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MedChem Final > DIETZ > Flashcards

DIETZ Flashcards

1
Q

Glucuronidation

Phase 2 Reaction

A

Most common

Addition of Sugar

detoxification of xenobiotics

–> phenols / alochols

–> aromatic amines / acids

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2
Q

Sulfate Conjugation

Phase 2 Reaction

A

Addition of Inorganic Sulfate

sulfate concentration is LIMITED, glucuronidation is more common

–> Phenols (most common) / alcohols

–> aromatic amines

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3
Q

Glutathione Conjugation

Phase 2 Reaction

A

Most common route for removal of Electrophiles

Major Detoxification Reaction

GSH - resistant to peptidases due to gamma linkage

Gamma lInkage prevents from peptidase degradation

Glutamine y-linkage + Cysteine + Glycine = GSH

Drug = Electrophile

GSH = Nucleophile

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4
Q

Glucuronide Conjugation

Enzymes & Cofactors

A

Conjugates glucuronic acid w/

billirubin / drugs / pesticides / carcinogens

Enzyme = UGT1 / UGT2

Catalyst = UDP

Co-factor = UDPGA

found in: liver / intestines / kidney / skin / brain / spleen/ nasal mucosa

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5
Q

Glucoronide Conjugation

Mechanism

A
  • Step 1) Formation of UDPGA
    • ​alpha glucose phosphate –> activated glucoronic acid
  • Step 2) Sn2 Displacement reaction
    • UDPGA = Electrophile
    • Drug/Substrate = Nucleophile
    • Enzyme = UGT –> UDT
      • INVERSION OF ALPHA –> BETA
      • product is always beta conjugate
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6
Q

Glucorinide Conjugation

UGT Substrates

A

Substrate = Nucleophile

UGT = electrophile

–> Produce ether linkage = polar metabolite

water soluble / excreted in kidney

  • Alcohols
    • 1* / 2* mainly
  • Phenols
  • Acids
    • Both aliphatic & aromatic
  • Amines
    • ​mainly aromatic
    • produce –> N-glucuronide
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7
Q

Crigler-Najjar Syndrome

Gilberts Disease

A
  • Caused by a deficiency in** **UGT
    • ​UGT conjugates unconjugated bilirubin
    • –> High concentration of unconj. Bilirubin
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8
Q

Gray Baby Syndrome

A
  • Caused by neonate inability to conjugate CHLORAMPHENICOL
    • ​antibacterial that needs UGT to break it down
    • UGT Deficiency
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9
Q

UGT Polymorphism

UGT1A1*28 Varient

A

Express Less UGT1A1 Enzyme

  • –> can lead to nonhemolytic unconjugated HYPERbilirubinemias
    • –> Jaundice
  • –> decreased enzyme activity effects Drug CLEARANCE
    • ​IRINOTECAN (anticancer PRODrug)
      • –> toxicity = diarrhea/neutropenia
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10
Q

UGT Enzyme INDUCER

A

Phenobarbital

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11
Q

UGT Enzyme Inhibitor

A

Protease Inhibitors

Lopinavir/Ritonavir

Flavonoids (phenolic phytochemicals)

= competitive substrate / inhibitor of UGT

but will need a very high concentration (not seen)

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12
Q

UGT Glucuronidation

Factors

A

Selective substrates / inibitors are LACKING

Low incidence of UGT Drug-Drug interactions

Important for detoxification reactions

inhibition –> reduce clearance of estradiol/bilirubin

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13
Q

Irinotecan

A

Prodrug

SN38 Topoisomerase for HIV

  • Protease Inhibitors & lopinavir/ritonavir
    • Inhibit metabolization of SN38 by UGT
      • ​–> INCREASED toxicity
    • lopinavir also inhibits 3A4 metabolism
      • ​–> increased toxicity
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14
Q

How to make a UGT substrate more stable towards Metabolism?

A

UGT Mechanism is Sn2

to make optimize it (keep it from being metabolized):

+Add Rigidity (sterics)

+Change Stereochemistry

-Reduce Lipohilicity

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15
Q

Why do Glucorinides have a relatively long

HALF LIFE?

