Nucleic Acid Biochemistry Practice Questions

Q: What is the cause of increased uric acid production in tumors?

Increased purine degradation. **Explanation:** The correct answer is **A. Increased purine degradation.** **1. Why it is correct:** Tumors are characterized by rapid cell turnover and high rates of cell death (lysis). When tumor cells break down—either spontaneously or due to chemotherapy (Tumor Lysis Syndrome)—large amounts of nucleic acids are released. The catabolism of **purines** (Adenine and Guanine) follows a specific pathway: they are converted into Xanthine and subsequently oxidized by the enzyme **Xanthine Oxidase** into **Uric Acid**. Because uric acid is the final metabolic end-product of purine metabolism in humans, massive cell turnover directly leads to hyperuricemia. **2. Why the other options are incorrect:** * **B & D (Pyrimidine degradation/synthesis):** Unlike purines, the end-products of pyrimidine catabolism (β-alanine and β-aminoisobutyrate) are highly water-soluble and do not form uric acid. Therefore, pyrimidine turnover does not contribute to gout or hyperuricemia. * **C (De novo purine synthesis):** While rapidly dividing tumor cells do increase de novo synthesis to create new DNA, the *excess* uric acid seen clinically in cancer patients is primarily a result of the **breakdown** of existing cellular bulk rather than the synthetic phase. **Clinical Pearls for NEET-PG:** * **Tumor Lysis Syndrome (TLS):** A metabolic emergency characterized by Hyperuricemia, Hyperkalemia, Hyperphosphatemia, and **Hypocalcemia**. * **Management:** Allopurinol (Xanthine Oxidase inhibitor) or Rasburicase (recombinant Urate Oxidase) is used to manage high uric acid levels. * **Key Enzyme:** Xanthine Oxidase is the rate-limiting step in uric acid formation and a frequent target for pharmacology questions.

Q: Allopurinol prevents the conversion of which of the following substances?

Hypoxanthine to xanthine. ### Explanation **Correct Option: A. Hypoxanthine to xanthine** Allopurinol is a structural analog of hypoxanthine and acts as a potent **suicide inhibitor** of the enzyme **Xanthine Oxidase (XO)**. In the purine degradation pathway, Xanthine Oxidase catalyzes two sequential steps: 1. **Hypoxanthine → Xanthine** 2. **Xanthine → Uric Acid** By inhibiting XO, allopurinol prevents the formation of both xanthine and uric acid, leading to an increase in more soluble precursors (hypoxanthine and xanthine) which are easily excreted by the kidneys. **Analysis of Incorrect Options:** * **B. Xanthine to hypoxanthine:** This is the reverse reaction. Purine catabolism is an irreversible pathway; xanthine does not convert back to hypoxanthine. * **C. Hypoxanthine to I.M.P:** This reaction is catalyzed by **HGPRT** (Hypoxanthine-Guanine Phosphoribosyltransferase) as part of the **Purine Salvage Pathway**. Allopurinol actually *promotes* this step because, when XO is inhibited, hypoxanthine levels rise and are diverted toward IMP synthesis, further reducing de novo purine production. * **D. All of the above:** Incorrect as only Option A describes the inhibited catabolic step. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Allopurinol is converted by XO into **Alloxanthine (Oxypurinol)**, which binds tightly to the enzyme's active site (suicide inhibition). * **Drug Interaction:** Since **6-Mercaptopurine** and **Azathioprine** are metabolized by Xanthine Oxidase, their dosage must be reduced by 75% if co-administered with Allopurinol to avoid toxicity. * **Lesch-Nyhan Syndrome:** Allopurinol is used to treat hyperuricemia in these patients but does not improve neurological symptoms.

