2. INTRODUCTION:-
Antinutritional Factors (ANFs):
• Defined as those substances present in the diet which by themselves or
their metabolic products arising in the system interfere with the feed
utilization, reduce production or affects the health of the animal.
• These anti-nutritive substances are often referred to as “toxic factors”
because of the deleterious effects they produce when eaten by animals.
According to their Chemical Properties
They are
Protein ,
Gylcosides,
Phenols,
Miscellaneous
3. This include
1. Saponins
2. Cyanogens
3. Glucosinolates (Goitrogens)
Glycosides
• Glycosides are usually compounds of plant origin.
They are made up of one or more sugars combined
with an alcohol, a phenol, or a complex molecule
such as a steroid nucleus.
• Contain CHO and non –CHO group (Aglycone)
4. • Saponins are a heterogenous group of naturally occurring
foam - producing triterpene or steroidal glycosides that
occur in a wide range of plants.
• characterized by bitter taste,
• foaming in aqueous solution,
• haemolyse RBC
Saponins:
They are able to form complexes with sterols,
including those associated with the plasma
membranes of animal cells.
5. Saponins are less important because their levels are low
in most common feed ingredients for monogastric animals.
In Ruminants they are toxic when fed in excess amount, because
their diet contain more saponins than monogastric.
The important common sources which cause saponin
poisoning of livestock are:-
• Sources of Saponins
Lucerne (Alfalfa)
Soya bean
Kidney bean (Rajma)
Lentil (Masoor)
Groundnut
Sunflower
6. Effects of Saponins
Bloat
Excess feeding of green lucerne or legume forages saponins lower the surface tension
of ruminal contents leading to accumulation of gas (CO2 and CH4), condition is known
as “bloat” This is also know as tympany/tympnitis.
Formation of Foam in the Rumen
The presence of saponins has been cited as one of the factors responsible for
formation of foam in the rumen and thereby gas is trapped in the rumen contents with
the result of which animals can not eliminate it by belching.
Haemolysis of RBC
Saponins are capable of destroying red blood cells (RBCs) by dissolving their
membranes, a process known as haemolysis, releasing free haemoglobin into the
bloodstream.
Saponins also have found to inhibit the actions of certain enzymes.
E.g., chymotrypsin because they interact with substrate-enzyme
interaction.
7. Other secondary effects of Saponin
In general the effects of ingestion of saponins include excessive salivation, increased
respiratory tract secretion, gastroenteritis, vomiting, diarrhoea, haemolysis, haematuria,
damage to livers and kidney tissues, cystitis, bloating, reduction of gastric motility,,
reduction of food intake, reduction of growth rate.
In Poultry 0.4 – 0.5 % saponin in feed depress feed consumption.
Egg production and body weights are also depress
TREATMENT AND PREVENTION OF SAPONIN TOXICITY
Turpentine and paraffin oil are helpful in reducing bloat.
For ruminants 1 to 2 kg dry fodder should be fed before letting the animals for legume
pastures or before excessive feeding of green legume fodders as a preventive
measure.
Water soaking and rinsing will remove their components in the feedstuffs. Chemically
saponins are glycosides which on hydrolysis yield surgars.
8. Cyanogens
• Cynogenetic glycoside compounds consist of α-hydroxynitrile
aglycones attached to a sugar moiety and are widely distributed
in the plant kingdom.
• In plants the Glycoside is non-toxic in the intact
tissues.
• These glycosides can be hydrolyzed to prussic
acid or hydrocyanic acid (HCN) by the enzyme
usually present in the same plant or as they are
being are being digested by animals.
• This reaction can take place in the rumen microbial
activity.
9. • The HCN is rapidly absorbed and some is eliminated through the lungs, but the greater
part is rapidly detoxified in the liver by conversion to thiocyanate.
• Ruminants are more susceptible to HCN poisoning than are horses and pigs because
the enzyme required for the release of HCN is destroyed in horses and pigs by the
gastric HCI.
There are three distinct glycosides:
• Amygdalin : Almonds
• Dhurrin : Jowar and other immature grasses
• Linamarin : Linseed, Cassava , Java Beans
Cynogens Plant source
• Heavy nitrate fertilization followed by an abundant irrigation or rainfall
may increase the potential of HCN poisoning of these crops.
10. 1. Cyanide taken to the body
2. It’s rapidly absorbed and circulated
3. It is merged with methemoglobin and forms cyanomethemoglobin.
4. The circulating cyanide inactivates cytochrome oxidase enzyme
by binding ferric (Fe+++) iron which is within this enzyme.
5. Normally the cytochrome oxidase enzyme catalyzes the last step
of oxidative phosphorylation.
6. The enzyme-cyanide complex prevents this task from being
performed.
7. The enzyme cannot combine with oxygen and electron
transportation become inhibited.
8. The animal cannot use oxygen and cellular respiration
stops immediately.
9. Death occurs due to histotoxic anoxia and ATP depletion.
Mechanism of action
11. Clinical signs of Cyanide Poisoning
• Dyspnea, labored breathing, restlessness, mental confusion,
ataxia, convulsions are the clinical signs in affected animals.
• Initially bright and cherry-red colored mucous membranes are
noticed.
• When patient becomes hypoxic, mucous membranes become
cyanotic
• Cyanide can cause death in a short amount of time, due to hypoxia
which is reduction of oxygen in tissues.
TREATMENT AND PREVENTION OF CYANIDE POISONING
For Cattle: I/V with 3.0g Sodium Nitrate and 15.0 g Sodium Thiosulphate
in 200 ml H2O.
For Sheep: I/V with 1.0g Sodium Nitrate and 2.5 g Sodium Thiosulphate
in 50 ml H2O.
12. Feeding of immature jowar green fodder should be avoided to
prevent HCN poisoning.
Drying plants decreases the cyanogenic potential over time.
Ensiling plants will significantly reduce the cyanogenic glycoside
content.
Sun-curing of hay will reduce HCN, especially if the hay is
crimped. Dhurrin will be hydrolyzed and HCN evaporates in
gaseous form.