Quiz
Enzyme Kinetics 5
This quiz has question types that open in the usual player.
Questions in this quiz (27)
1Drug metabolism involves pathways for the biosynthesis of endogenous substrates (eg hormones, cholesterol and bile acids) i.e. normal biosynthesis enzymes are involved in the metabolism of these drugs, to produce less pharamacologically active products. There are exceptions where metabolism will produce more active metabolites (e.g. prodrugs like aspirin) or the metabolite may be more toxic/carcinogenic.
- ATrue
- BFalse
2The kidney is the major site of drug metabolism, but specific drugs may undergo biotransformation in other tissues e.g. lungs
- ATrue
- BFalse
3Lipophilic compounds must be made more hydrophilic by drug metabolism for secretion. Why?
- AUnmetabolised lipophilic molecules will remain in the blood and tissues and maintain their pharmacological effects for less time
- BHydrophilic drugs go to the stomach and intestine before circulation
- CBoth lipophilic and hydrophilic drugs go to the kidney for metabolism, reducing toxicity and are then excreted in urine
- DLipophilic drugs first cross the duodenum
4The physical and chemical properties of a drug determine its success to reach its target
1. [blank_start]Chemical[blank_end] stability such as stability in the stomach
2. [blank_start]Metabolic[blank_end] stability no interaction with other metabolites
3. Successful Absorption ability to [blank_start]cross membranes[blank_end]
Dosage:
1. Depending on dosage, drugs can be therapeutic failures if the [blank_start]dosage is too low[blank_end] to have an effect
2. This could be if the drug is unable to [blank_start]enter the circulation[blank_end] too, or if it is broken down in the stomach and excreted quickly
3. If the drug dosage is too high, it may not be metabolised fast enough and will remain in the blood too long having a [blank_start]toxic effect/overdose[blank_end]
4. Have to consider all of these components – volume of distribution, clearance of the drug (metabolism) and absorption
5. Metabolic stability refers to the fact that after metabolism, [blank_start]chemical properties[blank_end] may change, and you may have new interactions- AChemical
- BProteolytic
- CMetabolic
- DBiosynthetic
- Ecross membranes
- Fenter cells
- Gdosage is too low
- Hdosage is too high
- Idrug isn't potent
- Jenter the circulation
- Kbe metabolised
- Ltoxic effect/overdose
- Mtolerance
- Nchemical properties
- Oconformation
5Phase I metabolism: involves small chemical changes that make compounds more hydrophilic, for effective clearance by the kidneys. What else is true?
- AUsually involve unmasking of a hydrophilic group (e.g. hydroxyl, amine, sulfhydryl)
- BUsually involve hydrolysis, oxidation or reduction mechanism
- CCytochrome P550 enzymes are responsible for most phase I reactions in the liver
- DHydrophobic groups may be added in the liver to increase biological half-life
- EMetabolites produced are often inactive and readily excreted
6If the drug remains lipophilic after phase I, it will continue to circulate and undergo phase II metabolism. What else is true of phase II?
- AOften involves addition of a large non-polar group in attempts to increase solubility
- BResults in secretion via faeces
- CIt is the final stage in drug metabolism
- DGenerate highly polar derivatives/conjugates for uptake
- EDerivatives include glucoronide, sulfate, acetate and amino acids
7Once modified the drugs undergo phase III metabolism. Which are true?
- AInvolves the use of membrane drug transporters to transport drugs across cellular barriers
- BCan target sites of accumulation
- CAll drugs undergo phase III
8Oxidation is the first and most common step involved in the drug metabolism. What else is true of oxidation in drug metabolism?
- AIt is the addition of oxygen, or removal of hydrogen.
- BKidney is the main organ whereas oxidation takes place by cytochrome P550
- CIncreased polarity of the oxidised products
- DDecreased water solubility and excretion in urine
- ETypes include: aliphatic or aromatic hydroxylation, N-, or S-oxidation, N-, O-, S-dealkylation
9Reduction is the removal of oxygen or addition of hydrogen. What else is true of it in drug metabolism?
- AMore common than oxidation in drug metabolism
- BExample: Nitro reduction to hydroxylamine/amine, carbonyl reduction to alcohol
- CCytochrome P450 system is involved in some reactions
- DModifications occur mainly in the kidney
10Which are true of hydrolysis in drug metabolism?