Q: What is a product of purine metabolism?

uric acid. **Explanation:** The correct answer is **D. uric acid**. **1. Why Uric Acid is Correct:** In humans, **uric acid** is the final metabolic breakdown product of purine nucleotides (Adenine and Guanine). The pathway involves the conversion of adenosine and guanosine into **Xanthine**, which is then oxidized by the enzyme **Xanthine Oxidase** to form uric acid. Because humans lack the enzyme *uricase*, we cannot further break down uric acid into allantoin, making it the terminal excretory product excreted via urine. **2. Why Other Options are Incorrect:** * **A. Beta-alanine:** This is a breakdown product of **pyrimidine** catabolism (specifically Uracil and Cytosine). * **B & C. Ammonia and Carbon Dioxide:** While these are produced during various metabolic cycles (like the Urea cycle or TCA cycle), they are the end products of **pyrimidine** catabolism (specifically Thymine breaks down into $\beta$-aminoisobutyrate, $CO_2$, and $NH_3$). In purine metabolism, the carbon skeleton remains largely intact as the purine ring is not cleaved into $CO_2$ and $NH_3$ in humans. **3. High-Yield Clinical Pearls for NEET-PG:** * **Gout:** Caused by hyperuricemia (elevated uric acid), leading to the deposition of **monosodium urate crystals** in joints (Tophi). * **Lesch-Nyhan Syndrome:** A deficiency of **HGPRT** (salvage pathway) leads to excessive de novo purine synthesis and massive overproduction of uric acid, characterized by self-mutilation and mental retardation. * **Pharmacology Link:** **Allopurinol** and **Febuxostat** treat gout by inhibiting **Xanthine Oxidase**, thereby reducing uric acid production. * **Von Gierke’s Disease:** Often presents with hyperuricemia due to increased pentose phosphate pathway activity, leading to increased PRPP and purine synthesis.

Q: Increased uric acid level in plasma is due to which of the following mechanisms?

Decreased purine reutilization. **Explanation:** The correct answer is **D. Decreased purine reutilization.** **Understanding the Mechanism:** Uric acid is the final metabolic breakdown product of purine nucleotides (Adenine and Guanine) in humans. Purines are managed by the body through two pathways: the **De Novo Synthesis** pathway (creating new purines) and the **Salvage Pathway** (reutilizing existing purines). The Salvage Pathway, primarily mediated by the enzyme **HGPRT** (Hypoxanthine-Guanine Phosphoribosyltransferase), recycles free purine bases back into nucleotides (IMP and GMP). When purine reutilization is decreased (as seen in **Lesch-Nyhan Syndrome**), two things happen: 1. Free purine bases are not recycled and are instead diverted to the degradation pathway, forming uric acid. 2. The lack of salvaged nucleotides leads to a loss of feedback inhibition on the *PRPP Amidotransferase* enzyme, significantly accelerating *de novo* purine synthesis, which further increases the purine load for degradation. **Why other options are incorrect:** * **A & B:** Increased utilization or decreased synthesis of purines would lead to a *reduction* in the pool of purines available for breakdown, thereby lowering uric acid levels. * **C:** Uric acid is the end product of purine degradation. Therefore, *increased* (not decreased) degradation leads to hyperuricemia. **High-Yield Clinical Pearls for NEET-PG:** * **Lesch-Nyhan Syndrome:** An X-linked recessive deficiency of **HGPRT**. Characterized by hyperuricemia, gout, intellectual disability, and distinctive **self-mutilation**. * **Von Gierke’s Disease:** Can cause hyperuricemia due to increased G6P entering the Pentose Phosphate Pathway, raising PRPP levels and driving purine synthesis. * **Drug Link:** **Allopurinol** treats hyperuricemia by inhibiting **Xanthine Oxidase**, the enzyme responsible for the final steps of uric acid production.

Q: To which nitrogen atom of the pyrimidine ring does the first carbon of the pentose sugar of a nucleic acid attach?

N-1 of pyrimidine. **Explanation:** In nucleic acid biochemistry, the formation of a **nucleoside** involves a covalent bond between the pentose sugar (ribose or deoxyribose) and a nitrogenous base. This specific linkage is known as a **β-N-glycosidic bond**. **Why Option B is correct:** The bond always forms between the **C-1 (anomeric carbon)** of the pentose sugar and a specific nitrogen atom of the base. For **pyrimidines** (Cytosine, Thymine, and Uracil), which are single-ring structures, the attachment occurs at the **N-1 position**. **Why other options are incorrect:** * **Option A (N-9 of pyrimidine):** This is incorrect because pyrimidines only have two nitrogen atoms (at positions 1 and 3). There is no N-9 in a pyrimidine ring. * **Option C (N-1 of purine):** This is incorrect. In **purines** (Adenine and Guanine), which are double-ring structures, the sugar attaches to the **N-9 position**, not N-1. **High-Yield Facts for NEET-PG:** * **Purines (A, G):** Attach via **N-9** to C-1 of sugar. (Mnemonic: "Pure As Gold" - Purines are larger, so they use the larger number, 9). * **Pyrimidines (C, T, U):** Attach via **N-1** to C-1 of sugar. * **Bond Type:** It is a **β-configuration** bond because the base lies above the plane of the sugar ring. * **Clinical Relevance:** Several antiviral and anticancer drugs (e.g., 5-Fluorouracil, Zidovudine) are **nucleoside analogues** that work by modifying these rings or the glycosidic linkage to inhibit DNA/RNA synthesis.

