Biochemistry high yield part 1

The medical biochemistry - FMGE

CARBOHYDRATE CHEMISTRY:-
 Formula:- Cn H2n On
 Glucose and mannose are epimers at C2 carbon
 Glucose galactose epimers at C4
 Enantimomers are mirror images to each other.
 α and β cyclic forms of D-glucose known as anomers
 C1 is anomeric carbon
 Benedict test reducing properties of sugars
 Sodium amalgam is used as reducing agent.
 Reduction of mono saccharides gives alcohols.
 Aldose reductase converts aldehydes to alcohols.
 Fructose is converted to sorbitol dehydrogenase (liver)
 Monosaccharides gives needle shaped osazones.
 Maltose gives sunflower shaped osazones
 Lactose gives powderpuff shaped osazones
 Maltose (α1-4) (glucose + glucose) – maltose (hydrolysed)
 Lactose (βgalactose – βglucose) (β1-4) – lactase (hydrolysed)
 Sucrose (glucose-fructose) (α1- β2)
 Glucosidic bond- bond between monosaccharides.
 Sucrose is hydrolysed by sucrase/invertase
 Dextrins are breakdown product of starch
 Inulin is a polymer of fructose
 Glycogen and starch are polymer of glucose
 Inulin is need to assess GFR
 Dietary fiber is cellulose (β-glycoside bond)
 D-glucoronic acid + N-acetyl glucosamine – Hyaluronic acid
 Keratin sulphate keeps cornea transparent

LIPID CHEMISTRY:-
 Saturated fatty acids does not contain double bond
 Unsaturated fatty acids has double bonds
 Linolecic, linolenic and arachidonic acid (PUFA)
 Deficiency of EFA – phyrnoderma (toad skin)
 Arachidonic acid gives Eicasonoids
 Unsaturated fatty acids exists in Cis form
 Hydrolysis of triacyl glycerin with alkali produces soaps (saponification)
 Vit.E is naturally occuring antioxidant, superoxide dismutase, urase

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 Purity of fatty acid is checked by iodine number
 RM number (Reichert-Meissl) – to check purity of butter
 Phospholipids – free fatty acids + alcohol + phosphate + nitrogen Base
 Lecithin – choline ( nitrogen base) - ( lung surfactant)
 Hormones like oxytocin and vasopressin action is mediated by phosphatidyl inositol
 Sphinogophospholipid :- cerebonic acid + sphingosine + phosphate + choline =
sphingomyelin.
 Phospholipases – A1, A2, C, D
 PLA2 (phospholipase A2)– give arachidonic acid
 Ganglioside GM2 accmulates in taysachs disease
 Cholesterol –C27 H46 O
 Cholesterol has ohg group at C3. Double bond between C5-C6
 Ergosterol is precussor for vit.D
 Zaks test is used to identify the qualitative analysis of cholesterol
 Emulsified fats in the intestine forms Micelles

PROTEINS AND AMINO ACID CHEMISTRY:-
 kjeldahi’s method is used to find out protein in biological fluids.
 the amino acid glycine has H as side chain
 alanine has –CH3 (methyl) as side chain.
 Cysteine and methionine are sulphur containing aminoacid.
 Aspartic acid and glutamic acid are acidic aminoacid
 Phenyl alanine, tyrosine, tryptophan –aromatic aminoacid
 Alanine is glucogenic aminoacid.
 Leucine and lysine – ketogenic aminoacid.
 Monosodium glutamate intolerance causes chinese restaurant syndrome
 D-penicilamine- used as chelating agent in Wilson’s disease (Accmulation of copper in
brain)
 N-acetyl cysteine used in cystic fibrosis and chronic renal failure.
 GABA-pentane is used as anticonvulsant
 Linear sequence of aminoacid seen in primary structure
 α helix and β sheath – secondary structure.3 diminsional arrangement of protein –teritary
 2 or more poly peptide chains- quartenary structure
 Peptide bond – bond between 2 aminoacid.
 Sangers reagent – used to determine aminoacid sequence
 Sangers reagent used to determin insulin structure
 Biurate is a compound formed by heating urea to 180 degrees . process is biurate reaction
 Copper sulphate is used for heatin in biurate reaction



 Glutathione is involved in transport of amino acfid in intestine and kidney via glutanyl
cycle/meister cycle.
 Aspertame – artifical sweetner.