A

Enterohepatic Recycling

  • Glucornides (w/ MW>500)
    • –> secreted into BILE
      • –> Gallbladder
      • –> B-glucoridase (bacterial)
        • ​–> REABSORBED
  • Ultimately increases time in body and can interact w/ other drugs
    • EX. CLORIPHENICOL
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16
Q

Sulfate Conjugation

Enzymes & Cofactors

A

Detoxification & bioactivation Pathways

Conjugates activated Sulfate to:

–> Phenols

–> alcohols / aromatic amines / N-hydroxyl Groups

Enzyme = SULT1/2

Cofactor = PAPS

found Ubiquitous / LIVER / placenta / intestine

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17
Q

Sulfate Conjugation

Mechanism

A
  • Step 1: Activation of inorganic sulfate –> PAPS
    • ATP-Sulfurylase / APS-Phosphokinase
      • –> Active PAPS
  • ​​Step 2: Sn2 Displacement Reaction
    • ​PAPS = Electrophile
    • Drug/Substrate = Nucleophile​
    • Enzyme = ST (sulfotransferase)
      • ​–> Sulfonated Product + PAP
      • enhanced water solubility –> excretion
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18
Q

Sulfate Conjugation

of Estradiol

A

Estradiol + PAPS/ST –> Sulfate Metabolite

  • Sulfate Metabolite = Water soluble –> Blood
    • In target tissues Sulfatase removes the sulfate
      • –> reactivated estradiol in tissue
    • “acts as a carrier”
      • so drug can travel
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19
Q

Sulfate Conjugation

DMBA Bioactivation

A

DMBA + ST/PAPS –> Sulfate metabolite

  • Sulfate –> Sn1 Rxn = Carbocation
    • carbocation is highly reactive can form TUMORS
    • DNA Adducts
    • ​Carbocation can also –> GSH –> detoxifcation
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20
Q

PAPS / ST

SUBSTRATES

A

Primarily with PHENOLS

alcohols

aromatic amines

N-hydroxyl groups

Drug = Nucleophile

PAPS = Electrophile

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21
Q

Glutathione Conjugation

Enzyme/Cofactors

A

Conjugates reactive/soft electrophiles such as

–> epoxides / RX / quinones

–> a/b-unsaturated carbonyls / quinone imines

Enzyme = GST = nu-

alpha/mu/pi-class of GST’s

Cofactor = Glutathione (nu-)

found in basicaly all mammalian tissues

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22
Q

GST Inducers

A

Phenobarbital

3-methylcholanthrene

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23
Q

Glutathione Conjugation

Mechanism

A

Can be conjugated w/o prior activation

Detoxification –> Inactive /nontoxic metabolites

  • Sn2 Reaction “INVERTED SN2”
    • ​GST = Nucleophile
    • Drug/substrate = electrophile
    • ​Product = ​Glutathione Conjugate(-GS)
      • REDUCES pKa
      • ​Can further be metabolized
        • ​–>Mercapturic Acid Derivative
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24
Q

Glutathione Conjugation

SUBSTRATES

A

Elimination of ELECTROPHILES

Epoxides

R-X (alkyl halides)

Quinones (QI’s / QM’s)

alpha/beta -unsaturated carbonyls

GSH = Nucleophile

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25
Q

GSH

Detoxification of Aflatoxins

A
  • Epoxide (Aflatoxin)
    • strong electrophile –> attack nu- proteins
      • ​–> protein modification
      • –> DNA adducts
        • Carcinogenic
  • ​​​Epoxide + GST/GSH –> Glutathione Product
    • ​Can be excreted, DETOXIFIED
    • *depletion of GST —> more epoxide as a carcinogen
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26
Q

N-Acetyltransferase (NAT)

Reaction

A

Transfer of Acetyl group to nitrogen atom of:

–> aromatic Amine

–> Hydrazine

Cofactor = Acetyl CoA

Enzyme = NAT

NAT1 found in urothelium / colon epithelial cells

NAT2 found in LIVER / intestine

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27
Q

N-acetyltransferase (NAT)