Q: Base unstacking of DNA results in which of the following phenomena?

Hyperchromicity. **Explanation:** **Correct Option: B. Hyperchromicity** Hyperchromicity refers to the increase in the absorption of ultraviolet (UV) light (at 260 nm) by DNA when it is denatured. In its native double-helical state, the nitrogenous bases are "stacked" tightly within the hydrophobic core, which limits their ability to absorb light. When DNA is heated or exposed to extreme pH, the hydrogen bonds break (denaturation), leading to **base unstacking**. This exposes the conjugated double bonds of the purines and pyrimidines, significantly increasing their UV absorbance. **Incorrect Options:** * **A. Hypochromicity:** This is the opposite effect; it refers to the *decrease* in light absorption. This occurs when single-stranded DNA renatures (anneals) back into a double helix, as the bases become restacked. * **C. Electrophoresis:** This is a laboratory technique used to separate DNA fragments based on their size and charge (DNA is negatively charged due to its phosphate backbone) using an electric field. It is not a direct optical consequence of base unstacking. * **D. Linear dichromicity:** This relates to the differential absorption of polarized light based on the orientation of molecules. While DNA exhibits this property, it is not the standard term used to describe the change in absorbance during denaturation. **High-Yield Clinical Pearls for NEET-PG:** * **Melting Temperature (Tm):** The temperature at which 50% of DNA is denatured. A higher **G-C content** increases the Tm because G-C pairs have three hydrogen bonds, whereas A-T pairs have only two. * **Absorbance Peak:** DNA and RNA absorb maximally at **260 nm**, while proteins absorb at **280 nm**. The 260/280 ratio is used to assess DNA purity. * **Reversibility:** Denaturation is reversible (renaturation/annealing), a principle fundamental to **PCR (Polymerase Chain Reaction)** and **Southern Blotting**.

Q: On complete hydrolysis of DNA, which of the following is NOT obtained?

Adenosine. **Explanation:** The fundamental structure of DNA consists of three components: a nitrogenous base, a pentose sugar (2-deoxy-D-ribose), and phosphoric acid. To understand the products of hydrolysis, one must distinguish between **Nucleosides** and **Nucleotides**. **1. Why Adenosine is the Correct Answer:** Adenosine is a **nucleoside** (Adenine + Ribose sugar). Upon **complete hydrolysis** of DNA, the glycosidic bonds between the sugar and the base, as well as the ester bonds to the phosphate group, are broken. This yields individual components: free nitrogenous bases, free pentose sugars, and inorganic phosphate. Adenosine does not exist as a free product of complete hydrolysis because it would further break down into Adenine and Ribose. Furthermore, "Adenosine" specifically contains ribose, making it a component of RNA, not DNA (where it would be Deoxyadenosine). **2. Analysis of Incorrect Options:** * **B. A purine base:** DNA contains the purine bases Adenine (A) and Guanine (G). Complete hydrolysis releases these as free bases. * **C. Phosphoric acid:** The backbone of DNA is held by phosphodiester bonds. Hydrolysis releases these as inorganic phosphoric acid ($H_3PO_4$). * **D. A deoxyribose pentose sugar:** The sugar in DNA is 2-deoxy-D-ribose. Complete hydrolysis cleaves the N-glycosidic linkage, releasing the free sugar. **High-Yield Clinical Pearls for NEET-PG:** * **Nucleoside vs. Nucleotide:** Nucleoside = Base + Sugar; Nucleotide = Base + Sugar + Phosphate (Nucleoside monophosphate). * **Chargaff’s Rule:** In double-stranded DNA, the amount of Purines (A+G) always equals the amount of Pyrimidines (C+T). * **Bonding:** Phosphodiester bonds form the backbone (3'-5'), while Hydrogen bonds connect the bases (2 between A=T, 3 between G≡C). * **DNA vs. RNA:** DNA has Thymine and Deoxyribose; RNA has Uracil and Ribose.