NUCLEIC ACIDS AND NUCLEOTIDES:-
 Nucleotides – nitrogen base + pentose sugar + phosphate
 Nucleoside – nitrogen base + sugar
 Ribose and deoxyribose differs in C2
 Purine nucleotide is Adenosin mono phosphate
 Pyramide nucleotide is Cyitidine MonoPhosphate, UradineMonoPhosphate
 Alopurinol used in the treatment of gout
 5- fluorouracil used in the treatment of cancers
 Azathioprine is used to suppress immunological rejection during transplantation
 The width of double helix of DNA – 20 Å / 2 nm
 Each turn of helix contains 10 base pairs
 Each turn of helix is 34 Å
 2 strands of double helixd are hold by H-bonds
 DNA protiens are known as histones
 B-DNA proposed by watson and crick in 1953
 A-DNA has 11 base pairs per turn.
 A and B- DNA are right handed helix
 Z-DNA is left handed helix
 Z-DNA has 12 base pairs per turn (zigzag)
 Formamide destahilses H-bonds, therefore it lowers Tm
 Formamide used in recombinant DNA technology
 The sugar in RNA kis ribose
 RNA is subjected to alkali hydrolysis and DNA cannot
 RNA can be identified lby orcinol colour reaction because of ribose
 Nucleolus synthesis r-RNA
 DNA converts M-RNA converts protein
 M-RNA has 7 methyl guicnosine at 5 prime end
 The 3 prime kend contains poly- A tail (MRNA)
 The stucture of t-RNA resembles clover leaf
 the acceptor arm of t-RNA has CCA cap (3prime)
 D-arm has dihyrouridine (t-RNA)
 TψC arm has T, pseudouridine and C (tRNA)



ENZYMES :-
 There are 6 cclasses of enzymes
 The functional unit of enzyme is holoenzyme
 Holoenzyme is made up of apoenzyme (protein part) and co-enzyme (non-protein part).
 Increase in concentration of substrate increase enzyme velocity
 Km = ½ Vmax
 Km = S (substrate concentration) Km-(michaelis-menten constant)
 Km is defined as the substrate concentration to produce ½ maximum velocity.
 Low Km denotes strong affinity between enzyme and substrate
 When enzymes are exposed to C and above temperatures denaturation occurs.
 All enzymes are active at neutral PH (7)
 The most common aminoacid at active site is serine

INHIBITORS:-
 Xanthine oxidase – allopurinol
 MAO (mono amino oxidase) – ephedrine, auphetamine
 Dihydrofolate reducatse – aminopterin, amethopterin, methotrexate
 Acetylcholine esterase – succinyl choline
 Dihydropteroate synthase – sulfanilamide
 Vit. Kepoxide reductase – dicumorol
 HMG co-A reducatse – lorastatin, compactin.
 Disulfiran is the drug used in the treatment of alcoholism
 Transketolase requires TPP
 Streptokinase is used to remove blood clots
 Streptokinase converts plasminogen to plasmin
 Asperginase is used in treatment of leukemias
 Increase amylase – acute pancreatitis
 Increase SGPT (serum glutamate pyruvate transaminase) – liver diseases
 Increase alkaline phosphatase – rickets and bone diseases
 Increase acid phosphatase – prostate carcinoma
 Increase aldolase – muscle dystrophy
 Increase troponin I – MI (first marker)
 Increase CPK1 – BB (brain)
 Increase CPK2 – MB (heart)
 Increase CPK3 – MM (skeletal muscle)



