and Aneshansley (1999); Beheshti, N. and
McIntosh, 2006).
Human catalase works at an optimum temperature of 37°C, which is
approximately the temperature of the human body. In contrast, catalase
isolated from the hyperthermophile archaea Pyrobaculum calidifontis has a
temperature optimum of 90°C. (Brioukhanov, et al., 2006). Catalase is
usually located in a cellular, bipolar environment organelle called the
peroxisome. Peroxisomes in plant cells are involved in photorespiration (the
use of oxygen and production of carbon dioxide) and symbiotic nitrogen
fixation (the breaking apart of diatomic nitrogen (N2) to reactive nitrogen
atoms) (Brioukhanov, et al., 2006). Hydrogen peroxide is used as a potent
antimicrobial agent when cells are infected with a pathogen. Catalase-
positive pathogens, such as Mycobacterium tuberculosis, Legionella
pneumophila, and Campylobacter jejuni, make catalase to deactivate the
peroxide radicals, thus allowing them to survive unharmed within the
host(Alberts, et al., 2006). Catalase contributes to ethanol metabolism in the
35

body after ingestion of alcohol, but it only breaks down a small fraction of
the alcohol in the body (Srinivasa et al., (2003).
DISTRIBUTION AMONG ORGANISMS
All known animals use catalase in every organ, with particularly high
concentrations occurring in the liver (Gaetani, et al., 1996). One unique use
of catalase occurs in the bombardier beetle. This beetle has two sets of
chemicals ordinarily stored separately in its paired glands. The larger of the
pair, the storage chamber or reservoir, contains hydroquinones and hydrogen
peroxide, whereas the smallest of the pair, the reaction chamber, contains
catalases and peroxidases. To activate the noxious spray, the beetle mixes
the contents of the two compartments, causing oxygen to be liberated from
hydrogen peroxide. The oxygen oxidizes the hydroquinones and also acts as
the propellant. The oxidation reaction is very exothermic (ΔH = −202.8
kJ/mol) which rapidly heats the mixture to the boiling point. Catalase is also
universal among plants, and many fungi are also high producers of the
enzyme. Almost all aerobic microorganisms use catalase. It is also present
in some anaerobic microorganisms, such as Methanosarcina barkeri ( ).
36

CATALASE USES AND APPLICATION
Catalase is used in the food industry for removing hydrogen peroxide
from milk prior to cheese production. Another use is in food wrappers
where it prevents food from oxidizing (Cook, et al., 1996) Catalase is also
used in the textile industry, removing hydrogen peroxide from fabrics to
make sure the material is peroxide-free (Hengge, 1999). A minor use is in
contact lens hygiene - a few lens-cleaning products disinfect the lens using a
hydrogen peroxide solution; a solution containing catalase is then used to
decompose the hydrogen peroxide before the lens is used again. Hengge,,
1999). Recently, catalase has also begun to be used in the aesthetics
industry. Several mask treatments combine the enzyme with hydrogen
peroxide on the face with the intent of increasing cellular oxygenation in the
upper layers of the epidermis
CHAPTER THREE
MATERIALS AND METHODS
3.1 MATERIALS
37

The materials used in this study include;
1. Chicken (Broiler)
2. Starter /growers mash
3. Wooden cage
4. Centrifuge
5. Spectrum lab 7555 Uv-vis spectrophotometer
6. Test-tube
7. Test tube racks
8. Glass cuvettes
9. EDTA bottles
10. masking tape
11. Syringes
12. Ceramic mortar and pestle
13. Beaker
14. Refrigerator
15. Weigh balance
16. Pipettes
17. pH-meter
38

18. measuring Cylinder
3.1.1 CHEMICALS
Potassium cyanide
Barbituric acid
Hydrodiloric acid
Orthophosphoric acid
Sodium acetate
Nitric acid
Ferric nitrate
Trichloroacetic acid
Chloramines T
3.1.2 EXPERIMENTAL BIRDS
Male and female chickens (Broilers) weighing 0.005kg
were used for the study. All birds were feed with growersmash
39

(live stock feeds Plc, Ikeja, Nigeria: protein 15%min, fat 3.5%,
fibre 7.5% max, calcium 1.0%min, phosphorus 0.4%min and net
energy 24gkcal/kgmin) and tap water.
3.2 METHOD
3.2.1 EXPERIMENTAL DIET
The chicken (Boilers) were divided into three (3) groups A,
B and C. Group A and B were experimental birds feed with
different concentration of potassium cyanide mixed with the
growers mash every morning and ordinary growers mash in the
might with tap water. Group C birds were the control, and they
were fed with growers mash and tap water.
The initial weights of the birds before and during the weeks
were recorded.
3.2.2. COLLECTIONS OF SAMPLES
40