Mechanism

A
  • Step 1) Transfer of Acetyl CoA –> NAT
  • Step 2) Transfer of Acetyl –> Substrate
    • ​substrate is aromatic amine or hydrazine
    • Produces Mercapturic Acid Derivative
      • ​as third step after GST metabolism
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28
Q

NAT

Polymorphisms

A

​Isoniazid (hydrazine group) = Substrate of NAT

  • Polymorphism in NAT2 (liver/intestine)
  • SLOW Acetylators
    • ​–Accumalate Isoniazid –> Neuropathy
      • ​found in many Caucasians /egyptians/moroccans
  • ​RAPID acetylators
    • ​Isoniazid –> more hydrolysis into acetyl radicals
      • –> Hepatic Damage
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29
Q

Mercapturic Acid Pathway

A
  • After GST Conjugation:
    • Product has Glutamine / Cysteine / Glycine
      • ​1) Y-glutamine Amide Hydrolysis
      • 2) Glycine Amide Hydrolysis
      • 3) Cys-N-Acytylation
        • ​NAT + AcetylCoA
        • PRODUCE MERCAPTURIC ACID
          • ​excreted in urine
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30
Q

Mercapturic Acid Products

A

Tridiphane = Herbicide

ACETAMINOPHEN

~only 2% of metabolism but is still found as a product

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31
Q

Chemical Toxicology

Drug ITSELF is Toxic

A
  • Exagerated on-target pharmacology
  • Off-Target Pharmacology
  • Trigger Immune response
    • ​–> inflammation​​
  • Structure Alerts from toxicity:
    • Sulfate
    • NO2 (nitrates)
    • Aziridiniums
    • Epoxides
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32
Q

Fenfluramine

A

Anti-suppresant drug

Found to cause Rare Valvular Disease

when in combo with Phenteramine

–> potentiation of serotonin effects

DRUG ITSELF WAS TOXIC

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33
Q

Vioxx

A

COX-2 Inhibitor (similar to Celecoxib)

Increased Risk of CV Problems

COX2–> in endothelial cells –> vessel constriction

DRUG ITSELF WAS TOXIC

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34
Q

DES

(diethylstilbestrol)

A

Teratogenic Drug

DRUG ITSELF WAS TOXIC​

used to prevent miscarriage –> led to increase in CERVICAL CANCER in DES daughters

Endocrine disrupting chemical

–> DNA methylation

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35
Q

Thalidomide

A

Teratogenic Drug

DRUG ITSELF WAS TOXIC

Used for sleep aid / morning sickness

caused severe birth defects

now used to treat leprosy & considered for HIV / multiple myeloma (cancer)

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36
Q

Metabolite Toxicity

A

Metabolite of the drug is the one that is TOXIC

Ex. ACETAMINOPHEN

37
Q

Metabolite Toxicity

3 Major Mechanisms

A
  • Adducted Protein/DNA
    • ​MAJOR one
    • Covalent bonding to cellular components
      • enzymes / regulatory proteins /DNA
  • ROS production
    • non-covalent interactions
  • Covalent Protein Adducts –> IMMUNOLOGICALLY mediated toxicity
    • ​
38
Q

Metabolite Toxicity

Sulfamethazole

A

Leads to Hypersensitivity reactions

Specifically for HIV Patients

–> Protein Adducts –> Sn2 –> More Immune Supression

39
Q

Metabolite Toxicity

Electrophile Reactivity/Selectivity Principle

A

The MORE REACTIVE the electropile

The LESS Selective

=MORE SIDE EFFECTS

  • ​Electrophile –> Water (nu-)
    • Most common reaction, b/c A LOT OF WATER
  • E+ –> GSH/GST
  • Toxic Reactions:
    • ​E+ –> Protein
      • Cytotoxic
    • E+ –> DNA
      • only a small amount reaches here but still Genotoxic
40
Q

