introduction of Purine and Pyrimidine metabolism, biosynthesis and degradation of nucleotides, biological functions and metabolic disorders, chemical analogues and therapeutic drugs, uric acid metabolism
introduction of Purine and Pyrimidine metabolism, biosynthesis and degradation of nucleotides, biological functions and metabolic disorders, chemical analogues and therapeutic drugs, uric acid metabolism
explains the breakdown of purine. source and excretion of purine is explained. hyperuricemia and hypouricemia is discussed. types of Gout, clinical features and treatment is included.
Nucleotide Biosynthesis involves 2 processes. one is Denovo synthesis and other is Salvage pathway. An outline of both the processes has given in this presentation.
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Pentose phosphate pathway is an alternative pathway to glycolysis and TCA cycle for oxidation of glucose. It is a shunt of glycolysis. It is also known as hexose monophosphate (HMP) shunt or phosphogluconate pathway. It occurs in cytoplasm of both prokaryotes and eukaryotes. While it involves oxidation of glucose, its primary role is anabolic rather than catabolic. It is an important pathway that generates precursors for nucleotide synthesis and is especially important in red blood cells (erythrocytes).
Substrate level phosphorylation and it's mechanism || Biochemistry || B Pharmacy || Project || slideshare || biology || chemistry
*images use in this ppt is only for educational purpose
In this presentation, i tell about substrate level phosphorylation
Phosphorylation involves the transfer of phosphate
group from one compound to other.
➢ Substrate level phosphorylation is a direct
phosphorylation of ADP with a phosphatase group by
using the energy obtain from a coupled reaction.
➢ Occurs in cytoplasm ( glycolysis – due to aerobic and
anaerobic condition) and in mitochondrial matrix ( krebs
cycle – anaerobic condition)
De novo and salvage pathway of nucleotides synthesis.pptx✨M.A kawish Ⓜ️
This slides explains Metabolism topic "De novo and salvage pathway of nucleotides synthesis. In which synthesis of Purines and pyrimidines synthesis has been occurred. In last there is a difference between these two pathways.
explains the breakdown of purine. source and excretion of purine is explained. hyperuricemia and hypouricemia is discussed. types of Gout, clinical features and treatment is included.
Nucleotide Biosynthesis involves 2 processes. one is Denovo synthesis and other is Salvage pathway. An outline of both the processes has given in this presentation.
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Pentose phosphate pathway is an alternative pathway to glycolysis and TCA cycle for oxidation of glucose. It is a shunt of glycolysis. It is also known as hexose monophosphate (HMP) shunt or phosphogluconate pathway. It occurs in cytoplasm of both prokaryotes and eukaryotes. While it involves oxidation of glucose, its primary role is anabolic rather than catabolic. It is an important pathway that generates precursors for nucleotide synthesis and is especially important in red blood cells (erythrocytes).
Substrate level phosphorylation and it's mechanism || Biochemistry || B Pharmacy || Project || slideshare || biology || chemistry
*images use in this ppt is only for educational purpose
In this presentation, i tell about substrate level phosphorylation
Phosphorylation involves the transfer of phosphate
group from one compound to other.
➢ Substrate level phosphorylation is a direct
phosphorylation of ADP with a phosphatase group by
using the energy obtain from a coupled reaction.
➢ Occurs in cytoplasm ( glycolysis – due to aerobic and
anaerobic condition) and in mitochondrial matrix ( krebs
cycle – anaerobic condition)
De novo and salvage pathway of nucleotides synthesis.pptx✨M.A kawish Ⓜ️
This slides explains Metabolism topic "De novo and salvage pathway of nucleotides synthesis. In which synthesis of Purines and pyrimidines synthesis has been occurred. In last there is a difference between these two pathways.
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http://sandymillin.wordpress.com/iateflwebinar2024
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Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
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The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
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2. Purine nucleotide can be synthesized by two
pathways….
De novo pathway (new synthesis from amphibolic
intermediates)
Salvage pathway
By phoshoribosylation of free purine bases and
By phosphorylation of purine nucleosides
In de novo synthesis, Purine nucleotides are
synthesized not the free purine bases.
3. Precursors for the de novo synthesis of purine
C2
C
6
N1
N
9
N
3
7
N
C5
C4
8C
Glutamine
Aspartate
Glycine
CO2
N10 Formyl
THF
N5 N10 Formyl
THF
In de novo synthesis, Purine ring is assembled on
ribose-5-phosphate, from a variety of precursors.
