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Enzyme Inhibition

ENZYME INHIBITION


ENZYME INHIBITION

  • Enzyme inhibitor binds with enzyme and decreases a catalytic activity.

Types of Enzyme Inhibition-

  1. Reversible
  2. Irreversible
  3. Allosteric
  4. Reversible Inhibition– binds through non-covalent bonds and activity of enzyme is restored. Divided into-

a) Competitive inhibitorKm increased, Vmax unchanged.

  • E.g.- Succinate dehydrogenase by melanate.

b) Non competitive inhibitor- Km unchanged, Vmax decrease, mostly irreversible.

  • E.g.- Cyanide by Cytochrome C Oxidase.
  • Carbonic anhydrase by Acetazolamide

2. Irreversible Inhibition– binds covalently with an enzyme.

a) Suicidal Inhibitor– irreversible binding to enzyme and inhibit enzyme.

  • E.g. Allopurinol inhibit Xanthine oxidase, cyclooxygenase.

3. Feedback Inhibition- called as end product inhibition.

  • E.g. AMP inhibits first step in purine synthesis.

Exam Important

  1. Reversible Inhibition- binds through non-covalent bonds and activity of enzyme is restored.
  2. Competitive inhibitor- Km increased, Vmax unchanged.
  3. Competitive inhibitor- Succinate dehydrogenase by melanate.
  4. Non competitive inhibitor- Km unchanged, Vmax decrease, mostly irreversible.
  5. Non competitive inhibitor- E.g.- Cyanide by Cytochrome C Oxidase.
  6. Suicidal Inhibitor- Allopurinol inhibit Xanthine oxidase.
Type of inhibitor Km Vmax
Reversible inhibbitor Increased No effect
Competitive No effect Decreased
Non-competitive Decreased Decreased
Uncompititive No effect Decreased
Irrversible inhibitor (same as reversible Increased No effect
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Codons & Genetic code

Codons & Genetic code


CODON &GENETIC CODE

  • Codon- is a sequence of three adjacent bases that corresponds to one of the amino acid.
  • There are 64 possible codon of sequence.
  • Four nucleotide bases A, G, C and U.
  • If 4 bases 44 = 256 amino acids.
  • Methionine has only 1 codon.
  • Genetic code is the system of nucleotide sequences of mRNA that determines the sequence of amino acids in protein.
  • Characteristics of genetic codes-

1.  Triplet codon– each amino acid has triplet sequence.

2. Degenerate (Redundant)

  • A given amino acid may have more than one codon.
  • Degeneracy of the codon lies in the 3rd base.

3. Universal– a specific codon represent a specific amino acid in all the  species.

  • Genetic coder are found in human mitochondria, code is-
  1. AUA codes for methionine instead of isoleucine.
  2. AGA and AGG serve as as stop codon.
  3. UGA also codes for Selenocysteine, a mechanism called translational recording.

4.Unambiguous/ Specific– a particular codon always codes for the same amino acid

5. Non overlapping and nonpuntate (comma less)– reading of genetic code does not involve overlapping sequence.

  • E.g.- AUGCUA GACUUU reads as AUG/CUA/GAC/UUU without punctuation (comma) between codons.

6. Stop or termination or nonsense codons

  • The three nucleotide triplets do not code for any amino acid are- UAA (amber), UAG (ochre), UGA (opal) called as nonsense codons that normally signal termination of polypeptide chains.
  • Wobble Hypothesis- states that a single tRNA can recognise more than one codon.
  • Base pairing of 3rd base of codon (at 31 end) often fails to recognize the specific complementary base codon (at 51 end at tRNA)
  • Wobble explains the degeneracy of genetic code.
  • A minimum of 31 tRNAs are required to translate all 61 different codons for the amino acids.
  • Gene- is the smallest functional unit of genome. 2 types
  1. Inducible gene
  2. Constitutive gene (housekeeping genes)- genes whose expression is not regulated
  • Cistron- is the smallest unit of genetic expression.
  • The codons that designate the same amino acid are called synonyms.