Carcinogens

Direct Acting Genotoxic Agents

A

Electrophiles

(usually w/o additional bioactivation)

Nitrogen Mustards

–> Aziridinium Ion –> DNA ALKYLATION

=apoptosis

41
Q

Carcinogens

Inderect Acting Genotoxic Agents

A

Need to be BIOACTIVATED to be toxic

= Ultimate Carcinogen/Toxin

Benzo(a)pyrane

42
Q

Carcinogens

NON-Genotoxic / Epigenetic Agents

A

–> Proteins but do not change genetically

Sustained Cytotoxity / Receptor Mediated

ER / AhR

Increase of Oxidative Stress

DNA Methylation

43
Q

Carcinogens:

Enzymes involved in

Bioactivation Reactions

A

Mainly p450 (phase 1)

Mainly Class 1 (1A1 / 1A2 / 1B1)

SULT

AKR

NAT

FMO / COX

44
Q

Enzymes Involved in

Detoxification Reactions

A

Mainly GST / UGT

AKR

P450

Little SULT / NAT / COMT / EH

45
Q

Types of Reactive Intermediates

A

Electrophiles (E+)

Free Radicals

Nucleophiles (Nu-)

46
Q

Nitrenium Ions

Carbacations

Aziridinium Ion

A

Positively Charged Electrophiles (E+)

MOST REACTIVE = Least selective

Can react with water

47
Q

Epoxide

Arene Oxide

Acyl Halide

Alkyl Halide

A

Neutral Electrophiles (E+)

Reactive intermediates

48
Q

Quinone

Quinone Imine

Quinone Methide

A

Neutral Electrophiles (+)

Reactive intermediates

MOST COMMON TOXIC METABOLITES

Quinone Methide = Not as bad as other quinones

does NOT undergo Redox Cycling –> ROS

49
Q

Reactive Intermediates

Epoxides

Aflatoxin

A

Metabolicly Activated

Mycotoxin / Aflatoxin B1

  • Haptic carcinogen / acute toxin
    • from mold Aspergillus flavus
  • Apurinic Sietes on DNA
    • ​Mutagenic Lesions
  • ​GST/GSH or EH–> detoxify the epoxide
  • ​Oltipraz = Chemopreventative for aflatoxin liver cancer
50
Q

Oltipraz

A

Induces GST & Quinone Reductase

INHIBITS 1A2 / 3A4

= CHEMOPREVENTATIVE for Aflatoxin Epoxide

  • Oltipraz –> More GST/GSH
    • More Detoxification of Aflatoxin Epoxide
  • Oltipraz -/-> inhibits P450
    • ​Less formation of epoxide
51
Q

Pulegone

A

From pennyroyal oil

used as a Abortifacient

P450 Oxidation –> Epoxide Electrophile (-)

= Liver Damage / Death @ high doses

52
Q

Benzo[a]pyrene

A

Found in Cigarettes

Potent Mutagen

1A1 metabolism –> Epoxide = DNA Adducts

also EH metabolism –> Diol –> AKR –> DNA Dmg

53
Q

Chloroform

A

Chloroform + 2E1 –> Phosgene (ACYL Halide)

Neutral Electrophile+

= Lung Toxin / rxns w/ amines of proteins

54
Q

Dichloroethylene

A

Found in dry cleaning solvents

Causes Lung Toxicity

  • 3 Bioactivation Pathways 2E1:
    • Chloroacetyl Chloride (most reactive electrophile)
    • DCE Epoxide
    • DCaldehyde
55
Q

Safrole

Tamoxifen

DMBA

A

Bioactivated into Genotoxic Carbocation

(Positively Charged Electrophile)

  • P450 –> PAPS/ST –> Sn1 Displacement
    • –> Carbocation
      • ​Attacks DNA = Forms DNA Adducts
      • Bulky adducts are stable
56
Q

Nitrenium Ion

A

Positively Charged Electrophile+

  • Amide –> 1A2 –> PAPS/ST –> Sn1 Displacement
    • ​= Nitrenium Ion
      • ​DNA Binding / Tumor Formations
57
Q

