Nucleic Acid Biochemistry Practice Questions

Q: Which of the following is not involved in the synthesis of pyrimidines?

Glycine. In pyrimidine synthesis, the parent ring structure is constructed from three simple precursors: **Glutamine**, **CO2**, and **Aspartic acid**. Unlike purine synthesis, which is a complex multi-step assembly on a ribose sugar, the pyrimidine ring is synthesized first and then attached to PRPP. **Why Glycine is the correct answer:** Glycine is a major contributor to the **purine** ring (providing carbons 4 and 5 and nitrogen 7), but it plays **no role** in the synthesis of pyrimidines. This is a classic "distractor" in biochemistry exams, as students often confuse the precursors of purines with those of pyrimidines. **Explanation of other options:** * **Glutamine (Option A):** Provides the amide nitrogen (N3) of the pyrimidine ring. It is the substrate for the rate-limiting enzyme, Carbamoyl Phosphate Synthetase II (CPS-II). * **CO2 (Option B):** Provides Carbon-2 of the pyrimidine ring. * **Aspartic acid (Option C):** This is the most significant contributor, providing the bulk of the ring (Nitrogen-1 and Carbons 4, 5, and 6). **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme:** CPS-II (located in the cytosol), inhibited by UTP and activated by PRPP. * **Leflunomide:** An immunosuppressant used in Rheumatoid Arthritis that inhibits **Dihydroorotate dehydrogenase**, blocking pyrimidine synthesis. * **Orotic Aciduria:** Caused by a deficiency of UMP Synthase; presents with megaloblastic anemia that does not respond to B12/Folate and the presence of orotic acid crystals in urine. * **Mnemonic for Pyrimidine atoms:** **"CAD"** — **C**O2, **A**spartate, and **D**erivative of Glutamine (Ammonia).

Q: Why is DNA selected for genetic information storage over RNA?

DNA is more stable than RNA.. **Explanation:** The primary reason DNA is the preferred molecule for long-term genetic storage is its superior **chemical stability** compared to RNA. This stability is driven by two key structural differences: 1. **Absence of 2'-OH group:** DNA contains deoxyribose, which lacks a hydroxyl (-OH) group at the 2' carbon. In RNA, this 2'-OH group makes the molecule susceptible to **nucleophilic attack** and spontaneous hydrolysis, especially in alkaline conditions. 2. **Thymine vs. Uracil:** DNA uses Thymine instead of Uracil. Cytosine can spontaneously deaminate to form Uracil. If DNA used Uracil naturally, the repair machinery could not distinguish between a "natural" Uracil and one formed by damage. By using Thymine (5-methyluracil), the cell can easily identify and repair deaminated Cytosine. **Analysis of Incorrect Options:** * **Option B & C:** While double-strandedness and complementarity facilitate replication and repair, they are not the fundamental reasons for "selection." RNA can also form double-stranded structures (e.g., in some viruses) and exhibit complementarity, yet it remains chemically unstable. * **Option D:** This is a circular argument. Both DNA and RNA can carry genetic information (genes); for example, many viruses use RNA as their primary genome. **NEET-PG High-Yield Pearls:** * **Alkali Lability:** RNA is degraded by 0.1M NaOH due to the 2'-OH group; DNA is only denatured (separated into strands) but not degraded. * **Self-Repair:** The presence of Thymine in DNA is a "quality control" mechanism to prevent mutations from Cytosine deamination. * **Catalytic Activity:** Because of its reactivity, RNA can act as an enzyme (**Ribozymes**, e.g., Peptidyl transferase), whereas DNA is chemically inert, making it safer for storage.

Q: Which of the following is NOT true about Ribozymes?