Q: The two strands of DNA are held together by:

Hydrogen bond. **Explanation:** The stability of the DNA double helix is primarily maintained by **Hydrogen bonds** between complementary nitrogenous bases. According to Watson-Crick base pairing, Adenine (A) pairs with Thymine (T) via **two** hydrogen bonds, while Guanine (G) pairs with Cytosine (C) via **three** hydrogen bonds. These bonds are weak enough to allow "unzipping" during replication and transcription but strong enough to maintain structural integrity. **Analysis of Options:** * **Hydrogen bond (Correct):** These are non-covalent interactions between a hydrogen atom and electronegative atoms (N or O). The triple bond between G-C makes GC-rich DNA more stable and harder to denature than AT-rich DNA. * **Covalent bond (Incorrect):** Covalent (phosphodiester) bonds form the **backbone** of a single DNA strand, linking the 3' carbon of one sugar to the 5' carbon of the next. They do not hold the two strands together. * **Van der Waals forces (Incorrect):** While these contribute to the "base-stacking" stability between adjacent bases on the *same* strand, they are not the primary force holding the two strands together. * **Ionic interaction (Incorrect):** DNA is negatively charged due to phosphate groups. Ionic interactions usually occur between DNA and positively charged proteins like **Histones**, not between the two DNA strands. **High-Yield Clinical Pearls for NEET-PG:** 1. **Melting Temperature (Tm):** The temperature at which 50% of DNA is denatured. High **G-C content** increases Tm because of the extra hydrogen bond. 2. **Chargaff’s Rule:** In double-stranded DNA, A=T and G=C; therefore, Purines = Pyrimidines. 3. **Denaturation:** Agents like heat, low salt concentration, and high pH (alkali) disrupt hydrogen bonds, leading to DNA strand separation.

Q: Hereditary orotic aciduria Type-I is due to a deficiency of which enzyme?

Orotate phosphoribosyl transferase. **Explanation:** Hereditary Orotic Aciduria (Type I) is an autosomal recessive disorder of **de novo pyrimidine synthesis**. The correct answer is **Orotate phosphoribosyl transferase (OPRT)** because, in Type I disease, there is a dual deficiency of both OPRT and **Orotidylate decarboxylase (ODC)**. These two enzymatic activities are part of a single bifunctional cytosolic protein called **UMP Synthase**. When these enzymes are deficient, Orotic acid cannot be converted to UMP (Uridine Monophosphate). This leads to an accumulation of orotic acid (excreted in urine) and a systemic deficiency of pyrimidines, which are essential for DNA/RNA synthesis and erythropoiesis. **Analysis of Incorrect Options:** * **B. Ribonucleotide reductase:** This enzyme converts ribonucleotides to deoxyribonucleotides (e.g., ADP to dADP). Its inhibition or deficiency affects DNA synthesis but does not cause orotic aciduria. * **C. Dihydroorotase:** This is the third enzyme in the pathway (converting Carbamoyl aspartate to Dihydroorotate). Deficiency would occur *before* the formation of orotic acid. * **D. Dihydroorotate dehydrogenase:** This mitochondrial enzyme converts dihydroorotate to orotate. Deficiency would lead to a decrease, rather than an increase, in orotic acid levels. **NEET-PG High-Yield Pearls:** 1. **Clinical Presentation:** Characterized by **megaloblastic anemia** that is refractory to Vitamin B12 and Folate, along with growth retardation and orotic acid crystals in urine. 2. **Treatment:** Oral **Uridine** supplementation. This bypasses the metabolic block and provides the necessary pyrimidines via the salvage pathway. 3. **Differential Diagnosis:** Differentiate from **Ornithine Transcarbamoylase (OTC) deficiency** (Urea cycle disorder). Both show orotic aciduria, but OTC deficiency presents with **hyperammonemia**, whereas Hereditary Orotic Aciduria does not.