At the end of 4, 8 and 12 weeks, three (3) birds were
weighed and killed from the three (3) different cages and their
kidneys were collected.
3.2.3 TREATMENT OF SAMPLE
10mg of the kidney were homogenized with 20ml of
orthophosphoric acid in a mortar and was then transferred back
to the plastic container for analysis.
3.2.4 DETERMINATION OF CYANIDE
0.1ml of homogenate is collected and placed in a test tube,
0.5ml phosphate buffer were added. 0.6ml ofNaOH and 2.8ml 6.0
pH buffer were added. Add 0.2ml of chloramineT, add 0.8ml of
colour reagent. Wait for 15minutes and read spec at 605mn.
3.2.5 PRINCIPLE
The method of rapid determination of the level of cyanide
in the kidney was carried out by the method of Esser´s 1993
3.2.6 STATISTICAL ANALYSIS
41

The data were analyses using the analysis of variance
(ANOVA) technique.
CHAPTER FOUR
PRESENTATION OF RESULT
The effect of Cyanide on the activities of Catalase in the organs of
Gallus Domesticus was investigated. The result is therefore presented below.
42

Table 4.1a; Level of Catalase activity in Gallus domesticus exposed to Cyanide invivo
after four weeks
Organ CONTROL 1mg 2mg 3mg
Liverxi
30.34±5.93a
22.43±4.24a
18.19±8.17b
12.34±3.21b
Kidneyxi
38.42± 3.50a
36.50±5.89a
29.36±5.87b
29.39±6.21b
Brainxi
38.32±6.05a
35.81±4.8a
28.59±2.89b
18.41±8.18b
Heartxi
40.26±6.91a
35.83±7.34a
28.41±6.10b
18.31±4.74b
All values are expressed as Mean ±SD. Values followed by different letters showed level of
significant difference (P<0.05) when compared across concentrations; Organs followed by
different superscript of x, y, z are significantly different across the weeks, organs followed by
different superscript of i and j are significantly different when compared food against in vivo.
Fig. 4.1a: Graph of Catalase activity after 4 weeks in birds dosed in vivo.
Table 4.1b: Level of Catalase activity in Gallus domesticus exposed to Cyanide in
food after four weeks
Liverxj
30.34±5.93a
28.45±5.9 a
25.43±7.17 a
20.74±7.85 b
Kidneyxj
38.42± 3.50 a
35.47±4.90 a
32.98±4.48 a
25.18±6.13b
43

Brainxi
38.32±6.05a
32.53±3.25a
28.42±6.9a
22.13±2.57b
Heartxj
40.26±6.91a
36.51±6.68a
32.29±7.9a
24.60±3.85b
Fig. 4.1b: Graph of Catalase activity in Birds Dosed Through Food after 4
weeks
Table 4.2a: Level of Catalase activity in Gallus domesticus exposed to
Cyanide in vivo after eight weeks
Liverxi
45.20±5.78a
40.59±6.68a
34.95±4.86b
29.56±7.76b
Kidneyxi
39.47±7.09a
34.80±7.73a
29.23±4.07b
22.22±6.18b
44

Brainxi
40.43±3.87a
36.12±4.67ab
32.02±6.61b
25.16±5.43b
Heartxi
40.52±3.17a
35.33±5.08a
30.31±6.96b
24.69±6.93b
Fig. 4.2a: Graph of Catalase activity in Birds Dosed in vivo after 8 weeks
Table 4.2b: Level of Catalase activity in Gallus domesticus exposed to
Cyanide in food after eight weeks
Liverxj
45.20±5.79 a
42.29±5.86 a
38.99±3.57 a
32.23±4.98b
Kidneyxj
39.47±7.09 a
37.95±4.5 a
32.51±5.24ab
28.17±3.02b
Brainxi
40.44±3.87a
37.98±3.47a
33.37±6.94a
28.01±5.04b
45

Heartxj
40.53±3.17a
37.33±7.98a
33.18±5.92a
27.30±5.04b
Fig. 4.2a: Graph of Catalase activity in birds dosed through food after 8
weeks
Table 4.3a: Level of Catalase activity in Gallus domesticus exposed
to Cyanide in vivo after Twelve weeks
Liverxi
47.50±5.88a
40.21±3.92ab
34.33±5.05b
23.08±8.97c
Kidneyxi
45.36±4.91a
40.13±5.39ab
33.23±6.03b
20.30±6.95c
Brainyi
48.85±2.21a
43.27±6.20ab
38.38±7.93b
28.64±5.33c
46

