ANSWER SCHEME 2010 I. DISCUSS 1.

a) Role of following compound in detoxication Glucuronate Active form UDP glucuronate Will conjugate with carboxyl, amino, sulfhydryl or hydroxyl groups (CASH) Examples carcinogens, aniline, benzoic acid meprobamate, phenol, steroids, bilir ubin, 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 additiv e) 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. a) How following substances can be synthesised dADP from IMP IMP to AMP by Addition of aspartate to IMP using adenylosuccinate synthethase to form adenylos uccinate 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 de carboxylase. 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 the pH Excess phytates form Ca salts 4.

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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 Catabolism of insulin organs involved liver, kidney, placenta Invove two enzyme systems Insulin specific protease

5.

Cleavage between amino acid 16 & 17 of B chain Hepatic glutathione- insulin transhydrogenase Reduce disulphide bonds so A and B chain are degraded TARGET ENZYME SECOND MESSENGER

6. Types of G protein G PROTEIN LIGAND TYPE OF RECEPTOR GS (stimulatory) Glucagon

Catecholamine Glucagon receptor B1 and B2 Both Adenylate cyclase Both cAMP (increase) GI (inhibitory) Norepinephrine 2 Adenyl te cycl se cAMP (decre se) GPLC (phospholip se) V sopressin DAG + C 2+

2) IP3 C 2+ + c lmodulin GT (tr nsducer) Light Rods cGMP phosphodiester se cGMP (decre se)

f its m tion b. f its dine) c. ition 2)

Mut ted PRPP synthet se Not subjected to llosteric regul tion by inorg nic phosph te or feed b ck inhib

So, le d to incre se PRPP which incre se phosphoribosyl mine nd thus purine. Biotin defiency Due to low biotin diet R w egg white cont in vidin th t bind biotin in non digestible form preventing its bsorption. Or l ntib cteri l decre se intestin l flor 3) Thi mine deficiency Antithi mine f ctors (thi min ses) cle ve thi mine Alcoholism Low int ke, m l bsorption, defective phosphoryl tion to TPP

III. 1)

ILLUSTRATE Role of vit min A in dim light vision Rhodopsin cycle

II. 1) .

GIVE REASONS Hyperuricemi m y occur in Von Gierkes dise se (G6P defiency) Decre se in G 6 Phosph t se will le d to incre se of G-6-phosph te due to l ck o conversion to glucose Incre se G-6-phosph te le d to incre se HMS ctivity which will incre se the for of R-5-P nd consequently incre se in PRPP After chemother phy Chemother phy le ds to tissue nd cell bre kdown which will le d to liber tion o DNA or RNA nd consequently their degr d tion into b ses ( purine or pyrimi nd ribose sug r

Norepinephrine V sopressin receptor 1 Both Phospholip se C 1)

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Mech nism of ction of gluc gon Gluc gon cts through G protein ( Gs) To dr w, ple se refer h ndout from professor or p ge224 ENUMERATE Sulphur cont ining compound (p/g 294) Mucoitin sulph te, Chondroitin sulph te (c rbohydr te) Sulfolipid (lipid) Ker tin, Immunoglobulin (protein) C thepsin, F tty cid syntheth se, Glycer ldehydes 3P dehydrogen se (enzymes) Vit min B1, lipoic cid, biotin (vit min) CoA, gluth thione, TPP (Coenzyme) Insulin ( hormone) Inorg nic sulph te, ethere l sulph te, neutr l sulph te (urine) Iron cont ining compound H emoglobin Myoglobin Cytochromes Cytochrome oxid se C t l se Peroxid se Criteri essenti l tr ce elements Present in he lthy tissue Concentr tion const nt Deficiency produce clinic l m nifest tion H s cert in biochemic l role Addition to diet prevent deficiency Pyridine cont ining vit min. Discuss function nd deficiency one of them Vit B3 (ni cin) required for synthesis NAD nd NADP deficiency le d to pell gr ( derm titis, di rhe , dementi ) Vit B6 (pyridoxine) Need in Tr ns min tion re ction Dec rboxyl tion re ction Coenzyme for non oxid tive de min tion of serine nd threonine Synthesis of amino levulinic aci ( precursor of heme) Generate niacin from tryptophan Biosynthesis of sphingosine Essential component of glycogen phosphorylase Deficiency lea to peripheral neuropathy, convulsion, anemia

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4) o o o

5) Vitamin whose eficiency lea to anemia. Explain it. a. Vitamin B6 (pyri oxine) because it is essential for heme biosynthesis b. Folic aci because it is nee e for purine biosynthesis an eoxythymi y lic aci ( TMP). Decrease in purine an TMP will inhibit DNA synthesis that wi ll slows own the maturation of RBC causing abnormally large macrocytic RBC with fragile membrane. c. Vitamin B12 (cobalamin) because of its effect on folate metabolism

IV. 1)