Aristolochic Acid

A

Form Nitrenium Ion (ultimate carcinogen)

Positively Charged Electrophile+

Dietary supplement for weight los

  • Nitro + Reductase –> Amine –> Amide –> P450
  • –> PAPS/ST –> Sn1 Displacement
    • ​= Nitrenium Ion
      • ​DNA Binding / Tumor Formations
      • Neprotoxicity Kidney
  • ​​Many patients had End-Stage Grenal Failure
  • & Urothelial Cancer
  • Misidentified chinese name that caused issues
58
Q

Quinoids

A

Neutral Electrophiles

Most Common Functional Group in Drugs

  • BENZENE + P450 + OXYGEN
    • ​–> Quinones
      • Can undergo REDOX RECYLING
      • –> ROS
59
Q

Phenytoin Bioactivation

A

Just Oxygen + P450

= Quinone (Electrophile)

Also undergoes Redox Cycle

–> ROS’s

60
Q

Endogenous Estrogen Bioactivation

A
  • Estrogen + p450 –> Quinones
    • ​Redox recycling –> ROS
    • Depurinating Adducts = GENOTOXICITY
      • ​COMT = Catecholamine METHYLTRANSFERASE
    • ​Also metablize estrogen and form
    • both Genotoxic Biomarkers
    • Non-Toxic Biomarkers
61
Q

Bioactivation of Equilenin

A

Form Redox Active / Electrophilic Quinones

+ Superoxide

= Carcinogen/Toxic

62
Q

HRT

Timing Hypothesis

A
  • Thought that using HRT PRE-MONOPAUSE
    • More benifits vs risks
      • stroke/cancer risk
  • Average age of HRT was >60 = POST-menopause
    • More risks vs benefits
      • heart disease / cognition / cancer / stroke risk
63
Q

Black Cohosh / Red Clover

A

P2 Clinical Trial proved that

They DO NOT reduce hotflashes in postmenopausal women

64
Q

Tamoxifen Bioactivation Pathway(s)

A

PAPS/ST –> CARBOCATION

P450 + Oxygen –> QUNONE / Quinone Methide

quinones can undergo GSH conjugation –> excreted

65
Q

STAR

Study of Tamoxifen & Raloxifene

(SERMS)

A

Both form Quinoids (electrophiles)

But can be GSH conjugated –> -GS excretion

  • ​Found that 3rd/4th generation SERMS (selective estrogen receptor modulators)
    • are ALSO CONVERTED TO QUINOIDS
    • ex. DMA / Acolbifene
66
Q

Etoposide

A

–> QUINONE PRODUCTS

as a side effect

  • A Anticancer agent from podophyllotoxin
    • –> Small cell lung / testicular cancer
  • ​INHIBITS Topoisomerase
    • ​–> unwinds supercoiled DNA
    • Inhibits tumor replication
67
Q

Kava Kava

A

Bioactivated to QUINONES

  • Methysticin / 7-8Dihydromethysican
    • –> Quinones –> Liver Toxicity
      • ​hepatitis / cirrhosis / liver failure
  • ​Marked as a SEDATIVE dietary supplement
68
Q

Acetaminophen/Diclofenac Bioactivation

A

APAP –> O/2E1 –> NAPQI

NAP- Quinone Imine

GI / Liver Toxicity

69
Q

Eugenol / BHT

Bioactivation

A

Eugenol = cloves/cigarettes / food / flavor agent

BHT = antioxidant / dried foods –> prevent lipid oxidation

Both metablolized to Quinone Methide

Quinone methide = tumor promotor

DOES NOT undergo rodox cyling

70
Q

Redox Cycling

A

Mechanism of toxicity for

QUINONES & QUINONE IMINES

not for quinone methides

  • Quinone + P450 Reductase –> Semiquinone Radical
    • ​O2 radical –> O2
    • ROS –> RADICAL DNA DMG
71
Q