LIPID METABOLISM:-
 TG – plasma concentration is 75-150 mg/dl
 Cholesterol – plasma concentration is 150-200 mg/dl
 Hypercholesteremia - >250mg/dl
 Hormone sensitive TG lipase removes fatty acid from C1 or C3 of TAG
 glucagon, epinephrine, thyroxine, ACTH – increase cAMP – increase lipolysis.
 Insulin – decrease cAMP – decrease lipolysis
 Glycerol is metabolized by liver.
 FFA from Adipose Tissue are transported to liver by albumin.
 Brain, erythrocytes cannot utilize FA
 FA activation – cytosol (ATP, Co-A, mg2+) requires 2 ATP
 Long chain FA are metabolized in peroxisomes
 Tangair’s disease – plasma HDL particles are almost absent
 Biosynthesis of FA in liver starts with glycerol and in adipose tissue with glucose and
acetyl Co-A
 Glycolipids act as receptors in cell membrane
 Absorption of cholesterol from intestine is by diffusion
 Cholesterol gives bile salts, vit.D, steroid hormones (sex hormone and corticoids)
 Prostaglandin exhibit platelet aggregation, increase cAMP and vasodilation
 Obesity gene – leptin
 β-oxidation – mitochondria
 activation of FA in β-oxidation – cytosol
 melanoyl Co-A inhibits – CAT-I, thus inhibits β-oxidation
 CAT-I – outer mitochondrial membrane
 CAT-II – inner mitochondrial membrane
 Medium chain aceyl Co-A dehydrogenase, rate limiting step of β-oxidation.
 β-oxidation of palmitate gives 106 ATP
 SIDS (sudden infant dead syndrome) – deficiency of medium chain aceyl Co-A
dehydrogenase (M-CAD.)
 Methyl melanoic academia – vit.B12 deficiency
 Methyl melanoic Co-A – requires Vit. B12
 Zellweger syndrome – absence of peroxisomes cerebrohepatorenal syndrome.
 Zellweger syndrome – defect in long chain fatty breakdown
 α-oxidation – Refsums disease – accumulation of phytanic acid.
 ω-oxidation requires – cytochrome P450 , NADPH, O2.
 Ketone bodies are synthesized in liver
 Ketone bodies are utilized by brain in prolonged starvation
 HMG – CoA synthase – rate limiting step in ketone bodies synthesis
 Ketone bodies cannot be utilized by liver because of deficiency of thiophorase
 Acetone exhaled by lungs – sweetish odur.


 Detection of ketone bodies in urine – rothers test
 Glucagon stimulates ketone bodies synthesis, insulin inhibits
 Treatment of keto acidosis – insulin
 Fatty acid bio-synthesis – cytosol.
 Acetyl Co-A for fatty acid biosynthesis (FAB) obtains from citrate lyase
 NADPH in FAB obtained form HMP- pathway and malic enzyme
 Acetyl Co-A carboxylase – rate limiting step in FAB
 Insulin stimulates FAB –glucagon inhibits
 Un-saturated fatty acids synthesized by fatty aceyl Co-A desaturase. Human lacks this
enzyme.
 TAG synthesis – adipose tissue
 Cerebronic acid + phyngosine = seramide
 Seramide + phosphate + choline = sphingomyelin
 Phospholipase A1 – cleaves FFA at C1
 Phospholipase A2 – cleavesFFA at C2
 Phospholipase C - cleaves phosphate and glycerol found in lysozomes of hepatocytes
 L-CAT found in lungs
 L-CAT activity is associated with apo-A1 of HDL
 Sphingomyelinase deficiency niemann’s pick’s desease
 Deficiency of seramidase Fauber’s disease
 Deficiency of β-galactidase krabbe’s disease
 Deficiency of β-glucosidase gauchers disease
 Deficiency of α-galactidase fabrys disease
 Deficiency of hexosaminidase A – Taysachs disease
 Cholesterol biosynthesis, liver- 50%, intestine- 15%
 Cholesterol synthesis- cytosol.
 HMG- CoA reductase – rate limiting step in cholesterol biosynthesis
 Cholesterol formulae :- C27 H46 O
 Glucagon – glucocorticoids – decrease cholesterol biosynthesis
 Compactin, lorastatin inhibits – HMG Co-A reductase
 HMG-CoA reductase also inhibited by bileacids
 7-α-hydroxylase – rate limiting step in bileacid biosynthesis
 95% of the bile is reabsorbed and return back to liver
 Primary bileacids – cholic acid chenodeoxycholic acid.
 Conjuation of bile acids done by – glycine , taurine
 Deoxycholic acid,lithocholic acid – secondary bile acids
 Chenodiol treat for cholilithiasisctiatn of chylomi
 Chylomicrons has B48
 VLDL has B100
 HDL has apoprotein-A



 Activation of chylomicrons and VLDL requires Apo-CII and Apo-E from HDL
 Lipoprotein lipase deficiency – hyperlipoprotenimia type I
 Defect in LDL receptors – type IIA
 Excess apoB – type IIB
 Abnormality in apo-E – type III
 Over production of TG – type IV
 Defect in HDL receptors – tangier’s disease