It is a protein. **Explanation:** **Why Option A is correct:** Ribozymes are **catalytic RNA molecules**, not proteins. While most biological catalysts are proteins (enzymes), ribozymes are unique because they consist of ribonucleic acid sequences that fold into complex three-dimensional structures to catalyze specific biochemical reactions. Therefore, the statement "It is a protein" is false. **Analysis of other options:** * **Option B (Transesterification):** Many ribozymes, such as **Group I and II introns** and the **Spliceosome** (specifically U2/U6 snRNA), catalyze transesterification reactions during RNA splicing to remove introns and join exons. * **Option C (Peptide bond formation):** This is a high-yield fact. The **23S rRNA** (in prokaryotes) and **28S rRNA** (in eukaryotes) of the large ribosomal subunit act as a **peptidyl transferase**. This ribozyme activity is responsible for forming peptide bonds during translation. * **Option D (Catalytic RNA):** This is the fundamental definition of a ribozyme. They function by lowering activation energy, similar to protein enzymes, but use nucleotides instead of amino acids. **High-Yield Clinical Pearls for NEET-PG:** * **First Ribozyme Discovered:** RNAse P (involved in tRNA processing) and the self-splicing Group I introns (by Thomas Cech). * **Ribozymes in Medicine:** Artificial ribozymes are being researched as therapeutic agents to "silence" specific genes by cleaving viral RNA or oncogenic mRNA. * **Key Example:** The **Ribosome** is essentially a ribozyme because the catalytic heart of the organelle is composed of RNA, not protein.

Q: Thermo-stability in DNA is contributed mostly by:

G≡C base pairs. **Explanation:** The thermo-stability of the DNA double helix refers to its resistance to denaturation (melting) when exposed to heat. **Why G≡C base pairs are the correct answer:** The stability of DNA is primarily determined by the hydrogen bonding between nitrogenous bases. According to Chargaff’s rules, Guanine (G) pairs with Cytosine (C) via **three hydrogen bonds**, whereas Adenine (A) pairs with Thymine (T) via only **two hydrogen bonds**. The additional hydrogen bond in G≡C pairs provides significantly higher thermal stability. Consequently, DNA sequences with a high **GC content** have a higher **Melting Temperature (Tm)**—the temperature at which 50% of the DNA becomes single-stranded. **Analysis of Incorrect Options:** * **A. A=T base pairs:** These contain only two hydrogen bonds, making them easier to break with heat compared to GC pairs. * **C. Molecular base stacking:** While hydrophobic interactions and van der Waals forces between stacked bases contribute to the overall structural stability of the helix, the specific "thermo-stability" tested in competitive exams traditionally focuses on the strength of the inter-strand hydrogen bonding (GC content). * **D. Antiparallel arrangement:** This refers to the 5'→3' and 3'→5' orientation of the strands. While essential for the double helix geometry, it is not the primary determinant of thermal resistance. **High-Yield Clinical Pearls for NEET-PG:** * **Tm (Melting Temperature):** Directly proportional to the GC content and the length of the DNA molecule. * **Hyperchromicity:** When DNA denatures (melts), its UV light absorption at **260 nm increases**. This is a common laboratory method to monitor DNA denaturation. * **TATA Box:** Promoters often contain AT-rich regions (like the TATA box) because the lower number of hydrogen bonds allows for easier "melting" or opening of the DNA strands during the initiation of transcription.

Q: What is the main catabolic product of purine nucleotides in humans?

Uric Acid. **Explanation:** In humans and higher primates, the final degradation product of purine metabolism (Adenine and Guanine) is **Uric Acid**. This process occurs primarily in the liver. Adenosine and Guanosine are converted into **Xanthine**, which is then oxidized by the enzyme **Xanthine Oxidase** to form Uric Acid. Because humans lack the enzyme *Urate Oxidase (Uricase)*, we cannot further break down uric acid into the more soluble allantoin, making uric acid the terminal excretory product excreted in urine. **Analysis of Options:** * **Option A & D (Ammonia, CO2, and Water):** These are the end products of **Pyrimidine** catabolism (Cytosine, Uracil, and Thymine). Pyrimidines are highly soluble and break down into β-alanine and β-aminoisobutyrate, eventually yielding CO2 and NH3. * **Option B (Ammonia):** While ammonia is produced during the deamination of amino acids and certain steps of nucleotide breakdown, it is not the "main" end product of the purine ring itself; it is typically converted to urea in the liver. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme:** PRPP Synthetase/Amidotransferase (Synthesis); **Xanthine Oxidase** (Catabolism). * **Gout:** Hyperuricemia (Uric acid >7 mg/dL) leads to the deposition of **Monosodium Urate crystals** in joints (Tophi). * **Lesch-Nyhan Syndrome:** 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.

Q: Amniocentesis conducted during genetic counseling of a pregnant woman reveals a fetal adenosine deaminase deficiency. This autosomal recessive immunodeficiency is usually associated with which of the following?

