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Chapter 3 Flashcards

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1
Q

Which of the following processes most directly determines whether a toxicant reaches its target site in the body?
A) Biotransformation
B) Absorption and Distribution
C) Enzymatic detoxification
D) Excretion

A

B) Absorption and Distribution
Explanation: Absorption and distribution are the initial steps that determine whether a chemical reaches its site of action (target organ). Biotransformation and excretion are important for clearance but come after distribution.

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2
Q

Which route of exposure generally leads to first-pass metabolism before systemic circulation?
A) Intravenous injection
B) Inhalation
C) Oral ingestion
D) Dermal absorption

A

C) Oral ingestion
Explanation: Oral ingestion subjects the toxicant to metabolism in the liver and intestinal wall before it enters systemic circulation (first-pass effect).

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3
Q

Which of the following best describes the blood-brain barrier?
A) Highly permeable to most charged molecules
B) Composed of fenestrated capillaries
C) A specialized barrier that restricts entry of many toxicants into the CNS
D) Only allows protein-bound chemicals to pass

A

C) A specialized barrier that restricts entry of many toxicants into the CNS
Explanation: The blood-brain barrier has tight junctions and is highly selective, allowing only certain substances (e.g., lipophilic, small) to enter.

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4
Q

A toxicant that is lipophilic and uncharged at physiological pH is most likely to accumulate in which tissue type?
A) Bone
B) Liver
C) Adipose tissue
D) Blood plasma

A

C) Adipose tissue
Explanation: Lipophilic toxicants tend to partition into fat and may accumulate in adipose tissue over time.

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5
Q

Which of the following processes converts a parent compound into a more reactive, potentially toxic metabolite?
A) Phase II conjugation
B) Phase I oxidation
C) Glucuronidation
D) Sulfation

A

B) Phase I oxidation
Explanation: Phase I enzymes like cytochrome P450 often convert xenobiotics into reactive electrophilic intermediates, increasing toxicity.

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6
Q

Which enzyme family is primarily responsible for oxidative metabolism of xenobiotics?
A) Glutathione S-transferases (GSTs)
B) Sulfotransferases
C) Cytochrome P450 monooxygenases
D) UDP-glucuronosyltransferases

A

C) Cytochrome P450 monooxygenases
Explanation: CYP450 enzymes carry out oxidation reactions in Phase I metabolism, introducing or exposing functional groups.

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7
Q

Which type of reactive metabolite can form adducts with DNA or proteins, leading to toxicity?
A) Nucleophiles
B) Electrophiles
C) Acids
D) Alcohols

A

B) Electrophiles
Explanation: Electrophiles are electron-deficient species that react with nucleophilic centers on DNA or proteins, often leading to mutagenesis or toxicity.

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8
Q

Which antioxidant tripeptide is critical in detoxifying reactive electrophilic species?
A) Cysteine
B) Glutathione
C) Histidine
D) Serotonin

A

B) Glutathione
Explanation: Glutathione (GSH) conjugates with electrophiles to form more water-soluble, less toxic compounds, often via glutathione S-transferases.

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9
Q

Redox cycling of certain chemicals can generate which of the following harmful species?
A) ATP
B) Free radicals
C) Proteins
D) DNA adducts

A

B) Free radicals
Explanation: Redox cycling leads to the formation of reactive oxygen species (ROS), including superoxide and hydroxyl radicals.

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10
Q

Which phase II enzyme catalyzes the conjugation of epoxides to dihydrodiols, aiding detoxification?
A) Epoxide hydrolase
B) Cytochrome P450
C) Peroxidase
D) Acetyltransferase DELIVERY TO THE TARGET (continued)

A

A) Epoxide hydrolase
Explanation: Epoxide hydrolase adds water to epoxides, converting them to less reactive and more water-soluble dihydrodiols.

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11
Q

Which tissue characteristic most influences passive diffusion of toxicants across capillaries?
A) Blood flow rate
B) Capillary fenestrae size
C) Protein synthesis rate
D) Membrane receptor density

A

B) Capillary fenestrae size
Explanation: Capillary permeability, determined by fenestrae size, affects how easily substances diffuse into tissues. Liver has large fenestrae; brain has small ones.

