INTRODUCTION

Molybdenum is present in the earth crest largely as

molybdenum disulphide and is a biogenic element of

microorganisms.
Trace amont of Mo is essential for a group of nitrogen fixing

bacteria,especially.
Molybdenum toxicity is most often seen in ruminants than in

other animals.
Molybdenum is an essential trace element and a component of

a number of enzymes, including sulphite oxidase ,xanthine

oxidase.

HISTORY
The element was discovered in
1778 byCarl Wilhelm Scheele
. The metal was first isolated in
1781 byPeter Jacob Hjelm.

Properties
Molybdenum is a high melting silver grey

metal with atomic number 42 and atomic

weight 95.94.
The transition element molybdenum exists
in five oxidation states 2-6 . The
predominent states are Mo 4 and Mo 6.
Molybdenum does not exists naturally in the
pure metallic state , but occurs in
assosiation with other elements.
The predominent form of molybdenum
occuring in soil and natural waters is the
molybdate anion .

SOURCES OF TOXICITY
Acidic soil, poorly drained soils, and those

contaminated with mining wastes.

Plants (legumes) can absorb and accumulate

water soluble molybdates from contaminated

soils.
Excessive use of molybdenum fertilizers.
Calves may be poisoned by milk from cows

on high molybdenum diets.

Molybdenum trioxide: exists as white to

slightly yellow to bluish powder chiefly used in

chemical analysis.
Molybdenum sesquioxide: exists as greyish

black powder. Often combined with iron as

Mol Iron and as haematinic.

DISTRIBUTION OF MOLYBDENUM

MOLYBDENUM PRODUCTS

FACTORS AFFECTING TOXICITY

Species-cattle are most susceptible , horses and

pigs are not usually affected.

Interactions-molybdenum has a strong inverse
relationship with copper and sulphur.
Form-water soluble form (tetramolybdate) is more
toxic than water insoluble form(molybdenum
disulfide).
Age -young animals are more susceptible.
Type of plant-legumes take up more of the
element than other plant species.
Season more seen in summer and early autumn.

TOXICITY
Molybdenum is present in all biological fluids

and tissues including bones .

In the diet , copper: molybdenum ratio of 6:1

is ideal.
Dietary molybdenum of 10 ppm can cause

toxicity regardless of copper intake.

TOXICOKINETICS
After oral administration , molybdenum compounds

are absorbed readily from the intestine.

In the blood molybdenum is bound to plasma

proteins and erythrocytes.

The highest concentration of Mo is present in bones

and liver but liver does not store molybdenum.

Lower concentration of Mo may be present in

kidneys,spleen,heart,and skeletal muscle.

Molybdenum is eliminated very rapidly via the

kidneys(80%)and bile hence under normal

conditions the element does not accumulate in
the body.
Normally only small amounts of Mo are

excreated in the faeces with exceptions in

certain GIT excretions
Molybdenum is also excreted in milk and may

affect young calves suckling the dam.

Mechanism of action
Mo toxicosis results primarily due to copper deficiency

induced by Mo.
It appears that the interaction of molybdates and

sulphides in the rumen give rise to thiomolybdates

which decreases the availability of dietary copper and,
when absorbed , impede the metabolism of tissue
copper.
Mo also promotes hepatic copper excretion by forming

a copper molybdate complex that is readily excreted

in urine causing a clinical copper deficiency.

Copper is present in many enzymes including

lysyl oxidase, thyrosinase, & cytochrome

oxydase.Other enzymes like lactase,ascorbic
acid oxidase,superoxide dismutase are also
affected. Deficiency of copper may reduce the
activity of these enzymes.
Copper is a cofactor for lysyl oxidase, an

enzyme that is responsible for the connective

tissue integrity by cross linking elastin .

The stensile strength of aorta and other major

vessel is markedly reduced in Cu deficiency.

Causes nerve damage and demyelination .
Decreases the activity of tyrosinase.
In ruminants and some other species ,

osteoporosis , spontanious fractures.

Copper deficiency affects the working of

superoxide dismutase.

Clinical sings
Molybdenum toxicity in animals is
commonly referred to as molybdinosis or
teart.
Clinical sings are predominant in ruminants.
In cattle: diarrhoea occurs 8-10days
following access to pasture which is
characterised by shooting diarrhoea &
watery faeces with unpleasant odour & full
of gas bubbles.
Other sings of acute toxicity in cattle may
includes:
Anorexia, excessive salivation, lacrimation,

PM FINDINGS
Fluid filled intestine bone rarification, exostosis,

depigmentation of skin & hair coat.

Haemorrhages & break down of periosteum

Diagnosis
Clinical signs, lesion & response to therapy.
Diagnosis is confirmed by demonstrating abnormal

concentration of molybdinum & Cu in blood (more

than 0.1ppm Mo & less than 0.6ppm Cu ) & liver
(more than 5ppm Mo & less than 10ppm Cu).
The specimens for chemical examination are, feed,
liver, kidneys, bone, urine, & hair.

Treatment and management

Copper: provision of Cu, orally, or parentrally, is

specific to molybdinum toxicosis.

For severe and sub acute cases, copper glycinate

may be injected s/c. Dose 60mg for calves &

120mg for cattle.
Coppersulphate in diet at the dose rate of 1-2 g

/adult cow/day in cattle & 0.25g/45kg body wt/day

in sheep is given un till symptoms disappers.

Copper sulphate
licks

Copper sulphate
crystals

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