- AThe addition of water gives more polar metabolites
- BEsterases and aminases catalyse the hydrolysis of drugs
- CCan convert ester or amide to acid and alcohol or amine
- DRequires just water and no enzyme
11What is the main enzyme responsible for the failure of most drugs in trials?
[blank_start]Cytochrome P450[blank_end]
Reduction e.g. [blank_start]NADPH-cytochrome P450 reductase[blank_end]
Oxidation e.g. [blank_start]Cytochrome P450 monooxygenase system[blank_end]- ACytochrome P450
- BNADPH cytochrome P450 reductase
- CCytochrome P450 monooxygenase system
12Phase I: Microsomal mixed-function oxidase system is cytochrome P450 dependent.
An [blank_start]oxygen and a reducing system[blank_end] (NADPH) is required—one atom of oxygen is transferred to the [blank_start]substrate[blank_end], and the other undergoes a two electron reduction and is converted to [blank_start]water[blank_end]. P450 functions together with membrane-bound [blank_start]NADPH oxidase[blank_end].
The mixed-function oxidase is found in [blank_start]microsomes[blank_end] (vesicle-like artefacts of endoplasmic reticulum) of many cells ([blank_start]liver[blank_end], kidney, lung, and intestine). There are different isozymes in other cells and it mostly modifies drugs in the [blank_start]liver[blank_end], despite presence elsewhere.- Aoxygen and a reducing system
- Breducing system
- Coxidising system
- Dsubstrate
- Ewater
- Facceptor
- Gwater
- Hhydrogen peroxide
- INADPH oxidase
- Jmonoamine oxidase
- Kmicrosomes
- Lendosomes
- Mphagosomes
- Nliver
- Olarge intestine
- Plymph nodes
- Qliver
- Rkidney
13Cytochrome P450 (CYP) 3A4
Structure
Contains a [blank_start]heme[blank_end] or [blank_start]protoporphyrin IX[blank_end] (an iron(III) porphyrin cofactor).
There are different isoforms of Cyt P450.
They are associated to the cell membrane (attached and close by).
Catalysis
Catalyses [blank_start]hydroxylation[blank_end] or [blank_start]epoxidation[blank_end] of various substrates.
Mechanism
Requires another enzyme [blank_start]NADPH-cytochrome P450 reductase[blank_end], which is a flavoenzyme that contains one molecule of flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). NADPH donates a proton to [blank_start]FAD[blank_end] and which is then transferred to a [blank_start]FMN[blank_end] and then an electron transfer occurs to the [blank_start]heme[blank_end] group. Molecular oxygen binds to the heme cofactor after [blank_start]reduction[blank_end] of [blank_start]ferrous (Fe2+)[blank_end] to [blank_start]ferric (Fe3+)[blank_end] and is converted to a reactive form. This activates oxygen, using 2 electrons, reducing it to water. The other oxygen is transferred to the substrate and is used in a number of [blank_start]oxygenation[blank_end] reactions.
Can oxygenate different compounds this way e.g. adding OH to aromatic ring to increase hydrophilicity. There is [blank_start]no real selectivity[blank_end] in terms of what it can modify – due to active site.- Aheme
- Bferric ring
- Chaemoglobin
- Dprotoporphyrin IX
- Eprotoporphyrin X
- Fporphyrin X
- Ghydroxylation
- Helimination
- Isubstitution
- Jepoxidation
- Kneutralisation
- LNADPH-cytochrome P450 reductase
- MReduced ferrous cytochrome P450
- NFAD
- OFMN
- PATP
- QNADPH
- RFMN
- SFAD
- TNADPH
- UATP
- Vheme
- Wprotoporphyrin IX
- Xreduction
- Yoxidation
- Zferrous (Fe2+)
- AAMg (2+)
- ABferric (Fe3+)
- ACMg (3+)
- ADoxygenation
- AEhydrolysis
- AFelimination
- AGno real selectivity
- AHno efficiency
- AIa limitation
14If the substrate for cytochrome P450 was an R-benzene product, what would the product be?
- AAn R-phenol product
- BAn benzoic acid group
- CCyclohexane
15Active site of cytochrome P450 can bind many substrates and modify them. It's large active site makes it [blank_start]promiscuous[blank_end].
