Enzymes Practice Questions

Q: Which trace element is present in carbonic anhydrase?

Zinc. **Explanation:** **Carbonic Anhydrase** is a classic example of a **metalloenzyme** where a metal ion is tightly bound and essential for catalytic activity. 1. **Why Zinc is correct:** Carbonic anhydrase contains a **Zinc ($Zn^{2+}$)** ion coordinated to three histidine residues at its active site. The Zinc ion facilitates the nucleophilic attack of water on carbon dioxide, catalyzing the reversible hydration of $CO_2$ to bicarbonate ($HCO_3^-$) and $H^+$. This reaction is vital for $CO_2$ transport in RBCs and acid-base regulation in the kidneys. 2. **Why other options are incorrect:** * **Molybdenum:** Found in enzymes like **Xanthine oxidase** (purine metabolism) and Sulfite oxidase. * **Copper:** Present in **Cytochrome c oxidase**, Superoxide dismutase (cytosolic), and Tyrosinase. * **Magnesium:** Acts as a cofactor for almost all enzymes utilizing ATP (e.g., **Hexokinase**, Phosphofructokinase) and DNA/RNA polymerases. **High-Yield Clinical Pearls for NEET-PG:** * **Carbonic Anhydrase Inhibitors:** Acetazolamide is a potent inhibitor used to treat glaucoma, altitude sickness, and idiopathic intracranial hypertension. * **Zinc-containing enzymes:** Other high-yield Zinc enzymes include **Alcohol dehydrogenase**, **Carboxypeptidase**, and **DNA polymerase**. * **Zinc Deficiency:** Characterized by growth retardation, impaired wound healing, and **Acrodermatitis enteropathica**. * **Speed:** Carbonic anhydrase is one of the fastest known enzymes, with a turnover number ($K_{cat}$) of $10^6$ reactions per second.

Q: Which enzyme is known as the 'suicidal enzyme'?

Cyclooxygenase. **Explanation:** **Cyclooxygenase (COX)**, also known as Prostaglandin H2 synthase, is termed a **'suicidal enzyme'** because of its unique mechanism of **self-catalyzed inactivation**. During the conversion of arachidonic acid into Prostaglandin $H_2$, the enzyme generates highly reactive free radical intermediates. These radicals attack the protein structure of the enzyme itself, leading to its irreversible denaturation and loss of activity. Thus, each molecule of COX can only perform a limited number of catalytic cycles before "killing" itself. **Analysis of Options:** * **Lipoxygenase (Option A):** This enzyme converts arachidonic acid into leukotrienes. While it is part of the eicosanoid pathway, it does not undergo the same self-inactivation process as COX. * **Thromboxane synthase (Option C):** This enzyme acts downstream of COX to convert $PGH_2$ into Thromboxane $A_2$. It is not characterized by suicidal inhibition. * **5' Nucleotidase (Option D):** This is a marker enzyme for the plasma membrane and canalicular membrane of hepatocytes; it is used clinically to differentiate the source of elevated alkaline phosphatase (ALP). **High-Yield Clinical Pearls for NEET-PG:** * **Aspirin Connection:** Aspirin is a **suicide inhibitor** (irreversible inhibitor) of COX. It acetylates a specific serine residue in the active site. Since platelets lack a nucleus, they cannot synthesize new COX enzymes, leading to the lifelong (7–10 days) anti-platelet effect of aspirin. * **Isoforms:** COX-1 is constitutive (gastric protection, renal blood flow), while COX-2 is inducible (inflammation, pain). * **Suicide Inhibition vs. Suicidal Enzyme:** While the terms are related, "suicidal enzyme" specifically refers to the enzyme's inherent property of self-destruction during its normal catalytic cycle.

Q: A kinetic analysis of the effect of a drug on an enzyme's activity was performed. Based on the results, into which of the following groups would the drug best fit?