Humoral Immunity - Deficient; Cellular Immunity - Deficient. ### Explanation **Adenosine Deaminase (ADA) deficiency** is the second most common cause of **Severe Combined Immunodeficiency (SCID)**, accounting for approximately 15% of cases. It is inherited as an autosomal recessive trait. #### Why Option D is Correct: The enzyme adenosine deaminase is essential for the purine salvage pathway. Its deficiency leads to the accumulation of toxic metabolites, specifically **deoxyadenosine** and **dATP**, within lymphocytes. These metabolites are lymphotoxic; they inhibit DNA synthesis and induce apoptosis. Because this metabolic defect affects the common lymphoid progenitor cell line, it results in the failure of both **T-cell and B-cell maturation**. Consequently, patients exhibit a profound lack of both **Cellular Immunity** (T-cells) and **Humoral Immunity** (B-cells/Antibodies). #### Why Other Options are Incorrect: * **Option A:** This describes an immunocompetent state. ADA deficiency is a primary immunodeficiency. * **Option B:** This pattern (Deficient Cellular, Normal Humoral) is characteristic of **DiGeorge Syndrome** (thymic hypoplasia), where T-cells are low but B-cells are initially preserved. * **Option C:** This pattern (Deficient Humoral, Normal Cellular) is characteristic of **X-linked Agammaglobulinemia (Bruton’s)**, where B-cell maturation is blocked but T-cell function remains intact. #### NEET-PG High-Yield Pearls: * **SCID Presentation:** Recurrent "failure to thrive," chronic diarrhea, and severe opportunistic infections (e.g., *Pneumocystis jirovecii*, *Candida*) in early infancy. * **Imaging:** Characteristically shows an **absent thymic shadow** on chest X-ray. * **Historical Significance:** ADA deficiency was the first disease treated with **Gene Therapy**. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the treatment of choice; Enzyme Replacement Therapy (PEG-ADA) is a temporizing measure.

Q: Gout is a disorder of-

Purine metabolism. **Explanation:** **Gout** is a clinical syndrome characterized by hyperuricemia (elevated serum uric acid levels), which leads to the deposition of monosodium urate crystals in joints and soft tissues. **1. Why Purine Metabolism is Correct:** Uric acid is the final metabolic breakdown product of **purine nucleotides** (Adenine and Guanine) in humans. The pathway involves the conversion of purines to Xanthine, which is then oxidized to Uric Acid by the enzyme **Xanthine Oxidase**. Gout occurs due to either the overproduction of uric acid (e.g., PRPP synthetase overactivity, Lesch-Nyhan syndrome) or, more commonly, decreased renal excretion of uric acid. **2. Why Other Options are Incorrect:** * **Pyrimidine Metabolism:** The end products of pyrimidine catabolism (Cytosine, Thymine, Uracil) are highly water-soluble compounds like **β-alanine and β-aminoisobutyrate**, which are easily excreted and do not cause gout. * **Ketone Metabolism:** Disorders here lead to ketoacidosis or hypoglycemia, not urate deposition. However, note that ketones can compete with uric acid for excretion in the kidneys, potentially triggering a gout flare. * **Protein Metabolism:** While purines are found in nucleoproteins, "protein metabolism" generally refers to amino acid breakdown, which primarily results in **urea** formation via the urea cycle. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Identification of **negatively birefringent, needle-shaped crystals** under polarized light microscopy. * **Drug of Choice:** **Allopurinol** (a suicide inhibitor of Xanthine Oxidase) for chronic gout; **NSAIDs** or Colchicine for acute attacks. * **Von Gierke’s Disease (G6PD deficiency):** A common biochemical association where lactic acidosis inhibits uric acid excretion, leading to secondary gout. * **Lesch-Nyhan Syndrome:** Deficiency of **HGPRT** (salvage pathway) leads to massive purine overproduction and self-mutilation.