- Apromiscuous
16Iron-oxo species:
1. Membrane bound [blank_start]NADPH oxidoreductase[blank_end] gives an electron to reduce Fe3+ to Fe2+ to give [blank_start]ferrous heme[blank_end]
2. O2 comes in and can bind [blank_start]ferrous heme[blank_end] and you form a [blank_start]ferrous oxy[blank_end] species
3. Another electron is gained from the oxidase, and you get oxidation to Fe3+ so you form [blank_start]ferric peroxy[blank_end] species (with an overall 2- charge)
4. Upon its formation you can take H from water to make [blank_start]ferric hydroperoxo[blank_end] species, and you still have the drug bound elsewhere
5. [blank_start]Ferric hydroperoxo[blank_end] species is also known as [blank_start]compound 0[blank_end] and is an active compound for drug modification
6. Gain another H and add to OH group and release water, so you get [blank_start]ferryl oxo[blank_end] species ([blank_start]compound 1[blank_end]) which can now make [blank_start]free radical attack[blank_end] on the drug substrate to affect its [blank_start]hydroxylation[blank_end]
7. Upon modification of drug, you lose the modified drug from the active site as a [blank_start]water[blank_end] comes in and displaces the drug, regenerating heme and rest of pathway
Return to ferric heme can occur before completion of the pathway if the drug is [blank_start]not tightly bound[blank_end], so you lose O2. If there is drug loss at compound 0, then you get regeneration of ferric heme and release of [blank_start]hydrogen peroxide[blank_end]. Gain of 2 protons and an electron will regenerate ferric heme. Entire pathway is tightly regulated.- ANADPH oxidoreductase
- Bcytochrome P450 monooxidase system
- Cepoxide hydrolase
- Dferrous heme
- Eferric heme
- Fferryl heme
- Gferrous heme
- Hferric heme
- Iferryl heme
- Jferrous oxy
- Kferrous peroxy
- Lferric oxy
- Mferric peroxy
- Nferric peroxo
- Oferryl peroxy
- Pferric hydroperoxo
- Qferrous hydroperoxo
- Rferric peroxo
- SFerric hydroperoxo
- Tferrous hydroperoxo
- Uferric peroxo
- Vferryl oxo
- Wferric oxo
- Xferryl oxy
- Ycompound 0
- Zcompound 1
- AAcompound 2
- ABcompound 1
- ACcompound 2
- ADcompound 0
- AEfree radical attack
- AFnucleophilic attack
- AGelectrophilic attack
- AHhydroxylation
- AIreduction
- AJoxidation
- AKwater
- ALheme
- AMnew drug
- ANnot tightly bound
- AOnot complementary
- APtightly bound
- AQhydrogen peroxide
- ARhydroxyl radical
17Aromatic hydroxylation
Hypothesised that aromatic compounds were metabolized first to the corresponding [blank_start]epoxides[blank_end] (a cyclic ether with a three-atom ring). This was confirmed by a group at NIH that isolated naphthalene 1,2-oxide from microsomal [blank_start]oxidation[blank_end] of naphthalene.
Arene oxide Formation
[blank_start]Kinetic isotope studies[blank_end] indicate that direct arene epoxidation is unlikely, but rather an activated heme [blank_start]iron-oxo[blank_end] species may add to the aromatic ring.
Arene oxides commonly formed by [blank_start]P450[blank_end], followed by NIH shift or 1,2- hydride shift
A tetrahedral intermediate is formed that can rearrange via the [blank_start]epoxide or ketone pathway[blank_end] to finally give an arenol.
The arene oxide can also undergo hydration by [blank_start]epoxide hydrolase[blank_end] to give a trans-diol, react with glutathione, catalyzed by [blank_start]glutathione S-transferase[blank_end] to form a β-hydroxy sulfide, as well as react with macromolecular nucleophiles.
Kinetic isotope studies were used to understand how epoxide is formed- Aepoxides
- Boxides
- Cethers
- Doxidation
- Ereduction
- FKinetic isotope studies
- GIsotopic labelling
- Hiron-oxo
- Iferroxo
- Jferroxy
- KP450
- Lepoxide hydrolase
- Mepoxide or ketone pathway
- Noxidation pathway
- Oreduction pathway
- Phydroxylation pathway
- Qepoxide hydrolase
- RP450
- SNADPH oxidoreductase
- Tglutathione S-transferase
- Uglutamate
- Vglutathione isomerase
18Epoxide hydrolyse opens the bottom epoxide ring or can modify the ring by adding glutathione, OH or another nucleophile.
