ANSWER SCHEME 2010

I. DISCUSS
1. Role of following compound in detoxication a) Glucuronate  Active form UDP glucuronate  Will conjugate with carboxyl, amino, sulfhydryl or hydroxyl groups (CASH)  Examples carcinogens, aniline, benzoic acid meprobamate, phenol, steroids, bilirubin, female sex hormone.  Enzyme- UDP glucuronyl transferase (in endoplasmic reticulum of liver) b) Glycine  Conjugate with benzoyl CoA from benzoic acid to form hippuric acid (food additive)  Conjugate with salicylic acid to form salicyluric acid.  Enzyme acyl CoA amino acid N- acyl transferase c) Sulphate  Active form PAPS (3 phosphoadenosine 5 phosphosulphate)  Conjugate with phenolic hydroxyl groups and amino groups  Example phenol, indoxyl and cresol  Enzyme sulfutransferase 2. How following substances can be synthesised a) dADP from IMP  IMP to AMP by Addition of aspartate to IMP using adenylosuccinate synthethase to form adenylosuccinate Release of fumarate by enzyme adenylosuccinase to form AMP  AMP to ADP By enzyme adenosine monophosphate kinase Involve phosphoryl transfer from ATP  ADP to dADP By reduction at carbon no2 of ribose moiety by ribonucleotide reductase to form 2-deoxy adenosine diphosphate (dADP) Require thioredoxin, thioredoxine reductase and NADPH b) First true nucleotide from orotate. Mention genetic disorder  The nucleotide is UMP  Orotate to AMP First, transfer of ribose phosphate moiety from PRPP to orotic acid to form OMP by orotate phosphoribosyl transferase. Then, decarboxylation of orotidylate to form UMP catalysed by orotidylic acid decarboxylase.  Genetic disorder orotic aciduria

3. Non hormonal regulation of blood calcium level Increase Ca absorption Decrease calcium absorption Protein (more soluble) Excess phosphorus insoluble Ca phosphate Acidity Excess oxalate precipitate Ca Lactose convert to lactic acid in intestine and Excess phytates form Ca salts lower the pH 4. Role of vitamin K in blood coagulation  Required for conversion of several blood clotting factor such as factor II, VII, IX and X to active state 5. Catabolism of insulin  organs involved liver, kidney, placenta  Invove two enzyme systems Insulin specific protease y Cleavage between amino acid 16 & 17 of B chain Hepatic glutathione- insulin transhydrogenase y Reduce disulphide bonds so A and B chain are degraded 6. Types of G protein G PROTEIN LIGAND GS (stimulatory) Glucagon Catecholamine Norepinephrine Vasopressin Norepinephrine GT (transducer) Light

TYPE OF RECEPTOR y Glucagon receptor y B1 and B2

2

TARGET ENZYME Both Adenylate cyclase Adenylate cyclase

SECOND MESSENGER Both cAMP (increase) cAMP (decrease) 1) DAG + Ca2+

GI (inhibitory) GPLC (phospholipase)

y y

Vasopressin receptor
1

Both Phospholipase C

Rods

2) IP3 Ca2+ + calmodulin cGMP cGMP phosphodiesterase (decrease)

II.

GIVE REASONS
1) Hyperuricemia may occur in a. Von Gierke s disease (G6P defiency)  Decrease in G 6 Phosphatase will lead to increase of G-6-phosphate due to lack of it s conversion to glucose  Increase G-6-phosphate lead to increase HMS activity which will increase the formation of R-5-P and consequently increase in PRPP b. After chemotheraphy  Chemotheraphy leads to tissue and cell breakdown which will lead to liberation of it s DNA or RNA and consequently their degradation into bases ( purine or pyrimidine) and ribose sugar

c. Mutated PRPP synthetase  Not subjected to allosteric regulation by inorganic phosphate or feed back inhibition  So, lead to increase PRPP which increase phosphoribosylamine and thus purine. 2) Biotin defiency  Due to low biotin diet  Raw egg white contain avidin that bind biotin in non digestible form preventing it s absorption.  Oral antibacterial decrease intestinal flora 3) Thiamine deficiency  Antithiamine factors (thiaminases) cleave thiamine  Alcoholism  Low intake, malabsorption, defective phosphorylation to TPP

III.

ILLUSTRATE
1) Role of vitamin A in dim light vision  Rhodopsin cycle RHODOPSIN (11 cis retinal + opsin)

Dark

Light

opsin

11 cis retinal Isomerase NADH Alcohol dehydrogenase

All trans retinal

Retinal dehydrogenase

NADPH

NADP NAD 11 cis retinol Isomerase All trans retinol

In liver Blood

In retina

2) Mechanism of action of glucagon  Glucagon acts through G protein ( Gs)  To draw, please refer handout from professor or page224

IV.

ENUMERATE
1) Sulphur containing compound (p/g 294)  Mucoitin sulphate, Chondroitin sulphate (carbohydrate)  Sulfolipid (lipid)  Keratin, Immunoglobulin (protein)  Cathepsin, Fatty acid synthethase, Glyceraldehydes 3P dehydrogenase (enzymes)  Vitamin B1, lipoic acid, biotin (vitamin)  CoA, gluthathione, TPP (Coenzyme)  Insulin ( hormone)  Inorganic sulphate, ethereal sulphate, neutral sulphate (urine) 2) Iron containing compound  Haemoglobin  Myoglobin  Cytochromes  Cytochrome oxidase  Catalase  Peroxidase 3) Criteria essential trace elements  Present in healthy tissue  Concentration constant  Deficiency produce clinical manifestation  Has certain biochemical role  Addition to diet prevent deficiency 4) Pyridine containing vitamin. Discuss function and deficiency one of them  Vit B3 (niacin) o required for synthesis NAD and NADP o deficiency lead to pellagra ( dermatitis, diarhea, dementia)  Vit B6 (pyridoxine) o Need in  Transamination reaction  Decarboxylation reaction  Coenzyme for non oxidative deamination of serine and threonine  Synthesis of amino levulinic acid ( precursor of heme)  Generate niacin from tryptophan  Biosynthesis of sphingosine  Essential component of glycogen phosphorylase o Deficiency lead to peripheral neuropathy, convulsion, anemia

5) Vitamin whose deficiency lead to anemia. Explain it. a. Vitamin B6 (pyridoxine) because it is essential for heme biosynthesis b. Folic acid because it is needed for purine biosynthesis and deoxythymidylic acid (dTMP). Decrease in purine and dTMP will inhibit DNA synthesis that will slows down the maturation of RBC causing abnormally large macrocytic RBC with fragile membrane. c. Vitamin B12 (cobalamin) because of it s effect on folate metabolism