NO is synthesized from:
If the percentage of thymine residues in DNA is 28%. What is the percentage of cytosine?
A patient complains of knee pain. Routine investigations are unremarkable and still, the patient is unsatisfied. Urine turns black on standing, what is the enzyme involved?
Vitamin B12 is found maximum in:
Female, on maize as a staple diet. History of diarrhoea and lesion in the neck region. This is due to deficiency of which of the following?
In a preterm baby with respiratory distress syndrome, which of the following lipids would be deficient?
Which of the following is the etiology of Werner syndrome?
Apolipoprotein B-48 is made by which process?
A child was fed on a staple diet of maize for a long time. Which of the following vitamin may get deficient in his body?
Which of the following is true about non-competitive inhibition?
NEET-PG 2020 - Biochemistry NEET-PG Practice Questions and MCQs
Question 11: NO is synthesized from:
- A. L-citrulline
- B. Glycine
- C. Lysine
- D. L-arginine (Correct Answer)
Explanation: ***L-arginine*** - **Nitric oxide (NO)** is synthesized from the amino acid **L-arginine** by the enzyme **nitric oxide synthase (NOS)**. - This reaction requires **molecular oxygen** and **NADPH** as cofactors, producing **L-citrulline** as a co-product. - **Three NOS isoforms** exist: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS). - **Clinical significance**: NO is crucial for **vascular smooth muscle relaxation**, **neurotransmission**, and **immune defense**. *L-citrulline* - **L-citrulline** is the co-product (not precursor) of the NO synthesis reaction. - While it can be recycled back to **L-arginine** via the **citrulline-arginine cycle**, it does not directly yield NO without first being converted to arginine. - This recycling pathway helps sustain NO production in endothelial cells. *Glycine* - **Glycine** is involved in various metabolic processes, including **heme synthesis**, **purine synthesis**, and as a neurotransmitter. - It plays no direct role in **nitric oxide** biosynthesis. - Not a substrate for any **NOS isoform**. *Lysine* - **Lysine** is an essential amino acid important for **protein synthesis**, **collagen formation**, and **carnitine synthesis**. - It is structurally distinct from arginine and is not recognized by **nitric oxide synthase**. - Not involved in the NO synthesis pathway.
Question 12: If the percentage of thymine residues in DNA is 28%. What is the percentage of cytosine?
- A. 36%
- B. 44%
- C. 22% (Correct Answer)
- D. 28%
Explanation: ***22%*** - According to **Chargaff's rules**, in a DNA molecule, the amount of **adenine (A) is equal to the amount of thymine (T)**, and the amount of **guanine (G) is equal to the amount of cytosine (C)**. - If thymine (T) is 28%, then adenine (A) is also 28%, making a total of 56% for A+T. The remaining 44% (100% - 56%) is split equally between guanine and cytosine, so cytosine (C) is 22%. *36%* - This percentage would be plausible if the sum of adenine and thymine were 28%, which is incorrect as A and T are equal and their sum would thus be 56%. - This value does not adhere to the principle of **base pairing complementarity** and the total percentage of all bases summing to 100%. *44%* - This would be the combined percentage of guanine and cytosine, not the percentage of cytosine alone. - If cytosine were 44%, then guanine would also be 44%, leading to a total of 88% for G+C, which is inconsistent with T being 28%. *28%* - This is the percentage of thymine, and by **Chargaff's rules**, it would also be the percentage of adenine, not cytosine. - Cytosine percentages are derived from the remaining proportion of bases after accounting for adenine and thymine.
Question 13: A patient complains of knee pain. Routine investigations are unremarkable and still, the patient is unsatisfied. Urine turns black on standing, what is the enzyme involved?
- A. Methylmalonyl-CoA mutase
- B. Homogentisate oxidase (Correct Answer)
- C. Xanthine oxidase
- D. Tyrosine hydroxylase
Explanation: ***Homogentisate oxidase*** - **Homogentisate oxidase** deficiency leads to **alkaptonuria**, where homogentisic acid accumulates and is excreted in urine, turning it black upon standing or exposure to air. The knee pain could be due to **ochronosis**, the deposition of oxidized homogentisic acid in cartilage and connective tissues. - The unremarkable routine investigations with persistent knee pain suggest a less common metabolic disorder, which is consistent with **alkaptonuria**'s chronic and insidious presentation. *Methylmalonyl-CoA mutase* - A deficiency in **methylmalonyl-CoA mutase** causes **methylmalonic acidemia**, a metabolic disorder typically presenting in infancy with neurological symptoms, feeding difficulties, and developmental delay. - It does not cause urine to turn black on standing or lead to specific joint pain like that seen in ochronosis. *Xanthine oxidase* - **Xanthine oxidase** is involved in purine metabolism, and its inhibition (e.g., by allopurinol) is used to treat **gout**. - While gout can cause knee pain, it is characterized by elevated uric acid and typically responds to conventional treatments and the urine does not turn black. *Tyrosine hydroxylase* - **Tyrosine hydroxylase** is the rate-limiting enzyme in catecholamine synthesis, converting tyrosine to L-DOPA. - Defects in this enzyme are rare and result in neurological disorders, such as **DOPA-responsive dystonia**, and do not cause urine to blacken or lead to direct joint damage.