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12
Q

Which of the following chemicals is known to accumulate in bone by replacing calcium?
A) Mercury
B) Lead
C) Cadmium
D) Arsenic

A

B) Lead
Explanation: Lead mimics calcium and can be stored long-term in hydroxyapatite crystals in bone.

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13
Q

Which transporters are responsible for exporting toxicants from cells, limiting intracellular accumulation?
A) OAT and OCT
B) P-gp and BCRP
C) SGLT1 and SGLT2
D) CYP1A1 and CYP3A4

A

B) P-gp and BCRP
Explanation: These are efflux transporters that reduce toxicant accumulation by actively exporting them out of cells.

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14
Q

What is enterohepatic circulation?
A) Detoxification of xenobiotics in the liver
B) Reabsorption of bile-excreted compounds in the intestine
C) Elimination of protein-bound toxins by kidneys
D) Blood flow from heart to intestine

A

B) Reabsorption of bile-excreted compounds in the intestine
Explanation: Enterohepatic recycling increases toxicant half-life and can lead to GI toxicity.

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15
Q

Which of the following best describes a direct-acting toxicant?
A) Requires metabolic activation to become toxic
B) Is only active in the kidney
C) Is toxic in its parent form without bioactivation
D) Generates ROS as a byproduct

A

C) Is toxic in its parent form without bioactivation
Explanation: Direct-acting toxicants do not require metabolic activation to exert toxicity.

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16
Q

What type of molecule is most likely to act as an electrophile in toxicity?
A) Molecule with an extra electron
B) Molecule with a partial or full positive charge
C) Nucleic acid with methyl groups
D) Amino acid with sulfur groups

A

B) Molecule with a partial or full positive charge
Explanation: Electrophiles seek electron-rich sites and can bind covalently to proteins or DNA.

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17
Q

Which toxicant undergoes redox cycling to generate ROS in cells?
A) Acetaminophen
B) Paraquat
C) Ethanol
D) Methotrexate

A

B) Paraquat
Explanation: Paraquat undergoes one-electron reductions and produces superoxide radicals through redox cycling.

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18
Q

What is the significance of the Fenton reaction in toxicology?
A) Produces energy via glucose metabolism
B) Generates reactive hydroxyl radicals from hydrogen peroxide
C) Detoxifies free radicals
D) Catalyzes protein synthesis

A

B) Generates reactive hydroxyl radicals from hydrogen peroxide
Explanation: The Fenton reaction produces highly damaging HO· radicals involved in oxidative stress and cell injury.

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19
Q

Which enzyme family plays a major role in detoxifying electrophiles?
A) Monoamine oxidases
B) Glutathione-S-transferases (GSTs)
C) P450 monooxygenases
D) Tyrosine kinases

A

B) Glutathione-S-transferases (GSTs)
Explanation: GSTs catalyze conjugation of glutathione to electrophiles, making them more water-soluble and less reactive.

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20
Q

Which phase II enzyme reduces quinones, preventing ROS generation?
A) Glutathione peroxidase
B) Catalase
C) NQO1
D) COMT INTERACTION WITH TARGET MOLECULES

A

C) NQO1
Explanation: NAD(P)H:quinone oxidoreductase (NQO1) detoxifies quinones by reducing them to hydroquinones, preventing redox cycling.

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21
Q

Which of the following best defines a “molecular initiating event” (MIE) in toxicology?
A) Onset of inflammation in target tissue
B) Binding of a toxicant to its molecular target initiating a toxic cascade
C) Absorption of a chemical through the GI tract
D) Inhibition of liver enzymes

A

B) Binding of a toxicant to its molecular target initiating a toxic cascade
Explanation: MIE is the first key interaction between a toxicant and a biomolecule, leading to downstream toxicological effects.

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22
Q

Which of the following types of interactions is typically irreversible and most likely to lead to toxicity?
A) Hydrogen bonding
B) Van der Waals interaction
C) Covalent binding
D) Ionic attraction

A

C) Covalent binding
Explanation: Covalent bonds are stable and irreversible, making the resulting adducts persistent and often toxic.