- ATrue
- BFalse
19Monoamine oxidases (MAO)
Catalyses [blank_start]oxidative deamination[blank_end] of endogenous catecholamines such as [blank_start]epinephrine[blank_end], and is located in [blank_start]nerve terminals[blank_end] and peripheral tissues. MAO inhibited by by [blank_start]antidepressants[blank_end], which affects levels of serotonin. Fatal drug-drug interactions [blank_start]increase release[blank_end] of catecholamine by-products or [blank_start]inhibit[blank_end] their reuptake in nerve terminals. Catecholamines ([blank_start]epinephrine[blank_end], norepinephrine, and dopamine) can lead to hypertensive crisis.- Aoxidative deamination
- Breductive deamination
- Chydrolysis
- Depinephrine
- Eglutamate
- Fnerve terminals
- Gmuscle tissue
- Hantidepressants
- Ichemotherapy drugs
- Jpainkillers
- Kincrease release
- Linhibit release
- Minhibit
- Nstimulate
- Oepinephrine
- Pglutamate
20Phase II transformations:
When phase I products are not sufficiently hydrophilic or inactive to be eliminated, the drugs or metabolites undergo phase II reactions where you add [blank_start]large polar compounds[blank_end] to make them more hydrophilic so that they get secreted in [blank_start]feces[blank_end].
Phase I reactions provide a functional group in the molecule to undergo phase II reactions. Phase II reactions modify functional groups by a [blank_start]conjugation[blank_end] reaction.
Phase II conjugation reactions are capable of converting these metabolites to more [blank_start]polar[blank_end] and water soluble products.
They often require [blank_start]coenzymes[blank_end].
Conjugation reactions are catalysed by [blank_start]transferases[blank_end] (liver).
Most conjugates are biologically inactive and nontoxic because they are highly polar and unable to cross cell membrane.- Alarge polar compounds
- Bsmall hydrophilic compounds
- Cfeces
- Durine
- Econjugation
- Fhydroxylation
- Gphosphorylation
- Hpolar
- Ilipophilic
- Jcoenzymes
- Kcofactors
- Ltransferases
- Mubiquitinases
21Phase II Metabolism
Glucuronidation by [blank_start]UDP-Glucuronosyltransferase[blank_end] (-OH, -COOH, -NH2, -SH)
Adding a sugar moiety increases solubility and ease of excretion as well. Conjugation to [blank_start]a-D-glucuronic acid[blank_end]. a-D-glucuronic acid. Products are often excreted in the [blank_start]bile[blank_end]. Enterohepatic ([blank_start]bile[blank_end] circulation) recycling may occur due to gut [blank_start]glucuronidases[blank_end]. Requires enzyme [blank_start]UDP-glucuronosyltransferase (UGT).[blank_end]
Example: [blank_start]Phosphorylase[blank_end] adds functional group from UDP to glucose-1-P → [blank_start]UDPG dehydrogenase[blank_end] oxidises the sugar, removing 2 H → End product is [blank_start]1-UDP-glucoronic acid.[blank_end]
N-glucuronidation occurs with [blank_start]amines[blank_end] (mainly aromatic), [blank_start]amides[blank_end] and [blank_start]sulfonamides[blank_end].
O-glucuronidation occurs by ester linkages with [blank_start]carboxylic acids[blank_end], [blank_start]phenols[blank_end] and [blank_start]alcohols[blank_end].
Sulfation by [blank_start]Sulfotransferase[blank_end]: (-NH2, -SO2NH2, -OH)
Major pathway for [blank_start]phenols[blank_end] (also alcohols, [blank_start]amines[blank_end] and thiols) and PAPS (3’-Phosphoadenosine-5’-phosphosulfate).
Sulfation occurs at [blank_start]low[blank_end] phase I substrate concentrations, whereas glucuronidation requires [blank_start]higher[blank_end] substrate concentrations.
Acetylation by [blank_start]acetyltransferase[blank_end] (-NH2, -SO2NH2, -OH)
Occurs on aromatic [blank_start]amines[blank_end] and sulfonamides, and requires N-acetyltransferase and the co-factor [blank_start]acetyl-CoA.[blank_end]
Important in sulfonamide metabolism because acetyl-sulfonamides are [blank_start]less[blank_end] soluble than the parent compound and may cause renal toxicity due to precipitation in the kidney.