4. Reactions of de
novo synthesis
of purine
α-D-Ribose-5-phosphate
PRPP synthase
ATP
AMP
Phosphoribosylpyrophosphate (PRPP)
PRPP Glutamyl
amidotransferase
Glutamine
Glutamate
5-phospho-β-D-Ribosylamine
Phosphoribosyl
glycinamide synthase
Glycine + ATP
ADP+Pi
Glycinamide ribosyl-5-phosphate
Formyl transferase
N5, N10 – methenyl
THF
THF
H2O
PPi
Mg++
Mg++
Formylglycinamide ribosyl-5-phosphate
Synthase
Glutamate
ATP, Mg++
Glutamine
Formylglycinamidine ribosyl-5-phosphate
Synthase
ATP Mg++
Ring closure
7. Formation of Purine Nucleoside Diphosphate
and Nucleoside Triphosphate
Nucleoside monophosphate
(AMP, GMP)
Nucleoside monophosphate
kinase
ATP
ADP
Nucleoside diphosphate
(ADP, GDP)
Nucleoside diphosphate
kinase
ATP
ADP
Nucleoside triphosphate
(ATP, GTP)
8. It is controlled by…
Concentration of PRPP
Feedback regulation
Concentration of PRPP
Increased conc. PRPP stimulates purine
nucleotide synthesis. Which in turn depends on…
Availability of ribose-5-phosphate and
The activity of PRPP synthase
10. Definition-
The conversion of free purines to the
corresponding nucleotides directly.
Sources of Purine
The free purines are formed in the cells
during the metabolic degradation of nucleic
acids & nucleotides.
Also obtained from the dietary sources.
11. -
This pathway provides purine nucleotide for
the tissues which are incapable of their
biosynthesis by de novo pathway.
e.g. human brain has low levels of PRPP
amidotransferase, & also RBCs and
polynuclear leukocyte cannot synthesize 5-
phoshoribosylamine.
Therefore, these tissues depends on this
pathway for purine nucleotide synthesis.
This is much simpler & required less energy.
13. Deoxyribonucleotides are synthesized by reduction of
ribonucleoside diphosphates (both purine & pyrimidine).
The –OH group on C2 of ribose is replaced by a H atom.
It is catalyzed by ribonucleotide reductase.
This enzyme is active only when cells have actively
synthesizing DNA (preparative to cell division).
The reaction also requires thioredoxin, thioredoxin
reductase and NADPH.
Ribonucleoside diphosphate
(ADP, GDP, CDP, UDP)
Ribonucleotide
reductase
Reduced
Thioredoxin
Oxidized
Thioredoxin
Deoxyribonucleoside diphosphate
(dADP, dGDP, dCDP, dUDP)
NADPH+H+NADP+
Thioredoxin
reductase
14. Purines (Adenine & guanine) are catabolised to
uric acid.
Purine Nucleotides are degraded by the pathway,
in which first phosphate group is removed by the
action of nucleotidase to give nucleoside.
Then it is further degraded to uric acid as
follows……
15. AMP
Nucleotidase
H2O
Adenosine
Adenosine
deaminase
H2O
NH3
Inosine
Xanthine oxidase
H2O H2O2
Xanthine
Xanthine oxidase
H2O
Uric acid
Hypoxanthine
Nucleotide
phosphorylase
Pi
GMP
Pi
Nucleotidase
H2O
Pi
Guanosine
Ribose-1-P
Nucleotide
phosphorylase
Pi
Ribose-1-P
Guanine
Guanase
H2O2
➢Xanthine oxidase contains FAD,
molybdenum and iron.
➢It is found in liver and small
intestine
➢X.O librates H2O2 which is
harmfull to the tissues.
➢Catalase convert H2O2 to H2O
16.
17. Uric acid is the end product of purine catabolism.
At physiological PH uric acid is mostly present in
plasma as sodium urate which is in soluble form.
The normal blood level of uric acid is 3-7 mg/dl.
The daily excretion varies from 500-700mg.
It excreted in to ways…
Via Kidney: majority of uric acid is excreted via kidney
(uricosuria).
Via gut: Smaller amount of urate is excreted via gut,
where it broken down by bacteria.
Significance of Uric acid
Uric acid plays an important role as antioxidant.
It is very effective scavenger of free radicals.