Doxorubin

A

Undergo Redox Cycling

Quinone –> Semiquinone

forms ROS

  • ROS = O2 radical
72
Q

Consequences of ROS

A
  • ROS = O2 Radical
    • O2 + 2H+ –> SOD (Superoxide Dismutase)
      • ​= H2O2 (hydrogen peroxide)
  • ​​H2O2 + Fe2+ (FENTON REACTION)
    • ​= HO- + HO RADICAL
  • ​​​​HO Radical can cause:
    • Lipid Peroxidation
    • Protein Oxidation
      • ​disulfide bond formation
    • DNA Oxidation
      • –> Mutagenic Lesion
        • Form (8-oxo-dG​) = Biomarker
73
Q

Fenton Reaction

A
  • Converts Hydrogen Peroxide with Fe2+​
    • ​= HO- + HO RADICAL
      • ​​​​HO Radical can cause:
        • Lipid Peroxidation
        • Protein Oxidation
        • ​DNA Oxidation
74
Q

Superoxide Dismutase

SOD

A

Converts ROS –> Hydrogen Peroxide

O2 Radical –> H2O2

–> fenton reaction

75
Q

Counterbalancing ROS

A
  • OH Radical formed from Fenton Rxn
    • can be counterbalanced by OXIDATIVE DEFENSE
      • Enzymatically
      • Non Enzymatically
        • Gutathione
        • 2GSH + 2OH Radicals –> GS-SG
          • –> excreted
76
Q

Lipid Peroxidation

A

Causes Many Diseases

End Product = Lipid Aldehyde (Biomarker)

  • Occur as a result from ROS –> Fenton RXN
    • OH RADICAL
  • Radicals KEEP CYCLING
    • until hit by GSH or another detoxifyer
77
Q

Vitamin C

Flavonoids (quercetin)

A

Antioxidants that SCAVANGE OH Radicals

  • Take OH Radicals –> Form WATER TWICE
    • –> forms a quinone, not as bad as the OH radicals
78
Q

Enzyme Catalyzed

ROS Scavanger

A

Scavange O2 Radicals

  • 2O2 + SOD –> Hydrogen peroxide
  • H2O2 can undergo two detoxification reactions
    • Glutathione Peroxidase
      • +2GSH –> 2x Water
    • Catalase
      • –> 2x Water
79
Q

Non-Enzymatic

ROS Scavenger

A
  • PHENOLS(from food) +OH Radical
    • abstracts the radical –> Water
  • BHT + OH Radical
    • Abstracts radical –> WATER
    • –> forms Quinone Methide
      • not as bad, does not go through REDOX RECLYING
80
Q

What metabolizes

Michael Acceptors

a/b -unsaturated carbonyls

A

GST

GSH = nucleophile -> Carbonyl (michael acceptor)

–> -GS product

81
Q

Bioactivation of Carbocation

A

P450 –> -OH group

PAPS / ST –> Sulfonated product

Sn1 Rxn –> CARBOCATION+

genotoxic molecule –> mutations on DNA

82
Q

Glutathione Peroxidase

A

Ezyme catalyzed

Scavenger of ROS

H2O2 + 2GSH –> 2x water + GSSG

83
Q

Catalase

A

Enzyme catalyzed

Scavenger of ROS

H2O2 + Catalase –> 2x Water + o2

84
Q

BHT

Phenols in food

A

Non-Enzyme Scavenger of ROS

Abstracts -OH Radicals

–> form Quinone Methide

does not go through redox recycling

85
Q

P450 1A1

A

Induced by POLYCYCLIC HYDROCARBONS

1-methyphenanthrene

If it has a lot of benzene rings it is likely oxidized by 1a1

86
Q

Redox Active

A

Means it can UNDERGO REDOX RECYCLING

Quinones

Epoxides are NOT redox active

87
Q

Aromatic Amines can be Metabolized by what?

A

NAT –> Acetyl group on the amine

PAPS/ST –> Sulfonated amine

UGT/UDPGA –> N-glucuronide

88
Q

What can react with Aromatic Nitro Groups

-NO2

AKA NITROSO

A

GST

glutathione s- transferase

89
Q
A

MedChem Final (8 decks)

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