Heartxi
47.27±7.03
a
41.32±2.10ab
37.27±4.94b
26.19±1.71c
Fig. 4.3a: Graph of Catalase activity in birds dosed cyanide invivo after
12 weeks
Table 4.3b: Level of Catalase activity in Gallus domesticus exposed
to Cyanide in food after Twelve weeks
Liverxj
47.50±5.89a
43.11±4.98ab
39.20±7.97a
33.26±8.07b
Kidneyyj
45.36±4.91a
41.74±3.52 a
37.83±2.22 a
31.28±4.25 a
Brainxi
48.85±2.21a
45.64±6.67a
41.26±5.89a
35.64±7.54a
Heartxj
47.27±7.03
a
44.61±1.49a
40.89±5.49a
32.35±6.82a
47

Fig. 4.3a: Graph of Catalase activity in birds dosed cyanide through food
after 12 weeks
Chapter Five
Discussion and Conclusion
The present study focused on the impact of cyanide toxicity on the
activities of Catalase in the organs (Liver; Kidney; Brain and Heart) of birds
(Gallus Domesticus). The findings from the study showed that there was a
48

reduction on the activities of catalase in the organs exposed to cyanide at
different concentrations invivo and through food after 4, 8 and 12 weeks
respectively. This reduction was significant after four and eight weeks in
the organs of the birds dosed 2mg and 3mg cyanide in vivo when compared
to control (P<0.05). However, the birds’ dosed cyanide through food had no
significant difference in the activities of catalase in all the organs assessed
except the birds dosed 3mg of cyanide. In the same vein, the birds exposed
to cyanide in vivo showed a significant difference in the level of catalase
activity in the organs of Gallus Domesticus dosed 2mg and 3mg except for
those dosed 1mg.
The birds dosed through food however, had no significant difference
in all of the organs except for the liver which showed variation in the liver at
the 3mg cyanide dose when compared to control. On comparing the level of
significance that exists relative to route of exposure and length of exposure,
catalase activity was not significant when compared across the weeks but
showed there was a rise on the activities of Catalase in all of the organs
irrespective of the route of exposure, and the differences that occured when
compared to control birds at various stages of the study. Although this
49

increase was not statistically significant, a level of differences on catalase
activity occurred when compared food versus in vivo.
The findings in this study show that cyanide intoxication in birds is
capable of reducing the activities of catalase in the (Liver, kidney, brain and
heart). Cyanide has been previously shown to induce oxidative stress and
damage in a number of biological systems (Johnson et al., 1987). Catalase is
a very important enzyme and is frequently used by cells to rapidly catalyze
the decomposition of hydrogen peroxide into less-reactive gaseous oxygen
and water molecules (Gaetani, et al., 1996). Cyanide on the other hand, has
been previously shown to induce oxidative stress and damage in a number of
biological systems. Administration of sub lethal doses of potassium cyanide
to CF1 mice induced lipid peroxidation in the brain (Johnson et al., 1987);
several other studies document an increase in reactive oxygen species
following cyanide exposure through the inhibition of the mitochondrial
respiratory chain at the ubiquinone-cytochrome b site, producing superoxide
anions and the hydro peroxides. In addition, the generation of
hydroxyperoxide was also seen in cyanide-treated PC12 cells (Ardelt et al.,
1994; Mills et al., 1996), rat leukemia 2H3 cells (Arai et al., 1999), and
50

cerebellar granule cells (Gunasekar et al., 1996) and have been identified as
a potent inhibitor of the enzymatic antioxidants such as catalase, superoxide
dismutase, and glutathione peroxidase (Ardelt et al., 1989; Kanthasamy et
al., 1997). These mechanisms may function in concert to produce the
oxidative stress and damage seen after cyanide exposure.
The observed increase in catalase activities as the study progressed
may have occurred due to the early rise of the enzyme to the challenge of
cyanide intoxication and auto-peroxidation. The reduction in catalase
activity in the organs of birds dosed cyanide relative to control birds could
be traceable to the rise in oxidative stress in the various organs leading to the
inhibition of the enzyme catalase (Kanthasamy et al., 1997). One reason
however, that may be adduced to a significant reduction in the activities of
catalase in the organs of birds dosed invivo compared to birds dosed through
food may be as a result of the detoxification processes that occurred
alongside the food in the digestive tract. Another factor may be as a result of
the binding of cyanide to other components of the food thus reducing its bio
availability to the binding site of the enzyme which may have led to the
inhibition of Catalase as well.
51

Conclusion
Based on the available evidences that exists in this study, this study
wishes to conclude that cyanide is a toxic substance which may give rise to a
number of biochemical challenges such as the auto-peroxidation of tissues
and the early induction of some enzymatic processes and later inhibition of
these same enzymes. This study has been able to establish that cyanide
toxicity is concentration dependent and also a factor of the route of exposure
to the metal and it is capable of inducing antioxidant response enzymes such
as catalase, and that catalase is a potent enzyme for early detection of
toxicity in tissues as it may serve as a second messenger and a signaling
enzyme to this effect.
52

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