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23
Q

An antagonist toxicant that binds a receptor without activating it would likely result in what type of effect?
A) Full receptor activation
B) Inverse agonism
C) Blocked downstream signaling
D) Enhanced receptor sensitivity

A

C) Blocked downstream signaling
Explanation: Antagonists bind to receptors and prevent endogenous agonists from activating signaling pathways.

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24
Q

What is a common target of alkylating agents such as mustard gas in biological systems?
A) Lipid bilayers
B) Mitochondrial DNA
C) Amino acid side chains and nucleophilic centers in DNA
D) Ribosomal RNA

A

C) Amino acid side chains and nucleophilic centers in DNA
Explanation: Alkylating agents covalently modify guanine bases or protein residues, disrupting function.

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25
Which statement best describes the concept of receptor occupancy theory in toxicology? A) Receptor binding always leads to toxicity B) Greater receptor occupancy correlates with greater biological effect C) Receptor binding blocks all metabolic activity D) Low receptor affinity leads to high toxicity
B) Greater receptor occupancy correlates with greater biological effect Explanation: The theory suggests a proportional relationship between the fraction of receptors occupied and the magnitude of response.
26
Which protein is a common target of reactive oxygen species, affecting signal transduction? A) Tubulin B) Actin C) Tyrosine kinases D) Protein thiols (e.g., cysteine residues)
D) Protein thiols (e.g., cysteine residues) Explanation: ROS often oxidize cysteine thiol groups, altering protein conformation and function.
27
Which statement about DNA adducts is most accurate? A) They are easily repaired and not biologically relevant B) They lead to reversible epigenetic changes only C) They can result in permanent mutations if unrepaired D) They never form with electrophiles
C) They can result in permanent mutations if unrepaired Explanation: DNA adducts can interfere with replication and, if not repaired, cause permanent mutations.
28
Which type of toxicant action involves replacement of an endogenous ligand? A) Oxidative phosphorylation uncoupler B) Competitive receptor antagonist C) Ion channel blocker D) DNA intercalator
B) Competitive receptor antagonist Explanation: These toxicants mimic the shape of natural ligands and compete for the same binding site.
29
A toxicant that disrupts cellular communication without altering genetic material is acting as a: A) Mutagen B) Endocrine disruptor C) Clastogen D) Alkylating agent
B) Endocrine disruptor Explanation: Endocrine disruptors interfere with hormonal signaling pathways without mutating DNA.
30
The toxicity of cyanide primarily results from its high affinity for which cellular component? A) DNA polymerase B) Mitochondrial cytochrome c oxidase C) Microtubules D) Calcium channels CELLULAR DYSFUNCTION AND TOXICITY
B) Mitochondrial cytochrome c oxidase Explanation: Cyanide binds irreversibly to the iron center of cytochrome c oxidase, halting oxidative phosphorylation.
31
Which organelle is most associated with intrinsic apoptosis following toxicant exposure? A) Nucleus B) Mitochondria C) Endoplasmic reticulum D) Golgi apparatus
B) Mitochondria Explanation: Mitochondria release cytochrome c into the cytosol, activating caspases and initiating apoptosis.
32
Which signaling molecule is directly involved in initiating extrinsic apoptosis? A) Bcl-2 B) TNF-α C) Cytochrome c D) Caspase-3
B) TNF-α Explanation: TNF-α binds to death receptors like Fas and initiates the extrinsic apoptotic pathway.
33
Which protein is an anti-apoptotic regulator that stabilizes mitochondrial membranes? A) p53 B) Caspase-9 C) Bax D) Bcl-2
D) Bcl-2 Explanation: Bcl-2 prevents cytochrome c release by maintaining mitochondrial membrane integrity.
34