Amino acid conjugation (-COOH)
Active [blank_start]CoA-amino acid[blank_end] conjugates that react with drugs by N-Acetylation include [blank_start]Gly, Glu and Arg[blank_end]
Glutathione conjugation by Glutathione-S-transferase:
Increases solubility and ease of secretion Glutathione is a tripeptide e.g. [blank_start]Gly-Cys-Glu[blank_end]. Drugs are conjugated by glutathione-S-transferase (GST). Conjugated compounds can subsequently be attacked by [blank_start]g-glutamyltranspeptidase[blank_end] and a peptidase and products can be further acetylated.
Fatty acid conjugation
Stearic and palmitic acids are conjugated to drug by [blank_start]esterification[blank_end] reaction.
Condensation reactions- Aa-D-glucuronic acid
- Bα-L-glucuronic acid
- Cβ-D-glucuronic acid
- Dbile
- Eurine
- Ffeces
- Gbile
- Hurine
- Ifeces
- Jglucuronidases
- Kglycosylases
- Luraminidases
- MUDP-glucuronosyltransferase (UGT).
- NUDP-glucosyltransferase (UGT)
- OUDP-glucuronosylases (UGN)
- PPhosphorylase
- QHydroxylases
- RUDPG dehydrogenase
- SUDPG oxidases
- TUDPG reductase
- U1-UDP-glucoronic acid.
- V3-UDP-glucoronic acid
- W1-UDP-glucoronosyl
- Xamines
- Yhydroxyls
- Zamides
- AAphosphates
- ABsulfonamides
- ACsulfates
- ADcarboxylic acids
- AEaldehydes
- AFphenols
- AGketones
- AHalcohols
- AIaldols
- AJphenols
- AKcarboxylic acids
- ALamines
- AMaldehydes
- ANlow
- AOhigh
- APhigher
- AQlower
- ARUDP-Glucuronosyltransferase
- ASUDP-Gluconotransferase
- ATGlucosyltransferases
- AUSulfotransferase
- AVSulfonases
- AWacetyltransferase
- AXhistone acetyltransferases
- AYamines
- AZhydroxyls
- BAacetyl-CoA.
- BBacetate.
- BCless
- BDmore
- BEGly, Glu and Arg
- BFGly, Cys and Glu
- BGGly-Cys-Glu
- BHAsp-His-Ser
- BIGly-Glu-Arg
- BJg-glutamyltranspeptidase
- BKtranspeptidase
- BLesterification
- BMconjugation
- BNaddition
- BOCoA-amino acid
- BPacetate-amino acid
22Removing functional groups that make drugs susceptible to enzymes will make them more resistant to metabolism. Remove methyl and replace with butyl in tolbutamide, to make it longer lasting – still degraded but takes longer.
- ATrue
- BFalse
23If a drug is too resistant to metabolism, it can pose problems as well (toxicity, long-lasting side effects). So you can add functional groups that are susceptible to metabolic enzymes to make drugs less resistant to metabolism. Reducing resistance e.g. adding acetate gives decreased lifetime and makes it more readily metabolised in phase I.
- ATrue
- BFalse
24Phase III
Efflux transporters detoxify cells from ‘toxic compounds’ e.g. [blank_start]P-glycoprotein[blank_end]. Can [blank_start]secrete[blank_end] compounds, even those that haven’t gone through phase 1 or 2.
They are one of the primary proteins involved in [blank_start]multidrug resistance[blank_end] in the treatment of cancers.
ATP-binding cassette (ABC) –superfamily- requires [blank_start]ATP hydrolysis[blank_end] to drive the export. ABC transporters can confer resistance to bacteria. Makes it difficult to circulate drugs – must modify them so they can’t go through ABC transporters and be [blank_start]excreted[blank_end] too quickly.- AP-glycoprotein
- Bg-glycoprotein
- Cglycopeptides
- Dsecrete
- Edegrade
- Fmultidrug resistance
- Gchemotherapy
- HATP hydrolysis
- IGTP hydrolysis
- JNADPH
- Kexcreted
- Ldegraded
- Mused
25Factors affecting metabolism
Rate and pathway of drug metabolism are affected by species, strain, [blank_start]sex[blank_end], age, [blank_start]hormones[blank_end], pregnancy, and liver diseases. Side effects may differ in individuals as drug metabolism [blank_start]efficiency[blank_end] will vary amongst individuals.