A noncompetitive inhibitor. ***A noncompetitive inhibitor*** - **Noncompetitive inhibition** decreases **Vmax** while keeping **Km unchanged**, resulting in lines that intersect on the **x-axis** of a Lineweaver-Burk plot. - The inhibitor binds to an **allosteric site** rather than the active site, reducing enzyme efficiency without affecting substrate binding affinity. *A competitive inhibitor* - **Competitive inhibition** increases **Km** while keeping **Vmax unchanged**, causing lines to intersect on the **y-axis** of a Lineweaver-Burk plot. - The inhibitor competes with substrate for the **active site**, which can be overcome by increasing substrate concentration. *An uncompetitive inhibitor* - **Uncompetitive inhibition** decreases both **Vmax** and **Km** proportionally, resulting in **parallel lines** on a Lineweaver-Burk plot. - The inhibitor binds only to the **enzyme-substrate complex**, preventing product formation and effectively reducing both parameters equally. *A competitive activator of the enzyme* - **Competitive activators** would increase **Vmax** while decreasing **Km**, showing enhanced enzyme efficiency and substrate affinity. - This would result in lines intersecting below the x-axis on a Lineweaver-Burk plot, indicating **improved catalytic activity**.

Q: Serum creatine kinase-3 (CK-3) is elevated in which of the following conditions?

Muscular dystrophy. ### Explanation Creatine Kinase (CK) is a dimeric enzyme composed of two subunits: **M (Muscle)** and **B (Brain)**. These subunits combine to form three distinct isoenzymes. **CK-3 (CK-MM)** is the predominant form found in skeletal muscle (98%) and cardiac muscle. **1. Why Muscular Dystrophy is Correct:** Elevated levels of CK-3 are a hallmark of skeletal muscle damage. In **Duchenne Muscular Dystrophy (DMD)**, the lack of dystrophin leads to increased membrane permeability, causing massive leakage of CK-MM into the serum. It is often elevated even before clinical symptoms appear. **2. Analysis of Incorrect Options:** * **Myocardial Infarction (MI):** While CK-3 is present in the heart, **CK-2 (CK-MB)** is the specific diagnostic marker for MI. CK-MB levels rise within 4–8 hours of an infarct. * **Alcoholic Cirrhosis:** Liver diseases typically involve elevations in ALT, AST, and GGT. CK is not found in significant quantities in hepatocytes; therefore, cirrhosis does not elevate serum CK-3. * **Brain Tumors:** The brain contains the **CK-1 (CK-BB)** isoenzyme. Damage to the blood-brain barrier or neural tissue (like tumors or infarction) may lead to an increase in CK-BB, not CK-3. **3. High-Yield Clinical Pearls for NEET-PG:** * **Isoenzyme Distribution:** * **CK-1 (BB):** Brain, Prostate, Gastrointestinal tract. * **CK-2 (MB):** Cardiac muscle (20–30%), Skeletal muscle (1–2%). * **CK-3 (MM):** Skeletal muscle (98%), Cardiac muscle (70–80%). * **Highest Elevations:** The highest serum CK levels (often >50 times normal) are seen in **Duchenne Muscular Dystrophy** and **Rhabdomyolysis**. * **Electrophoretic Mobility:** On electrophoresis (pH 8.6), CK-1 (BB) moves fastest toward the anode, while CK-3 (MM) moves slowest.

Q: Which of the following is a serum marker of rickets?