Which reactive oxygen species is most damaging due to its reactivity and inability to be enzymatically detoxified? A) Hydrogen peroxide B) Superoxide anion C) Hydroxyl radical (OH·) D) Nitric oxide
C) Hydroxyl radical (OH·) Explanation: OH· is extremely reactive and damages DNA, lipids, and proteins; it cannot be detoxified enzymatically.
35
Which phase of the cell cycle is targeted by many DNA-damaging toxicants to arrest cell proliferation? A) G0 B) S C) M D) G1
B) S Explanation: DNA damage checkpoints in the S phase halt replication to allow for repair or trigger apoptosis.
36
What is the major cellular consequence of calcium overload induced by toxicants? A) Increased ATP synthesis B) Activation of proteases and phospholipases C) DNA methylation D) Protein glycosylation
B) Activation of proteases and phospholipases Explanation: Elevated cytosolic calcium activates destructive enzymes that degrade cellular components.
37
Which of the following represents a hallmark of necrotic cell death? A) Caspase activation B) Mitochondrial swelling and membrane rupture C) DNA laddering D) Apoptotic bodies
B) Mitochondrial swelling and membrane rupture Explanation: Necrosis is associated with energy failure, membrane disruption, and inflammation.
38
Which of the following is a hallmark of apoptosis but not necrosis? A) Membrane rupture B) Caspase activation C) Cell swelling D) Loss of ion homeostasis
B) Caspase activation Explanation: Caspase enzymes cleave cellular components in a regulated manner during apoptosis.
39
Which form of cell death involves cellular digestion of organelles through lysosomes? A) Apoptosis B) Necrosis C) Autophagy D) Pyroptosis
C) Autophagy Explanation: Autophagy uses autophagosomes and lysosomes to degrade damaged organelles and proteins.
40
Which organ is particularly vulnerable to toxicants that deplete glutathione? A) Kidney B) Lung C) Liver D) Spleen
C) Liver Explanation: The liver relies heavily on glutathione for detoxification; its depletion leads to oxidative damage and necrosis.
41
Which enzyme is most associated with lipid peroxidation in oxidative stress? A) Superoxide dismutase (SOD) B) Catalase C) Lipoxygenase D) Glutathione peroxidase
C) Lipoxygenase Explanation: Lipoxygenases oxidize polyunsaturated fatty acids, initiating lipid peroxidation cascades.
42
Which toxicant is well known to inhibit protein synthesis by targeting ribosomes? A) Cyanide B) Ricin C) Arsenic D) Carbon monoxide
B) Ricin Explanation: Ricin is a potent inhibitor of protein synthesis; it inactivates ribosomal RNA.
43
Which mitochondrial complex is inhibited by rotenone, leading to impaired ATP production? A) Complex I B) Complex II C) Complex III D) Complex IV
A) Complex I Explanation: Rotenone inhibits NADH dehydrogenase (Complex I), reducing electron transport and ATP generation.
44
Which nuclear protein acts as a master regulator of the cellular response to DNA damage? A) Bcl-2 B) p53 C) NF-κB D) PARP
B) p53 Explanation: p53 is a tumor suppressor protein that halts the cell cycle or induces apoptosis upon DNA damage.
45
Which toxic mechanism underlies acetaminophen-induced liver injury at high doses? A) Inhibition of cytochrome c oxidase B) Formation of stable DNA adducts C) Glutathione depletion and reactive metabolite formation D) Membrane pore formation by ROS
C) Glutathione depletion and reactive metabolite formation Explanation: Acetaminophen is converted to a reactive metabolite (NAPQI) which depletes glutathione and causes hepatic necrosis.
46
What is the key event in ER stress-induced apoptosis? A) Release of calcium from the mitochondria B) Activation of PERK and CHOP pathways C) Membrane rupture D) Oxidative phosphorylation inhibition
B) Activation of PERK and CHOP pathways Explanation: ER stress triggers the unfolded protein response (UPR); prolonged stress activates PERK and CHOP, leading to apoptosis.
47
Which of the following events characterizes pyroptosis? A) Cell shrinkage and membrane blebbing B) Inflammation and caspase-1 activation C) ATP depletion and chromatin condensation D) Non-inflammatory cell death