Drug metabolism is [blank_start]stereospecific[blank_end]. Enantiomers act as two different xenobiotics, with different metabolites and [blank_start]pharmacokinetics[blank_end]. Sometimes the inactive enantiomer produces [blank_start]toxic[blank_end] metabolites or may inhibit metabolism of active isomer.- Ahormones
- Bneurotransmitters
- Csex
- Dphenotype
- Eefficiency
- Factivity
- Gstereospecific
- Hgeneral
- Ipharmacokinetics
- Jthermodynamics
- Kefficacy
- Ltoxic
- Minactive
26Plasma binding:
Drugs can bind to plasma proteins and only [blank_start]unbound[blank_end] compound is available for distribution into tissues.
Acidic drugs tend to bind to [blank_start]albumin[blank_end]. Basic drugs bind to [blank_start]alpha-1 acid glycoprotein[blank_end].
0-50% bound = [blank_start]negligible[blank_end] effect on drug activity
50-90% = moderate
90-99% = high
>99% = very high
The % dose reaching the bloodstream is the [blank_start]bioavailability[blank_end].
If you take aspirin, only 10% of the compound is available as 90% binds plasma – only [blank_start]10[blank_end]% can be distributed and active. Therefore some drugs are more active compounds than others at lower doses.
Want plasma binding to be in [blank_start]50-90[blank_end]% range. If the percentage is higher, then you need to take higher doses or dose more often to have desired effect.- Anegligible
- Bsignificant
- Cmoderate
- Dunbound
- Ebound
- Falbumin
- Galpha-1 acid glycoprotein
- Hkeratin
- Ialpha-1 acid glycoprotein
- Jalbumin
- Kcyanohydroxycinnamin
- Lbioavailability
- Mdosage
- N10
- O20
- P90
- Q50-90
- R0-50
- S>99
27Prodrug metabolism:
Prodrugs are compounds that are [blank_start]inactive[blank_end], but are converted in the body to an [blank_start]active[blank_end] drug by metabolic enzymes in the liver.
The drugs have to cross the [blank_start]intestine[blank_end]. By modifying, can influence drug so it can access [blank_start]membrane proteins[blank_end], making it active. Might want to prevent membrane crossing, so can modify the metabolic processes it undergoes so it stays in bloodstream.
They can improve membrane permeability:
May be present as [blank_start]esters[blank_end]. If a carboxylic acid is important for drug binding to its target, but it prevents the drug from [blank_start]crossing a membrane[blank_end], prodrugs can temporarily “hide” it as an ester. Once in the blood, it is hydrolysed to the active form by [blank_start]esterases[blank_end] e.g. aspirin and salicyclic acid.
N-methylation:
N-demethylation is a common liver metabolic reaction, amines may be methylated to increase [blank_start]hydrophobicity[blank_end]. These [blank_start]N-methyl[blank_end] groups will be removed in the liver.
Membrane transporter- mimic substrate to cross membrane
Dopamine transport:
Dopamine can’t cross the blood brain barrier as its too [blank_start]polar[blank_end] initially, so a [blank_start]carboxy[blank_end] group is added to make [blank_start]levodopa[blank_end]. Once modified and moved across the membrane, P450 will modify again and a [blank_start]decarboxylase[blank_end] removes the carboxy group to produce active dopamine again.
Extend life:
[blank_start]6-mercaptopurine[blank_end] is an immune suppressant (organ transplants), but is eliminated from the body [blank_start]quickly[blank_end]. It is a prodrug that slowly is converted to the active drug, giving a longer life and reducing toxicity.
Less toxic or side effects:
Salicylic acid is a painkiller, but phenolic -OH causes gastric bleeding. Aspirin has an ester to mask this toxic group until it is hydrolysed.- Ainactive
- Balways active
- Cactive
- Dinactive
- Eintestine
- Fliver
- Gmembrane proteins
- Htransporters
- Itransport vesicles
- Jesters
- Kethers
- Lcrossing a membrane
- Macting on target
- Nesterases
- Ohydrolases
- Phydrophobicity
- Qhydrophilicity
- RN-methyl
- Sbutyryl
- Tbutyl
- Upolar
- Vbig
- Wlevodopa
- XL-dopa
- Ycarboxy
- Zhydroxyl
- AAdecarboxylase
- ABesterase
- AC6-mercaptopurine
- ADβ-mercaptoethanol
- AE6-chloropurine
- AFquickly
- AGslowly
Information
- Description
- Degree Biochemistry (Enzyme Kinetics) Quiz on Enzyme Kinetics 5, created by Davina Jugnarain on 30/05/2016.
- Author
- Davina Jugnarain
- Language
- English
- Views
- 36
- Tags
- Rating
- No ratings yet Rate this quiz