Alkaline phosphatase. **Explanation:** In rickets (and osteomalacia), the primary biochemical hallmark is an **elevation in serum Alkaline Phosphatase (ALP)**. This occurs because rickets is characterized by a failure of osteoid mineralization. To compensate for the weakened bone structure, **osteoblastic activity** increases. Since ALP is a byproduct of osteoblast activity (reflecting bone turnover), its levels rise significantly. It is often the earliest and most sensitive biochemical marker of the disease, frequently rising before radiological changes appear. **Analysis of Incorrect Options:** * **Acid Phosphatase (ACP):** This is a marker of **osteoclast** activity and is primarily used as a marker for prostatic carcinoma or Gaucher’s disease, not metabolic bone disease like rickets. * **Decreased Serum Calcium:** While calcium can be low, it is often **normal** in early or moderate rickets due to compensatory secondary hyperparathyroidism, which mobilizes calcium from bones to maintain serum levels. Therefore, it is not as reliable a marker as ALP. * **Urinary Phosphates:** While phosphate metabolism is affected, urinary phosphate levels are variable and influenced by PTH; they are not considered a primary diagnostic "serum marker" for the condition. **NEET-PG High-Yield Pearls:** * **Earliest sign of Rickets:** Increase in serum Alkaline Phosphatase. * **Most specific radiological sign:** Cupping, splaying, and fraying of the metaphysis (best seen at the wrist). * **Biochemical Profile:** Low/Normal Calcium, Low Phosphate, **High ALP**, and High PTH (Secondary Hyperparathyroidism). * **Vitamin D-dependent Rickets Type II:** Characterized by end-organ resistance to 1,25(OH)₂D (mutated receptors) and often presents with alopecia.

Q: Copper is a constituent of which enzyme?

Lysyl oxidase. **Explanation:** **1. Why Lysyl Oxidase is the Correct Answer:** Lysyl oxidase is a copper-dependent enzyme essential for the cross-linking of collagen and elastin fibers. It oxidatively deaminates the side chains of lysine and hydroxylysine residues to form reactive aldehydes (allysine). these aldehydes then undergo spontaneous condensation to form stable covalent cross-links, providing structural integrity and tensile strength to the extracellular matrix. **2. Analysis of Incorrect Options:** * **Glucose oxidase:** This is a flavoprotein (containing **FAD**) used primarily in laboratory assays to measure blood glucose levels. * **Xanthine oxidase:** This enzyme, involved in purine catabolism (converting hypoxanthine to xanthine and xanthine to uric acid), requires **Molybdenum**, Iron, and FAD as cofactors. * **Transketolase:** A key enzyme in the Pentose Phosphate Pathway (HMP Shunt), it requires **Thiamine pyrophosphate (Vitamin B1)** and Magnesium ($Mg^{2+}$) as cofactors. **3. High-Yield Clinical Pearls for NEET-PG:** * **Menkes Kinky Hair Syndrome:** An X-linked recessive disorder caused by impaired copper absorption. The resulting deficiency in **Lysyl oxidase** activity leads to weak collagen, causing brittle hair, skeletal deformities, and arterial aneurysms. * **Other Copper-containing enzymes:** * **Cytochrome c oxidase** (Complex IV of the ETC) * **Superoxide dismutase (SOD)** (Cytosolic form; contains Cu and Zn) * **Tyrosinase** (Deficiency leads to Albinism) * **Ceruloplasmin** (Ferroxidase activity) * **Dopamine $\beta$-hydroxylase** (Converts dopamine to norepinephrine) * **Wilson’s Disease:** Characterized by excessive copper accumulation due to defective biliary excretion (ATP7B mutation).

Q: Which of the following is true regarding Nitric Oxide Synthase?