Its antioxidant property can be compared with vitamin C
18. Due to ↓ U.A ExcretionDue to ↑ U.A synthesis
Secondary due toPrimary
idiopathic
✓Renal insufficiency
✓Metabolic acidosis
✓Lactic acidosis
✓Diabetes Mellitus
✓Starvation
✓ Unknown reason✓ PRPP synthetase
✓ PRPP amidotransferase
✓ HGPRTase
Secondary
due to
Primary
(genetic)
✓↑ Dietary intake
✓↑ Nucleic acid turnover
✓Various cancers Such as..
(Leukemia, polycythemia.)
✓Von Gierkes disease
19. Gout is a metabolic disease associated with overproduction
of uric acid.
An elevated serum uric acid conc. is known as hyperuricemia
In sever hyperuricemia, crystals of sodium urate get
deposited in the soft tissues, particularly in the joints.
Such deposits are commonly known as tophi.
This causes inflammation in the joints resulting in the
painful gouty arthritis.
Sodium urate or uric acid may precipitate in kidneys and
ureters that results in renal damage and stone formation.
Prevalence of gout is about 3 per 1,000 persons.
Mostly affecting males and post-menopausal womens are
also equally susceptible.
21. Gout is of two type…
Primary gout
Secondary gout
Primary gout:-
It is an inborn error of metabolism due to defect in
enzymes of purine biosynthesis. Such as…
PRPP synthetase
PRPP amidotransferase
HGPRTase
Secondary gout:-
It is due various diseases causing increased synthesis or
decreased excretion of uric acid.
↑ Dietary intake
↑ Nucleic acid turnover
Various cancers Such as..
(Leukemia, polycythemia.)
starvation
Renal insufficiency
Lactic acidosis
Diabetes Mellitus
22. SecondaryPrimary (Genetic)
Due to enzyme defect Due to decreased
excretion
Due to increased
synthesis
✓Renal
insufficiency
✓Lactic acidosis
✓Diabetes Mellitus
✓↑ Dietary intake
✓↑ Nucleic acid turnover
✓Various cancers Such as..
(Leukemia, polycythemia.)
✓Starvation
✓Von Gierkes disease
✓ PRPP synthetase
✓ PRPP amidotransferase
✓ HGPRTase
23. Gout
(Hyperuricemia)
Secondary
Due to decreased
excretion
Renal insufficiency
Lactic acidosis
Diabetes Mellitus
Due to increased
synthesis
↑ Dietary intake
↑ Nucleic acid turnover
Various cancers
Starvation
Primary (Genetic)
Due to enzyme
defect in …
- PRPP synthetase
- PRPP
amidotransferase
- HGPRTase
24. Gout can be treated combination of nutritional
therapy and drug therapy.
Foods rich in nucleotides and nucleic acids such as
liver, coffeine and tea should restrict in the diet. And
also the alcohol.
Drug for the treatment of primary gout is allopurinol.
Allopurinol is structural analog of hypoxanthine that
competitively inhibits the enzyme xanthine oxidase.
Allopurinol acts as suicide inhibitor in this reaction.
It get oxidized to alloxanthine by XO.
Alloxanthine is more effective inhibitor of XO.
This leads to the accumulation of hypoxanthine and
xanthine. These two compounds are more soluble than
uric acid, hence easily excreaed in the urine.
25. It is due to the deficiency of enzyme HGPRTase.
It was first described in 1964 by Michael Lesch (a
medical student) and Wiliam L. Nyhan (his teacher).
It is an X-linked inherited disorder, that affect only
males.
In absence of HGPRTase, the salvage pathway is inoperative
and purine cannot reconverted to nucleotides; instead they
are degraded to uric acid.
And also cause the accumulation of PRPP, which stimulate
synthesis and degradation of purine.
This results in increased conc of uric acid in plasma and urine
26. Symptoms:-
Hyperuricemia
Neurological abnormalities such as…
Mental retadation
Aggressive behavior
Learning disability
Biting of fingers and lips (self-mutilation)
Gout
Urinary tract stones
Treatment:-
Allopurinol helps to reduces uric acid formation, has
no affect on the neurological manifestation in these
patients.
27. Purine Nucleoside phosphorylase deficiency:-
Purine Nucleoside phosphorylase deficiency is
associated with impaired T-cell function with normal
B-cell function.
In the cells of patients with this deficiency, dGTP
accumulates.
Like dATP, dGTP allosteric inhibits ribonucleotide
reductase.
Both are autosomal recessive disorders with
symptoms of recurrent and chronic infection.