OXIDATIVE PHOSPHORYLATION AND ETC:-
 Phosphophenol pyruvate is 14.8 cal/mole.
 S-adenosyl methionane is 10 cal/mole
 cAMP is 12 cal/mole
 ATP is 7.3 cal/mole
 The inner mitochondrial membrane is impermeable to H+, K+ and Na+
 Co-enzyme Q is also known as ubiquione
 Complex-I – NADH-co-encyme Q reductase inhibited by – amytal, rotenone,
pricydine-A
 Complex III – Co-enzyme Q-cytC reductase inhibited by antimycin A,
BAL (british anti lewisite)
 Comple IV – cytochrome oxidase inhibited by cyanide, CO, Na-azide.
 otation of -subunit is 12
 ATP synthatase has F0 and F1 subunits.
 F0 – channel protein C
 F1 – central γ subunit, 3α, 3β
 Mutation of mitochondrial DNA – oxiphos disease AKA (lebers hereditary optic
neuropathy)
 2, A dinitrophenol – uncoupler of oxiphosphorylation
 Digomycin inhibits oxidative phosphorylation by binding to ATP synthetase 2 blockes
proton channels
 Atractyloside inhibits oxidative phosphorylation by blocking the adequate supply of
ADP.



VITAMINS:-
Vit.A:-
 Retinol is present in animals in the form of retinylester
 Retinal,retinol and retinoic acid are vitamers of vitamin A
 β- carotene gives l2 moles of retinal by 1 ’-1 ’ di-oxygenase
 retinyl esters are transported by chylomicrons and stored in liver
 retinol is transported in circulation by RBP 9retinal binding protein)
 rods – dim light vision
 cones – bright light
 vit-A required for rods
 rhodopsin present in rods
 rhodopsin = 11-cis retinal + opsin
 during walds visual cycle rhodipsin is bleached to metarhodopsin-II which increases C-
GMP an degenerates nerve impulse
 Vit-A deficiency night blindness
 Serene deficiency of vit-A causes xerophthalmia, characterized of dryness of conjunctiva
and cornea, white triangular plaques, bitot’s spots are seen
 Xerophthalmia leads to keratomalacia causing total blindness

Vit. D
 Ergosterol (plants) ergocalciferol – vit. D2
 Cholecalciferol (animals)- vit.D3
 Vit-D synthesis takes place in skin.
 1,25- Di-hydroxycholecalciferal is known as calcitriol i.e., active form of vit-D
 25- α -hydroxylase and 1-α-hydroxylase requires cyt-p-450, NADPH and O2
 Vit.D is essential for bone formation
 Vit-D deficiency:- pickets – bowlegs – children; osteomalacia – Adults.
 Alkaline phosphatase activity elevated in rickets
 Vit-D is more toxic in over doses
 Vit-D is transported in the circulation by α2-globulin
 1-α-hydroxylase present in kidney and stimulated by PTH
 25- α –hydroxylase present in liver

Vit-E:-
 Anti sterility vitamin
 Also known as tocopherols α,β,γ,δ out of these α-tocopherols more active
 Vit-E is transported by VLDL and LDL in the circulation
 Normal plasma levels of tocopherols <1mg/dl


 Vit-E naturally occurring antioxidant and it requires selenium
 Vit-E prevents peroxidation reactions of PUFA
 ALA-synthase requires vit.E

Vit-K:-
 Vit-K also synthesized by intestinal bacteria
 Bile salts are essential for absorption of vit- K
 Transported to liver by means of LDL
 Vit-K is responsible for post transitional modification of 2,7,9,10 clotting factors by
carboxylation of glutamic acid
 Carboxylation of glutamic acid is inhibited by dicumarol
 Deficiency of vit-K leads to lack of acive prothrobin in circulation
 High doses of vit-K causes hemolytic anemia

Vit-C :-
 Vit-C is required for collagen formation
 Vit-C is co-enzyme for hydroxylation of proline and lysine, where protocollagen is
converted to collagen
 Deficiency of vit-C leads to scurvy, delayed wound healing

Vit-B1 :-
 co-enzyme – TPP
 TPP required for PDH transketolase
 Deficiency seen in the people who consume polished rice as a staple food
 Elevation of pyruvate in plasma and excrets in urine
 Wet-beriberi – edema – systolic increase – diastolic decrease – bouncing pulse.
 Dry-beriberi – no edema – neurological manifestations are seen
 Decrease transketoplase activity – Wernick’s korsakoff syndrome
 Thyamine deficiency more commonly seen in alcoholics.


Biochemistry high yield part 1

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Biochemistry high yield part 1