Q: What is the pentose sugar found in nucleic acids?

Ribose. **Explanation:** **1. Why Ribose is Correct:** Nucleic acids (DNA and RNA) are polymers of nucleotides. Each nucleotide consists of a nitrogenous base, a phosphate group, and a **pentose (5-carbon) sugar**. In **RNA**, the sugar is **D-ribose**. In **DNA**, it is **2-deoxy-D-ribose**, where the hydroxyl (-OH) group at the C2 position is replaced by a hydrogen atom. Ribose provides the structural backbone for these genetic molecules, allowing for the formation of phosphodiester bonds. **2. Analysis of Incorrect Options:** * **Ribulose (Option A):** This is a ketopentose sugar. While it is an isomer of ribose, its primary biological role is as an intermediate in the **Pentose Phosphate Pathway (PPP)** (as Ribulose-5-phosphate) and not as a structural component of nucleic acids. * **Xylulose (Option B):** This is also a ketopentose. L-xylulose is a key intermediate in the **Uronic Acid Pathway**. Deficiency of the enzyme *xylitol dehydrogenase* leads to Essential Pentosuria, where xylulose is excreted in the urine. * **Xylase (Option D):** This is an incorrect term in this context; "Xylanase" is an enzyme that breaks down xylan (a plant polysaccharide). It is not a sugar. **3. High-Yield Clinical Pearls for NEET-PG:** * **Sugar Chemistry:** Ribose is an **aldopentose**, while Ribulose and Xylulose are **ketopentoses**. * **DNA vs. RNA:** The absence of the 2'-OH group in deoxyribose makes DNA chemically more stable than RNA, which is why DNA is the primary genetic material. * **Essential Pentosuria:** A rare, benign genetic condition characterized by high levels of **L-xylulose** in the urine, often giving a false-positive result on Benedict’s test (reducing sugar). * **PPP Link:** The Pentose Phosphate Pathway is the body's primary source of Ribose-5-phosphate for *de novo* nucleotide synthesis.

Question 1

What is the cause of increased uric acid production in tumors?

Accepted Answer

Increased purine degradation

Answer

Increased pyrimidine degradation

Answer

Denovo purine synthesis

Answer

Increased pyrimidine synthesis

Question 2

Allopurinol prevents the conversion of which of the following substances?

Accepted Answer

Hypoxanthine to xanthine

Answer

Xanthine to hypoxanthine

Answer

Hypoxanthine to I.M.P

Answer

All of the above

Question 3

What is a product of purine metabolism?

Accepted Answer

uric acid

Answer

beta-alanine

Answer

ammonia

Answer

carbon dioxide

Question 4

Increased uric acid level in plasma is due to which of the following mechanisms?

Accepted Answer

Decreased purine reutilization

Answer

Increased purine utilization

Answer

Decreased purine synthesis

Answer

Decreased purine degradation

Question 5

To which nitrogen atom of the pyrimidine ring does the first carbon of the pentose sugar of a nucleic acid attach?

Accepted Answer

N-1 of pyrimidine

Answer

N-9 of pyrimidine

Answer

N-1 of purine

Answer

None of the above

Question 6

Base unstacking of DNA results in which of the following phenomena?

Accepted Answer

Hyperchromicity

Answer

Hypochromicity

Answer

Electrophoresis

Answer

Linear dichromicity

Question 7

On complete hydrolysis of DNA, which of the following is NOT obtained?

Accepted Answer

Adenosine

Answer

A purine base

Answer

Phosphoric acid

Answer

A deoxyribose pentose sugar

Question 8

The two strands of DNA are held together by:

Accepted Answer

Hydrogen bond

Answer

Van der Waal bond

Answer

Covalent bond

Answer

Ionic interaction

Question 9

Hereditary orotic aciduria Type-I is due to a deficiency of which enzyme?

Accepted Answer

Orotate phosphoribosyl transferase

Answer

Ribonucleotide reductase

Answer

Dihydroorotase

Answer

Dihydroorotate dehydrogenase

Question 10

What is the pentose sugar found in nucleic acids?

Accepted Answer

Ribose

Answer

Ribulose

Answer

Xylulose

Answer

Xylase

Nucleic Acid Biochemistry — MCQs

Nucleic Acid Biochemistry — MCQs

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