URIC ACID

PRESENTED BY: PRODUCTION

NEHA SRIVASTAVA
BBT-2-08047
INTRODUCTION

 Uric acid (or urate) is a

heterocyclic compound of carbon,
nitrogen, oxygen, and hydrogen
with the formula C5H4N4O3


PRODUCTION OF URIC ACID FROM
PURINES
 Purines are metabolized into uric
acid
 When cells die and get recycled, the
purines in their genetic material
also get broken down. Uric acid is
the chemical formed when purines
have been broken down completely.
It's normal and healthy for uric acid
to be formed in the body from
breakdown of purines.

Reaction:

Uric acid is produced by xanthine



oxidase from xanthine and

hypoxanthine, which in turn are
produced from purine. Uric acid is
more toxic to tissues than either
xanthine or hypoxanthine

ROLE OF URIC ACID IN HUMAN

 uric acid serves as an antioxidant

and helps prevent damage to our
blood vessel linings, so a
continual supply of uric acid is
important for protecting our
blood vessels. .



 In humans, over half the
antioxidant capacity of
blood plasma comes from uric
Research article about role of uric
acid
 Towards the physiological function of uric acid.
 Becker BF.

Department of Physiology, University of Munich, Germany.

Uric acid, or more correctly (at physiological pH values), its
monoanion urate, is traditionally considered to be a metabolically inert
end-product of purine metabolism in man, without any physiological
value. However, this ubiquitous compound has proven to be a
selective antioxidant, capable especially of reaction with hydroxyl
radicals and hypochlorous acid, itself being converted to innocuous
products (allantoin, allantoate, glyoxylate, urea, oxalate). There is now
evidence for such processes not only in vitro and in isolated organs,
but also in the human lung in vivo. Urate may also serve as an
oxidisable cosubstrate for the enzyme cyclooxygenase. As shown
for the coronary system, a major site of production of urate is the
microvascular endothelium, and there is generally a net release of
urate from the human myocardium in vivo. In isolated organ
preparations, urate protects against reperfusion damage induced
by activated granulocytes, cells known to produce a variety of
radicals and oxidants. Intriguingly, urate prevents oxidative
inactivation of endothelial enzymes (cyclooxygenase, angiotensin
converting enzyme) and preserves the ability of the endothelium
to mediate vascular dilatation in the face of oxidative stress,
suggesting a particular relationship between the site of urate
formation and the need for a biologically potent radical
URICOTELISM

 Uricotelism

Elimination of uric acid as the main
nitrogenous waste material is called
uricotelism. Animals showing
uricotelism are called uricotelic
animals.
 Occurrence

It is a common method seen in birds,
land reptiles, insects, land snails and
some land crustaceans.

THE THREE MODES OF EXCRETION
OF NITROGENOUS COMPOND
Uric acid excretion

 In humans and higher primates, uric acid is

the final oxidation (breakdown) product
of purine metabolism and is excreted in
urine.
 In birds and reptiles, and in some desert
dwelling mammals (e.g., the
kangaroo rat), Uric acid is formed from
ammonia mostly in the liver and to some
extent in the kidneys apart from this

uric acid also is the end product of purine
metabolism, but it is excreted in feces as a
dry mass.
Uric acid from ammonia

 Uric acid is formed from ammonia

mostly in the liver and to some extent
in the kidneys. The process is highly
energy dependant, but is much less
toxic than both ammonia and urea
and it is almost insoluble in water and
can be eliminated from the body in
nearly a solid state, saving a lot of
water.
 In humans, about 70% of daily uric acid
disposal occurs via the kidneys
Excretion of uric acid in human

, Uric acid is produced as the
major end-product of purine
metabolism by muscles, liver and
intestine. b, After the blood is
filtered at the glomerulus, the
resulting fluid enters the tubules
of the kidneys to allow waste
substances to be excreted as
urine. Many substances, however,
such as uric acid, are useful and
so are reabsorbed. This is
achieved by the cells that line the
walls of the tubules, as seen in
detail at the right. As shown by
Enomoto et al.1, the transporter
URAT1 mediates uptake of uric
acid across the apical membrane,
in exchange for anions, which
enter cells either by Na+-coupled
transport through the apical
membrane or organic anion
transport (through OAT proteins)
across the basolateral membrane.
Uric acid leaves the cell across the
basolateral membrane through an
unknown channel or transporter,
possibly in exchange for anions
through an OAT protein
URIC ACID RELATED
DISORDERS
 In human blood plasma, the reference range of
uric acid is between 3.6 mg/dL (~214µmol/L)
and 8.3 mg/dL (~494µmol/L) (1 mg/dL=59.48
µmol/L). This range is considered normal by
the American Medical Association. Uric acid
concentrations in blood plasma above and
below the normal range are known,
respectively, as hyperuricemia and
hypouricemia.
 Similarly, uric acid concentrations in urine above
and below normal are known as
hyperuricosuria and hypouricosuria. Such
abnormal concentrations of uric acid are not
medical conditions, but are associated with a
variety of medical conditions
HIGH URIC ACID
Gout
Excess serum accumulation of uric acid can lead to a type of arthritis known as gout.
Gout

Gout can be controlled by diet and/or

a drug called allopurinol which
inhibits the enzyme which produces
uric acid.
 Lesch-Nyhan syndrome


Lesch-Nyhan syndrome,
an extremely rare
inherited disorder, is also
associated with very high
serum uric acid levels.
URIC ACID STONE

 5-25% of humans impaired renal

(kidney) excretion leads to uric
kidney stone

LOW URIC ACID


Multiple sclerosis

Lower serum values of uric acid have
been associated with
Multiple Sclerosis.


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Oxidative stress

 Oxidative stress

Uric acid may be a marker of
oxidative stress, and may have a
potential therapeutic role as an
antioxidant.



Oxidative stress

Antioxidant – prooxidant urate redox shuttle. The antioxidant –



prooxidant urate redox shuttle is an important concept to understand

regarding accelerated atherosclerosis. This shuttle is important in
understanding the role of how the antioxidant uric acid becomes prooxidant in
this environmental milieu, which results in its damaging role to the
endothelium and arterial vessel wall remodeling with an elevated tension of
oxidative – redox stress (ROS), accelerated atherosclerosis and arterial vessel
wall remodeling.
Sources of uric acid
 In humans Purines are excreted as uric acid. Purines are
found in high amounts in animal food products, such as
liver and sardines
 Moderate intake of purine-containing food is not associated
with an increased risk of gout, A moderate amount of
purine is also contained in beef, pork, poultry, fish and
seafood, asparagus, cauliflower, spinach, mushrooms,
green peas, lentils, dried peas, beans, oatmeal, wheat
bran and wheat germ.
 In many instances, people have elevated uric acid levels for
hereditary reasons. Diet may also be a factor; eating
large amounts of sea salt can cause increased levels of
uric acid.
 Serum uric acid can be elevated due to reduced excretion
by the kidneys, and or high intake of dietary purine.[
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