B) Inflammation and caspase-1 activation Explanation: Pyroptosis is an inflammatory form of cell death initiated by inflammasomes and caspase-1.
48
Which toxicant leads to oxidative DNA damage via hydroxyl radical generation in the presence of iron? A) Benzene B) Toluene C) Hydrogen peroxide D) Ethanol
C) Hydrogen peroxide Explanation: H2O2 can react with Fe2+ in the Fenton reaction to produce hydroxyl radicals that damage DNA.
49
What is the primary cellular function disrupted by microcystin? A) Mitochondrial DNA transcription B) Protein phosphatase inhibition C) Calcium channel blocking D) Lipid biosynthesis
B) Protein phosphatase inhibition Explanation: Microcystin inhibits protein phosphatases 1 and 2A, leading to cytoskeletal collapse and hepatotoxicity.
50
Which type of damage is caused by reactive nitrogen species like peroxynitrite? A) DNA alkylation B) Protein nitration and lipid oxidation C) Hydrolysis of proteins D) Iron chelation
B) Protein nitration and lipid oxidation Explanation: RNS like ONOO− modify tyrosine residues in proteins and cause lipid peroxidation.
51
Which organ is most vulnerable to toxicants due to its role in concentrating urine? A) Liver B) Kidney C) Lung D) Spleen
B) Kidney Explanation: The kidney concentrates substances during filtration and reabsorption, increasing exposure to potential toxins.
52
What is the role of cytochrome P450 enzymes in bioactivation? A) Conjugate xenobiotics with glutathione B) Oxidize xenobiotics, potentially forming reactive intermediates C) Reduce reactive nitrogen species D) Transport xenobiotics across membranes
B) Oxidize xenobiotics, potentially forming reactive intermediates Explanation: Cytochrome P450s often convert stable compounds into reactive metabolites capable of binding DNA or proteins.
53
Which structure is the primary site of xenobiotic metabolism? A) Mitochondria B) Smooth endoplasmic reticulum C) Nucleus D) Ribosome
B) Smooth endoplasmic reticulum Explanation: Many Phase I enzymes, including CYPs, are located in the smooth ER.
54
Which organ is a major target for inhaled toxicants due to its large surface area and vascularization? A) Liver B) Brain C) Lung D) Skin
C) Lung Explanation: The lungs offer high surface area and direct access to blood, making them vulnerable to airborne toxins.
55
How does arsenic exert toxic effects at the cellular level? A) Alkylates DNA bases B) Inhibits ATP production by targeting pyruvate dehydrogenase C) Chelates intracellular calcium D) Promotes histone acetylation
B) Inhibits ATP production by targeting pyruvate dehydrogenase Explanation: Arsenic inhibits critical enzymes in energy metabolism, impairing ATP synthesis and causing cell death.
56
Which biomolecule is most susceptible to peroxidation during oxidative stress? A) DNA B) RNA C) Proteins D) Lipids
D) Lipids Explanation: Polyunsaturated fatty acids in membranes are primary targets for lipid peroxidation.
57
Which toxicant is most associated with inhibiting mitochondrial Complex IV? A) Rotenone B) Cyanide C) Aflatoxin B1 D) Mercury
B) Cyanide Explanation: Cyanide inhibits cytochrome c oxidase (Complex IV), halting oxidative phosphorylation.
58
How does cadmium exert nephrotoxic effects? A) Forms protein-DNA adducts in hepatocytes B) Accumulates in mitochondria disrupting ATP synthesis C) Binds to metallothionein and accumulates in proximal tubules D) Promotes oxidative DNA fragmentation in glomeruli
C) Binds to metallothionein and accumulates in proximal tubules Explanation: Cadmium–metallothionein complexes are reabsorbed in proximal tubules, leading to chronic kidney damage.
59
Which cytokine plays a major role in initiating inflammatory responses to tissue injury? A) IL-10 B) TGF-β C) TNF-α D) EGF
C) TNF-α Explanation: Tumor necrosis factor alpha (TNF-α) is a central mediator in inflammation following toxic injury.
60
Which of the following is the primary defense against superoxide anions in cells? A) Catalase B) Superoxide dismutase (SOD) C) Peroxidase D) NQO1