It requires NADH, FAD, FMN & Heme iron. **Explanation:** Nitric Oxide Synthase (NOS) is a complex enzyme responsible for the synthesis of Nitric Oxide (NO) from **L-arginine**. **Why Option D is correct:** NOS is a unique enzyme that functions as both a reductase and an oxygenase. To catalyze the conversion of L-arginine to L-citrulline and NO, it requires five essential cofactors: **NADPH** (electron donor), **FAD**, **FMN**, **Heme iron (protoporphyrin IX)**, and **Tetrahydrobiopterin (BH4)**. The enzyme transfers electrons from NADPH through the flavins (FAD/FMN) to the heme center to activate molecular oxygen. **Analysis of Incorrect Options:** * **Option A:** Most isoforms of NOS (specifically eNOS and nNOS) are **activated by Ca++-Calmodulin** binding, not inhibited by it. * **Option B:** NOS is a **monooxygenase** (mixed-function oxidase), not a dioxygenase. It incorporates only one atom of molecular oxygen into the product (NO), while the other is reduced to water. * **Option C:** The primary electron donor for NOS is **NADPH**, which is generated via the Pentose Phosphate Pathway, not NADH. **High-Yield Clinical Pearls for NEET-PG:** * **Isoforms:** There are three types: **nNOS** (Neuronal/Type I), **iNOS** (Inducible/Type II - Ca++ independent), and **eNOS** (Endothelial/Type III). * **Substrate:** L-Arginine is the precursor; L-Citrulline is the byproduct. * **Inhibitor:** Asymmetric dimethylarginine (ADMA) acts as an endogenous inhibitor of NOS. * **Function:** NO is a potent vasodilator that acts by increasing **cGMP** levels via activation of soluble guanylyl cyclase.

Q: Which of the following is a selenium-containing enzyme?

Glutathione peroxidase. **Explanation:** **Glutathione Peroxidase (GPx)** is the correct answer because it is a key antioxidant enzyme that contains **Selenium** in the form of the 21st amino acid, **Selenocysteine**, at its active site. Its primary role is to protect cells from oxidative damage by reducing lipid hydroperoxides and free hydrogen peroxide (H₂O₂) into water, using reduced glutathione as a hydrogen donor. **Analysis of Incorrect Options:** * **A. Xanthine Oxidase:** This enzyme, involved in purine catabolism (converting hypoxanthine to xanthine and then to uric acid), requires **Molybdenum**, Iron, and FAD as cofactors. * **C. Superoxide Dismutase (SOD):** There are different forms of SOD, but none contain selenium. The cytosolic form requires **Copper and Zinc**, while the mitochondrial form requires **Manganese**. * **D. Lysyl Oxidase:** This enzyme is essential for the cross-linking of collagen and elastin fibers in the extracellular matrix. It is a **Copper-dependent** enzyme. **High-Yield Clinical Pearls for NEET-PG:** * **Selenium Deficiency:** Associated with **Keshan disease** (an endemic cardiomyopathy) and **Kashin-Beck disease** (an osteoarthropathy). * **Other Selenoenzymes:** Apart from GPx, other important selenium-containing enzymes include **Thioredoxin reductase** and **Deiodinases** (specifically Type 1 and 2 iodothyronine deiodinases, which convert T4 to the active T3). * **Antioxidant Synergy:** Selenium works synergistically with **Vitamin E**; while Vitamin E prevents the formation of lipid peroxides in membranes, GPx removes them once formed.

Q: NAD+ is reduced to NADH + H+ by dehydrogenases of all the following substrates, except?

Succinate. ### Explanation The core concept here is the specificity of electron acceptors in the mitochondrial respiratory chain and metabolic pathways. Dehydrogenases catalyze the removal of hydrogen atoms from substrates, but they utilize different coenzymes—typically **NAD+** or **FAD**—based on the energy change of the reaction. **1. Why Succinate is the Correct Answer:** Succinate is oxidized to Fumarate by the enzyme **Succinate Dehydrogenase** (Complex II of the Electron Transport Chain). This specific reaction uses **FAD** as the electron acceptor, reducing it to **FADH₂**, not NADH. This occurs because the free energy change associated with the oxidation of a C-C single bond to a C=C double bond is insufficient to reduce NAD+, but is enough to reduce FAD. **2. Analysis of Incorrect Options:** * **Pyruvate:** Converted to Acetyl-CoA by the *Pyruvate Dehydrogenase Complex*. This reaction involves the reduction of **NAD+ to NADH**. * **Glyceraldehyde-3-phosphate:** In glycolysis, *G3P Dehydrogenase* oxidizes G3P to 1,3-bisphosphoglycerate, reducing **NAD+ to NADH**. * **Malate:** In the TCA cycle, *Malate Dehydrogenase* oxidizes malate to oxaloacetate, reducing **NAD+ to NADH**. **3. High-Yield Clinical Pearls for NEET-PG:** * **Succinate Dehydrogenase** is unique because it is the only TCA cycle enzyme that is **membrane-bound** (inner mitochondrial membrane) and functions as **Complex II** of the ETC. * **Riboflavin (Vitamin B2)** is the precursor for FAD; hence, B2 deficiency directly impairs succinate oxidation. * **Mnemonic:** Most "Dehydrogenases" in the TCA cycle produce NADH (Isocitrate, α-Ketoglutarate, Malate), except for Succinate Dehydrogenase, which produces FADH₂.