 Exam Important

  • Information for synthesis of protein is contained in the mRNA.
  • Thymine is not involved in codons.
  • 64 (43) possible codon sequences.
  • tRNA acts as the adapter molecule between the codon and specific amino acid.
  • UUU is the codon for phenylalanine.
  • Degeneracy of the codon lies in the 3rd base.
  • Amino acid with maximum number codons are Serine, Arginine, Leucine.
  • Monocistronic- e.g. eukaryotic mRNA
  • Polycistronic- e.g. Prokaryotic mRNA
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Phospholipids

PHOSPHOLIPIDS


PHOSPHOLIPIDS

  • Phospholipid= Fatty acid+ Glycerol+Phosphoric acid+ nitrogenous base
  • Function is transduction of signals in cell membrane.

2 types-

  1. Glycerophospholipids
  2. Sphingophospholipids

1. Glycerophospholipids (phosphoglycerides)- that contains glycerol as alcohol. They are-

a) Phosphatidylcholine (lecithin)

  • Most abundant phospholipids in cell membrane.
  • Dipalmitoyl lecithin in lungs
  • Insufficient production of Dipalmitoyl lecithin- acute pulmonary distress syndrome in premature infants.

b) Phosphatidylethanolamine (Cephalin)- contains ethanolamine.

c) Plasmogens- platelet activating factor

d) Cardiolipin (Diphosphatidylglycerol) – is a major lipid of inner mitochondrial membrane.

  • It has antigenic properties (only humans).
  • Deficiency causes- Barth syndrome.

Exam Important

1.Glycerophospholipids (phosphoglycerides)- that contains glycerol as alcohol. They are-

a) Phosphatidylcholine (lecithin)

  • Most abundant phospholipids in cell membrane.
  • Dipalmitoyl lecithin in lungs
  • Insufficient production of Dipalmitoyl lecithin- acute pulmonary distress syndrome in premature infants.

 b) Phosphatidylethanolamine (Cephalin)- contains ethanolamine.

c) Plasmogens- platelet activating factor

d) Cardiolipin (Diphosphatidylglycerol) – is a major lipid of inner mitochondrial membrane.

  • It has antigenic properties (only humans).
  • Deficiency causes- Barth syndrome.
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Severe Combined Immunodeficiency (Scid)

SEVERE COMBINED IMMUNODEFICIENCY (SCID)


SEVERE COMBINED IMMUNODEFICIENCY (SCID)

It is caused due to –

  • Deficiency of Adenosine Deaminase (ADA)
  • Adenosine accumulates and converted to ribonucleotides and deoxyribonucleotides (dATP).
  • dATP inhibits ribonucleotidereductase which decreases production of deoxyribose nucleotides.
  • There is decrease in T and B cells leading to immunodeficiency.
  • X Linked Type is the Most Common Pattern of Inheritance

Clinical features-

  •  Chronic diarrhea
  •   failure to thrive.

Treatment-

  • Gene therapy is the first order to be treated.
  • Enzyme Replacement Therapy with Polyethyleneglycol modified bovine adenosine deaminase (PEGADA).

Exam Important

  • There is a decrease in T and B cells.
  • Adenosine accumulation is seen in SCID.
  • DNA synthesis decreases.
  • X Linked Pattren of Inheritance is most common
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Metabolism of Triacylglycerol

Metabolism of Triacylglycerol


METABOLISM OF TRIACYLGLYCEROL

  • Triacylglycerol contains one molecule of glycerol and 3 molecules of fatty acid.
  • Occurs in liver, adipose tissue, intestinal mucosal cells.
  • Organelle- endoplasmic reticulum.

3 steps-

  1. Fatty acid to acyl CoA by Acyl CoA synthase (thiokinase)
  2. Glycerol to glycerol-3-phosphate (formed from glucose-3- phosphate dehydrogenase in adipose tissue) by glucose kinase.
  3. Phosphatidate undergoes hydrolytic dephosphorylation which is esterified to form triacylglycerol.
  • In adipose tissues- insulin enhances triacylglycerol synthesis.
  • In Diabetes, glycerol-3-phosphate is hampered leading to decrease triglyceride synthesis.
  • Triglyceride is the major lipid for adipose tissues.

Triacylglycerol hydrolysis (lipolysis)-

  • Triacylglycerol (stored fat) is degraded.
  • Enzyme- hormone sensitive lipase.
  • Lipolysis refers to hydrolysis of triacylglycerol in adipose tissues.