B) Superoxide dismutase (SOD) Explanation: SOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which is less reactive.
61
Which protein functions as a sensor of oxidative stress by modifying thiol groups? A) Bcl-2 B) Keap1 C) Caspase-8 D) PPAR-γ
B) Keap1 Explanation: Keap1 binds to and regulates Nrf2 under basal conditions. Oxidative stress modifies Keap1, allowing Nrf2 to activate antioxidant genes.
62
Which toxicant inhibits Complex III of the mitochondrial electron transport chain? A) Rotenone B) Cyanide C) Antimycin A D) Dinitrophenol
C) Antimycin A Explanation: Antimycin A blocks electron flow at Complex III, disrupting ATP synthesis and increasing ROS.
63
Which biochemical parameter is most useful in diagnosing hepatocellular injury? A) Increased creatinine B) Increased ALT and AST C) Decreased hemoglobin D) Elevated LDH and CK-MB
B) Increased ALT and AST Explanation: ALT and AST are released from damaged hepatocytes and serve as biomarkers of liver injury.
64
Which cellular organelle is most sensitive to calcium dysregulation induced by toxicants? A) Golgi apparatus B) Mitochondria C) Nucleolus D) Peroxisome
B) Mitochondria Explanation: Mitochondria buffer calcium; excess Ca2+ disrupts membrane potential and induces apoptosis.
65
What is the function of caspase-3 in cell death pathways? A) DNA repair B) Lipid oxidation C) Execution of apoptosis D) Cell proliferation
C) Execution of apoptosis Explanation: Caspase-3 is a key executioner caspase that cleaves cellular proteins during apoptosis.
66
Which biomarker is most closely associated with oxidative DNA damage? A) 8-oxo-dG B) Creatinine C) Bilirubin D) GSH
A) 8-oxo-dG Explanation: 8-oxo-deoxyguanosine is a product of DNA oxidation and is a common biomarker for oxidative DNA damage.
67
Which enzyme detoxifies lipid hydroperoxides? A) Catalase B) Glutathione peroxidase C) SOD D) CYP3A4
B) Glutathione peroxidase Explanation: GPx reduces lipid hydroperoxides to non-toxic alcohols using glutathione as a cofactor.
68
Which signaling pathway is most commonly activated by oxidative stress? A) JAK/STAT B) Nrf2/Keap1 C) Wnt/β-catenin D) Notch
B) Nrf2/Keap1 Explanation: Oxidative stress disrupts Keap1, allowing Nrf2 to upregulate antioxidant and detoxification genes.
69
Which process leads to mitochondrial outer membrane permeabilization in apoptosis? A) Cytochrome c degradation B) Bcl-2 overexpression C) Bax/Bak activation D) Activation of mTOR
C) Bax/Bak activation Explanation: Bax and Bak oligomerize and form pores in the mitochondrial membrane, releasing cytochrome c.
70
Which key cellular molecule neutralizes hydrogen peroxide? A) NQO1 B) Catalase C) SOD D) GSH-S-transferase
B) Catalase Explanation: Catalase decomposes hydrogen peroxide into water and oxygen, preventing oxidative damage.
71
Which toxicant causes lipid accumulation in hepatocytes by inhibiting mitochondrial β-oxidation? A) Acetaminophen B) Ethanol C) Carbon tetrachloride D) Aflatoxin B1
B) Ethanol Explanation: Chronic ethanol exposure impairs mitochondrial function and fatty acid oxidation, leading to steatosis.
72
Which mechanism is primarily involved in gentamicin-induced nephrotoxicity? A) DNA methylation in glomeruli B) Inhibition of hepatic CYP enzymes C) Accumulation in proximal tubule and lysosomal damage D) Increased glomerular filtration rate
C) Accumulation in proximal tubule and lysosomal damage Explanation: Gentamicin accumulates in proximal tubular cells, leading to lysosomal rupture and necrosis.
73
What is a major site of reactive oxygen species generation in the cell? A) Endoplasmic reticulum B) Mitochondrial electron transport chain C) Nucleolus D) Golgi apparatus
B) Mitochondrial electron transport chain Explanation: Electron leakage from complexes I and III of the mitochondrial ETC leads to ROS formation.
74
Which of the following enzymes helps regenerate reduced glutathione (GSH) from GSSG? A) Glutathione peroxidase B) Glutathione S-transferase C) Glutathione reductase D) Thioredoxin reductase