Question 1

Which trace element is present in carbonic anhydrase?

Accepted Answer

Zinc

Answer

Molybdenum

Answer

Copper

Answer

Magnesium

Question 2

Which enzyme is known as the 'suicidal enzyme'?

Accepted Answer

Cyclooxygenase

Answer

Lipoxygenase

Answer

Thromboxane synthase

Answer

5'Nucleotidase

Question 3

A 28-year-old female presents with fluctuating fatigue, drooping of her eyelids, difficulty swallowing, and slurred speech. The patient is given a drug that affects an enzyme's activity, and kinetic analysis of the enzyme-catalyzed reaction, in the presence and absence of the drug, is shown below. The effect of this medication can best be described by which set of terms below?

Accepted Answer

Type of Inhibition - Competitive; Effect on Km (as Compared to No Drug) - Increased; Effect of Vmax(as compared to No drug - No change

Answer

Type of Inhibition - Competitive; Effect on Km (as Compared to No Drug) - Decreased; Effect of Vmax(as compared to No drug - Decreased

Answer

Type of Inhibition - Non-competitive; Effect on Km (as Compared to No Drug) - Increased; Effect of Vmax(as compared to No drug - No change

Answer

Type of Inhibition - Non-competitive; Effect on Km (as Compared to No Drug) - Decreased; Effect of Vmax(as compared to No drug - Increased

Question 4

A kinetic analysis of the effect of a drug on an enzyme's activity was performed. Based on the results, into which of the following groups would the drug best fit?

Accepted Answer

A noncompetitive inhibitor

Answer

A competitive inhibitor

Answer

An uncompetitive inhibitor

Answer

A competitive activator of the enzyme

Question 5

Serum creatine kinase-3 (CK-3) is elevated in which of the following conditions?

Accepted Answer

Muscular dystrophy

Answer

Myocardial infarction

Answer

Alcoholic cirrhosis

Answer

Brain tumours

Question 6

Which of the following is a serum marker of rickets?

Accepted Answer

Alkaline phosphatase

Answer

Acid phosphatase

Answer

Decreased serum calcium

Answer

Urinary phosphates

Question 7

Copper is a constituent of which enzyme?

Accepted Answer

Lysyl oxidase

Answer

Glucose oxidase

Answer

Xanthine oxidase

Answer

Transketolase

Question 8

Which of the following is true regarding Nitric Oxide Synthase?

Accepted Answer

It requires NADH, FAD, FMN & Heme iron

Answer

It is inhibited by Ca++

Answer

It catalyzes a dioxygenase reaction

Answer

It accepts electrons from NADH

Question 9

Which of the following is a selenium-containing enzyme?

Accepted Answer

Glutathione peroxidase

Answer

Xanthine oxidase

Answer

Superoxide dismutase

Answer

Lysyl oxidase

Question 10

NAD+ is reduced to NADH + H+ by dehydrogenases of all the following substrates, except?

Accepted Answer

Succinate

Answer

Pyruvate

Answer

Glyceraldehyde-3-phosphate

Answer

Malate

Enzymes — MCQs

Enzymes — MCQs

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