Regulation of lipolysis-

  1. Hormone sensitive lipase activated by-
  2. Epinephrine
  3. Catecholamines
  4. Thyroid hormones
  5. Growth hormone
  6. ACTH
  7. Glucocorticoids

Hormone sensitive lipase inactivated by-

  1. Insulin
  2. Prostaglandin

Exam Important

  • Triacylglycerol contains one molecule of glycerol and 3 molecules of fatty acid.
  • Occurs in liver, adipose tissue, intestinal mucosal cells.
  • Organelle- endoplasmic reticulum.

3 steps-

  1. Fatty acid to acyl CoA by Acyl CoA synthase (thiokinase)
  2. Glycerol to glycerol-3-phosphate (formed from glucose-3- phosphate dehydrogenase in adipose tissue) by glucose kinase.
  3. Phosphatidate undergoes hydrolytic dephosphorylation which is esterified to form triacylglycerol.
  • In adipose tissues- insulin enhances triacylglycerol synthesis.
  • In Diabetes, glycerol-3-phosphate is hampered leading to decrease triglyceride synthesis.
  • Triglyceride is the major lipid for adipose tissues.
  • Triacylglycerol hydrolysis (lipolysis)-
  • Triacylglycerol (stored fat) is degraded.
  • Enzyme- hormone sensitive lipase.
  • Lipolysis refers to hydrolysis of triacylglycerol in adipose tissues.

Regulation of lipolysis-

Hormone sensitive lipase activated by-

  1. Epinephrine
  2. Catecholamines
  3. Thyroid hormones
  4. Growth hormone
  5. ACTH
  6. Glucocorticoids

Hormone sensitive lipase inactivated by-

  1. Insulin
  2. Prostaglandin
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Lesch- Nyhan Syndrome

LESCH- NYHAN SYNDROME


LESCH- NYHAN SYNDROME

Main Features

  • It is X-linked Recessive disorder.
  • It is caused due to complete deficiency of Hypoxanthine guanine phosphoribosyl transferase (HGPRT deficiency).
  • It affects only males.
  • Increased production of purine nucleotide from PRPP via De Novo pathway.
  • Purine degraded into uric acid and its level increases.

Clinical features

  • Hyperuricemia
  • Gouty arithritis
  • Urinary stones
  • Intellectual disability
  • Dystonic movement
  • Dysarthric speech
  • Self mutilation (irresistible urge to bite the fingers and lips)
  • Megaloblastic anaemia

Diagnosis

  • Hyperuricemia
  • HGPRTase enzyme acitivity in RBCs is deficient

Treatment

  • Allopurinol
  • Alkalanization of urine
  • High fluid intake

Exam Important

  • It is a sex linked disorder. (X Linked Recessive Disorder)
  • The structural gene of HGPRT is located on X-chromosome.
  • There is a complete deficiancy of HGPRT 
  • Self mutilation is one of the characteristic feature of the syndrome.
  • Allopurinol is used in the treatment.
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Different types of Fatty Oxidation

Different types of Fatty Oxidation


DIFFERENT TYPES OF FATTY ACID OXIDATION

Oxidation of Very Long Chain Fatty Acid-

  • It takes place in Peroxisomes till Octanoyl CoA.
  • Oxidation in peroxisome produces Acetyl CoA and H2O2.

Clinical Corelation-

  1. Peroxisomal Ghost
  2. Zellweger’s syndrome- is a rare inborn error of peroxisomal fatty acid oxidation.
  3. Neonatal adrenoleukodystrophy
  4. Infantile Refsum disease

Oxidation of Unsaturated Fatty Acid-

  • It occurs in mitochondria
  • The energy yield by oxidation of Unsaturated Fatty Acid is 1.5 ATP less per double bond.

Oxidation of Odd Chain Fatty Acid-

  • It takes place in mitochondria
  • Odd chain fatty acids are also Beta-oxidized normally but the last step produces a 3-carbon propionyl.
  • This three carbon units (propionl CoA) from odd chain fatty acids is the only part of a fatty acid that is glucogenic. 

Alpha- oxidation of fatty acids

  • It occurs in endoplasmic reticulum and mitochondria

Exam Important

  • Oxidation of Very Long Chain Fatty Acid- It takes place in Peroxisomes till Octanoyl CoA.
  • Oxidation in peroxisome produces Acetyl CoA and H2O2
  • Oxidation of Unsaturated Fatty Acid- It occurs in mitochondria
  • The energy yield by oxidation of Unsaturated Fatty Acid is 1.5 ATP less per double bond.
  • Odd chain fatty acids are also Beta-oxidized normally but the last step produces a 3-carbon propionyl.
  • Alpha- oxidation of fatty acids–  It occurs in endoplasmic reticulum and mitochondria.
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Rapoport- Leubering Cycle

Rapoport- Leubering Cycle


  • Rapoport- Leubering Cycle occurs in RBCs (erythrocytes).