C) Glutathione reductase Explanation: Glutathione reductase uses NADPH to reduce oxidized glutathione (GSSG) back to GSH.
75
Which of the following describes mitochondrial permeability transition (MPT)? A) DNA fragmentation in mitochondria B) Reversible opening of voltage-dependent calcium channels C) Sudden loss of mitochondrial membrane potential and swelling D) Fusion of inner and outer mitochondrial membranes
C) Sudden loss of mitochondrial membrane potential and swelling Explanation: MPT involves opening of a pore in the mitochondrial membrane, leading to swelling and release of apoptotic factors.
76
What is the primary function of thioredoxin (Trx) in cells? A) Transport of iron B) Antioxidant defense through disulfide bond reduction C) DNA base excision repair D) Hydrolysis of peroxides
B) Antioxidant defense through disulfide bond reduction Explanation: Thioredoxin reduces disulfide bonds in proteins, helping to maintain redox homeostasis.
77
What is the fate of cells undergoing irreversible ATP depletion? A) Cell proliferation B) Controlled autophagy C) Necrosis D) Differentiation
C) Necrosis Explanation: Lack of ATP impairs membrane pumps and energy-dependent processes, leading to cell lysis and necrosis.
78
Which of the following proteins is released from mitochondria to activate apoptosis? A) p53 B) TNF-α C) Cytochrome c D) NF-κB
C) Cytochrome c Explanation: In intrinsic apoptosis, cytochrome c is released into the cytosol and helps activate caspases.
79
Which mitochondrial protein complex is responsible for ATP synthesis? A) Complex I B) Complex II C) ATP synthase (Complex V) D) Complex IV
C) ATP synthase (Complex V) Explanation: Complex V uses the proton gradient generated by the ETC to produce ATP from ADP and Pi.
80
Which cellular event best characterizes the early phase of oxidative stress response? A) ATP depletion B) Nuclear condensation C) Induction of antioxidant gene transcription via Nrf2 D) Cytoskeletal collapse REPAIR AND ADAPTATION
C) Induction of antioxidant gene transcription via Nrf2 Explanation: Activation of Nrf2 leads to transcription of detoxification and antioxidant defense genes.
81
Which protein is activated in response to oxidative stress to upregulate antioxidant defense genes? A) NF-κB B) AP-1 C) Nrf2 D) p53
C) Nrf2 Explanation: Nrf2 translocates to the nucleus after being released from Keap1, promoting expression of detoxifying and antioxidant genes.
82
Which enzyme directly repairs O6-methylguanine adducts in DNA? A) PARP B) MGMT C) DNA polymerase δ D) Ligase III
B) MGMT Explanation: MGMT (O6-methylguanine-DNA methyltransferase) transfers the methyl group from guanine to itself, repairing the lesion directly.
83
Which DNA repair pathway corrects bulky adducts caused by UV damage? A) Base excision repair B) Nucleotide excision repair C) Mismatch repair D) Non-homologous end joining
B) Nucleotide excision repair Explanation: NER removes large, helix-distorting lesions such as pyrimidine dimers.
84
Which protein complex initiates autophagy during cellular stress? A) Atg12–Atg5–Atg16 B) ULK1 complex C) LC3-II D) AMPK–mTOR
B) ULK1 complex Explanation: The ULK1 complex is the first to activate autophagosome formation in response to nutrient depletion or stress.
85
Which organelle is primarily responsible for degrading damaged organelles during autophagy? A) Nucleus B) Golgi apparatus C) Lysosome D) Peroxisome
C) Lysosome Explanation: Lysosomes fuse with autophagosomes and degrade their contents, completing autophagy.
86
Which repair enzyme is essential for sealing nicks in the phosphodiester backbone of DNA? A) DNA glycosylase B) DNA ligase C) DNA polymerase β D) Topoisomerase I
B) DNA ligase Explanation: DNA ligase completes the repair process by sealing breaks after damaged bases are removed and replaced.
87
Which antioxidant vitamin is most important in protecting membranes from lipid peroxidation? A) Vitamin A B) Vitamin B6 C) Vitamin E (α-tocopherol) D) Vitamin K