Q: Pyrimidine overproduction results in all of the following except:

Hyperuricemia. **Explanation:** The correct answer is **Hyperuricemia** because the catabolism of pyrimidines (Cytosine, Uracil, Thymine) results in highly water-soluble end products: **$\beta$-alanine** and **$\beta$-aminoisobutyrate**. Unlike purine catabolism, which produces insoluble uric acid leading to hyperuricemia and gout, pyrimidine breakdown does not contribute to uric acid levels. **Analysis of Options:** * **Hyperuricemia (A):** This is a hallmark of **purine** overproduction or impaired excretion. Pyrimidine metabolism is independent of the xanthine oxidase pathway that produces uric acid. * **Reye Syndrome (B):** In Reye syndrome, mitochondrial damage leads to hyperammonemia. This causes an accumulation of Carbamoyl Phosphate in the mitochondria, which leaks into the cytosol and enters the pyrimidine synthesis pathway, causing secondary overproduction of orotic acid. * **Orotic Aciduria (C):** This is a direct result of pyrimidine pathway derangement. Hereditary Orotic Aciduria (Type I) occurs due to a deficiency of **UMPS (Uridine Monophosphate Synthase)**, leading to a massive buildup and excretion of orotic acid. * **Megaloblastic Anemia (D):** In Hereditary Orotic Aciduria, the inability to synthesize pyrimidines leads to a lack of TTP and dCTP required for DNA synthesis in RBC precursors. This results in megaloblastic anemia that is **refractory** to Vitamin B12 and Folate. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme of Pyrimidine synthesis:** Carbamoyl Phosphate Synthetase II (CPS-II), located in the cytosol (inhibited by UTP). * **Differentiating Orotic Aciduria:** If Orotic aciduria is accompanied by **hyperammonemia**, suspect **OTC (Ornithine Transcarbamylase) deficiency** (Urea cycle defect). If ammonia levels are normal, suspect **Hereditary Orotic Aciduria**. * **Treatment:** Hereditary Orotic Aciduria is treated with **Oral Uridine**, which bypasses the metabolic block.

Question 1

Which of the following is not involved in the synthesis of pyrimidines?

Accepted Answer

Glycine

Answer

Glutamine

Answer

CO2

Answer

Aspartic acid

Question 2

Why is DNA selected for genetic information storage over RNA?

Accepted Answer

DNA is more stable than RNA.

Answer

DNA is double-stranded, whereas RNA is typically single-stranded.

Answer

The two strands of DNA are complementary.

Answer

DNA contains genes.

Question 3

Which of the following is NOT true about Ribozymes?

Accepted Answer

It is a protein

Answer

Involved in transesterification

Answer

Involved in peptide bond formation

Answer

Catalytic RNA

Question 4

Thermo-stability in DNA is contributed mostly by:

Accepted Answer

G≡C base pairs

Answer

A=T base pairs

Answer

Molecular base stacking

Answer

Antiparallel arrangement

Question 5

What is the main catabolic product of purine nucleotides in humans?

Accepted Answer

Uric Acid

Answer

Ammonia and CO2

Answer

Ammonia

Answer

CO2 and Water

Question 6

Amniocentesis conducted during genetic counseling of a pregnant woman reveals a fetal adenosine deaminase deficiency. This autosomal recessive immunodeficiency is usually associated with which of the following?

Accepted Answer

Humoral Immunity - Deficient; Cellular Immunity - Deficient

Answer

Humoral Immunity - Normal; Cellular Immunity - Normal

Answer

Humoral Immunity - Normal; Cellular Immunity - Deficient

Answer

Humoral Immunity - Deficient; Cellular Immunity - Normal

Question 7

Gout is a disorder of-

Accepted Answer

Purine metabolism

Answer

Pyrimidine metabolism

Answer

Ketone metabolism

Answer

Protein metabolism

Question 8

Pyrimidine overproduction results in all of the following except:

Accepted Answer

Hyperuricemia

Answer

Reye syndrome

Answer

Orotic aciduria

Answer

Megaloblastic anemia

Question 9

Which statement is true about the structure of DNA?

Accepted Answer

It has a deoxyribose-phosphate backbone with bases stacked inside.

Answer

Purines are adenine and guanine, and pyrimidines are uracil and cytosine.

Answer

Watson and Crick discovered the DNA structure in 1973.

Answer

It mainly consists of a left-handed helix.

Question 10

Which of the following statements is NOT true regarding hypoxanthine-guanine phosphoribosyltransferase?

Accepted Answer

Requires phosphoribosyl pyrophosphate (PRPP) as a substrate.

Answer

Predominantly present in the liver.

Answer

Involved in purine metabolism.

Answer

Its deficiency leads to Lesch-Nyhan disease.

Nucleic Acid Biochemistry — MCQs

Nucleic Acid Biochemistry — MCQs

On this page

Practice by Chapter

Want unlimited practice?