  • In this cycle, 1,3 – BPG is converted into 2, 3 –BPG by an enzyme biphosphoglycerate  mutase.
  • 2,3- BPG is then converted into 3- phosphoglycerate by enzyme 2,3- biphosphoglycerate phosphatase. 

Significance of Rapaport- Leubering Cycle-

  • The 2, 3 – BPG combines with haemoglobin and reduces the affinity towards oxygen. So, its presence has oxyhemoglobin unloads more oxygen to the tissues.
  • 2,3BPG shifts the oxygen Dissociation curve to right.
  • If the glycolysis of RBCs is impaired there will be impaired synthesis of 2, 3 – BPG  which causes left shift of O2  dissociation curve and increase oxygen affinity of haemoglobin.
  • Under hypoxic, high altitude, fetal tissues, anaemic condition the 2, 3- BPG concentration in the RBC increases.

Exam Important

  • Rapoport Leubering cycle occurs in erythrocytes
  • 2, 3 –bisphosphoglycerate combines with hemoglobin & reduces affinity towards oxygen.
  • 2,3 BPG shifts the oxygen Dissociation curve to right due to reduced affinity towards oxygen
  • No ATP is generated (only one molecule generated through glycolysis in RBC utilized)
  • Under hypoxic conditions, 2, 3- BPG increases in RBCs
  • Cancer cells switching to glycolysis even in the presence of adequate O2 for oxidative phosphorylation c/d Warburg effect
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Metabolism of Chylomicron

Metabolism of Chylomicron


LIPOPROTEIN METABOLISM

Chylomicron Metabolism

  • Chylomicrons transport the dietry lipid from intestine to liver.
  • Function of chylomicrons is to transport exogenous triglyceride to adipose tissue (for storage).
  1. Step I- Formation of Nascent Chylomicron- contains triglyceride, cholestryl ester, cholesterol, lipid, apo B-48 & apo A.
  2. Step II- Formation of Mature Chylomicron- by receiving apo C-II and apo E from HDL.
  3. Step III- Formation of Remanant Chylomicron– Apo C-II activates Lipoprotein Lipase
  4. Step IV- Uptake of Remnant Chylomicron
  • Chylomicron remnant is taken up by the liver.
  • Uptake is mediated by apo E via two apo E dependent recptors, LDL  receptor and LDL receptor related protein-I (LRP-I).

Exam Important

  • Chylomicrons transport the dietry lipid from intestine to liver.
  • Function of chylomicrons is to transport exogenous triglyceride to adipose tissue (for storage).
  1. Step I- Formation of Nascent Chylomicron
  2. Step II- Formation of Mature Chylomicron- by receiving apo C-II and apo E from HDL.
  3. Step III- Formation of Remanant Chylomicron- Apo C-II activates Lipoprotein Lipase
  4. Step IV- Uptake of Remnant Chylomicron-
  • Chylomicron remnant is taken up by the liver.
  • Uptake is mediated by apo E via two apo E dependent recptors, LDL  receptor and LDL receptor related protein-I (LRP-I).
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Cholesterol Synthesis

CHOLESTEROL SYNTHESIS


CHOLESTEROL SYNTHESIS

  • Cholesterol is the major sterol in humans.
  • Major component in plasma membrane.

Synthesis of Cholesterol

  • Major sites- Liver, adrenal cortex, testis, ovaries and intestine.
  • Cell organelle- endoplasmic reticulum and cytoplasm
  • First material is Acetyl CoA.
  • Acetyl- CoA condenses with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)
  • Then HMG-CoA is converted to mevalonate by HMG-CoA reductase, (the key regulatory enzyme of cholesterol synthesis)

Exam Important

  • Cholesterol is the major sterol in humans.
  • Major sites- Liver, adrenal cortex, testis, ovaries and intestine.
  • Cell organelle- endoplasmic reticulum and cytoplasm
  • First material is Acetyl CoA.
  • Acetyl- CoA condenses with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)
  • Then HMG-CoA is converted to mevalonate by HMG-CoA reductase, (the key regulatory enzyme of cholesterol synthesis)
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