C) Vitamin E (α-tocopherol) Explanation: Vitamin E is lipid-soluble and acts as a chain-breaking antioxidant in lipid membranes.
88
What role does glutathione reductase play in the antioxidant system? A) Conjugates xenobiotics B) Reduces GSSG to GSH using NADPH C) Removes peroxides D) Binds heavy metals
B) Reduces GSSG to GSH using NADPH Explanation: Glutathione reductase maintains reduced glutathione levels, essential for antioxidant defenses.
89
Which transcription factor complex is activated downstream of Nrf2 to induce antioxidant enzymes? A) AP-1 B) ARE (Antioxidant Response Element) C) HRE (Hypoxia Response Element) D) GRE (Glucocorticoid Response Element)
B) ARE (Antioxidant Response Element) Explanation: ARE is the DNA sequence Nrf2 binds to initiate transcription of detoxifying and antioxidant genes.
90
What is the role of metallothioneins in cellular protection? A) Catalyze lipid peroxidation B) Store vitamin C C) Bind and detoxify heavy metals D) Activate p53
C) Bind and detoxify heavy metals Explanation: Metallothioneins are cysteine-rich proteins that chelate metals like cadmium and zinc, reducing toxicity.
91
Which enzyme family is primarily involved in repairing single-strand breaks in DNA? A) DNA ligase IV B) PARP (Poly ADP-ribose polymerase) C) RecA D) Caspase-9
B) PARP (Poly ADP-ribose polymerase) Explanation: PARP detects and helps initiate repair of single-strand breaks by recruiting repair proteins.
92
Which signaling pathway promotes cell survival and growth under stress conditions? A) MAPK–ERK B) PI3K–Akt–mTOR C) JAK–STAT D) p53–Bax
B) PI3K–Akt–mTOR Explanation: This pathway enhances survival and growth by promoting protein synthesis and inhibiting apoptosis.
93
Which enzyme repairs apurinic/apyrimidinic sites in base excision repair? A) DNA glycosylase B) AP endonuclease C) DNA polymerase γ D) UvrABC complex
B) AP endonuclease Explanation: AP endonuclease cleaves the phosphodiester bond at abasic sites to allow repair synthesis.
94
Which process is critical for removing misfolded proteins from the cytoplasm? A) Apoptosis B) Ubiquitination and proteasomal degradation C) Autolysis D) Endocytosis
B) Ubiquitination and proteasomal degradation Explanation: Misfolded proteins are tagged with ubiquitin and degraded in the proteasome to maintain proteostasis.
95
Which marker protein is recruited to autophagosome membranes? A) Atg4 B) LC3-II C) Caspase-9 D) GSK3β
B) LC3-II Explanation: LC3-II integrates into autophagosome membranes and is widely used as an autophagy marker.
96
How does the cell remove oxidatively damaged lipids? A) Through increased DNA methylation B) Via lipid hydrolysis and β-oxidation C) Through passive diffusion D) By lysosomal binding
B) Via lipid hydrolysis and β-oxidation Explanation: Damaged lipids are broken down and catabolized in mitochondria through β-oxidation.
97
Which protein inhibits mTOR and promotes autophagy under nutrient stress? A) Akt B) AMPK C) Caspase-8 D) Bcl-2
B) AMPK Explanation: AMPK senses low energy and inhibits mTOR, activating autophagy and energy-saving processes.
98
Which protein serves as a scaffold for DNA repair and replication at damage sites? A) PCNA (Proliferating Cell Nuclear Antigen) B) HSP70 C) ATM D) Keap1
A) PCNA Explanation: PCNA acts as a sliding clamp for DNA polymerases and coordinates repair machinery.
99
Which small antioxidant molecule is regenerated from its oxidized form by glutathione reductase? A) NADPH B) Cysteine C) GSH D) Vitamin C
C) GSH Explanation: GSH (reduced glutathione) is restored from GSSG using glutathione reductase and NADPH.
100
What is the end result of successful cellular adaptation and repair after toxicant exposure? A) Mutagenesis B) Cell death C) Return to homeostasis D) Oncogenesis ✅ You’ve reached the end of the 100-question ABT-style toxicology review!
C) Return to homeostasis Explanation: Repair and adaptation mechanisms aim to restore normal function and maintain cellular integrity.
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