Question 14: Vitamin B12 is found maximum in:
- A. Sunlight
- B. Green leafy vegetables
- C. Animal products (Correct Answer)
- D. Roots and tubers
Explanation: ***Animal products*** - **Vitamin B12**, or cobalamin, is primarily synthesized by bacteria and accumulates in animal tissues, making **meat, fish, poultry, eggs, and dairy** the richest dietary sources. - Humans generally cannot synthesize vitamin B12 and must obtain it from dietary sources, with **animal-derived foods** being the most concentrated and bioavailable forms. *Sunlight* - **Sunlight** is primarily critical for the synthesis of **Vitamin D** in the skin, not Vitamin B12. - Exposure to sunlight has no direct role in the production or absorption of **Vitamin B12**. *Green leafy vegetables* - **Green leafy vegetables** are excellent sources of nutrients like **folate, Vitamin K, and iron**, but they are generally devoid of naturally occurring **Vitamin B12**. - While some fortified plant-based foods may contain Vitamin B12, naturally, these vegetables do not provide it. *Roots and tubers* - **Roots and tubers** like potatoes, carrots, and sweet potatoes are good sources of carbohydrates, fiber, and various vitamins and minerals such as **Vitamin C and potassium**. - They do not contain significant amounts of **Vitamin B12**, as they are plant-based foods.
Question 15: Female, on maize as a staple diet. History of diarrhoea and lesion in the neck region. This is due to deficiency of which of the following?
- A. Pyridoxine
- B. Niacin (Correct Answer)
- C. Thiamine
- D. Zinc
Explanation: ***Niacin*** * The constellation of **diarrhea**, **dermatitis** (neck lesion, often a "Casal's necklace"), and the exclusive reliance on a **maize staple diet** is highly characteristic of **pellagra**, which is caused by a **niacin (vitamin B3) deficiency**. * Maize contains niacin in a bound form (niacytin) that is largely **unbioavailable** unless treated with alkali (e.g., historical limewater soaking in some cultures). *Pyridoxine* * Deficiency of **pyridoxine (vitamin B6)** can lead to symptoms such as **skin inflammation (seborrheic dermatitis)**, **glossitis**, **cheilosis**, and neurological issues like **peripheral neuropathy** or **seizures**. * It does not typically present with the classic **diarrhea** and **dermatitis** pattern associated with pellagra in the context of a maize-based diet. *Thiamine* * **Thiamine (vitamin B1) deficiency** is associated with **beriberi**, characterized by cardiovascular symptoms (**wet beriberi** with edema and heart failure) or neurological symptoms (**dry beriberi** with neuropathy and muscle wasting). * It does not cause the specific dermatological lesion on the neck or the triad of symptoms (dermatitis, diarrhea, and dementia) seen with niacin deficiency. *Zinc* * **Zinc deficiency** can manifest as **dermatitis (acrodermatitis enteropathica)**, **diarrhea**, **impaired immune function**, and **poor wound healing** or **growth retardation**. * While it can cause skin lesions and diarrhea, the distinct **photosensitive dermatosis** on the neck and the strong association with a maize staple diet specifically point away from zinc deficiency and towards pellagra.
Question 16: In a preterm baby with respiratory distress syndrome, which of the following lipids would be deficient?
- A. Cardiolipin
- B. Sphingomyelin
- C. Phosphatidylinositol
- D. Lecithin (Correct Answer)
Explanation: ***Lecithin*** - **Lecithin** (also known as **phosphatidylcholine**) is the primary component of **surfactant** in the lungs, which reduces surface tension and prevents alveolar collapse. - In **preterm babies**, insufficient production of lecithin due to immature lung development leads to **respiratory distress syndrome (RDS)**. *Cardiolipin* - **Cardiolipin** is a major phospholipid found in the **inner mitochondrial membrane**, crucial for oxidative phosphorylation. - Deficiency is associated with mitochondrial disorders like **Barth syndrome**, not primary respiratory distress. *Sphingomyelin* - **Sphingomyelin** is a significant component of **cell membranes** and **myelin sheaths**, important for nerve insulation. - While present in the lungs, its primary role is not in surface tension reduction, and its deficiency is not directly linked to RDS. *Phosphatidylinositol* - **Phosphatidylinositol** is a precursor for various **signaling molecules** and plays a role in cell membrane structure. - While involved in cellular processes, it is not the critical surfactant component whose deficiency causes RDS.
Question 17: Which of the following is the etiology of Werner syndrome?
- A. Increased length of telomere
- B. Increased advanced glycation end products
- C. Decreased lipid peroxidation
- D. Short telomere with damaged DNA and loss of helicase (Correct Answer)
Explanation: ***Short telomere with damaged DNA and loss of helicase*** - **Werner syndrome** is an **autosomal recessive disorder** characterized by **premature aging** due to mutations in the *WRN* gene, which codes for a **RecQ-type DNA helicase**. - The dysfunctional helicase leads to defects in **DNA replication, repair, and transcription**, resulting in **genomic instability**, **damaged DNA**, and **accelerated telomere attrition** (short telomeres). *Increased length of telomere* - **Increased telomere length** is generally associated with a **reduced rate of cellular aging** and is not characteristic of Werner syndrome or other premature aging disorders. - In most aging processes and syndromes like Werner, **telomeres tend to shorten** over time due to incomplete replication and oxidative stress. *Increased advanced glycation end products* - **Advanced glycation end products (AGEs)** accumulate in various tissues during normal aging and in conditions like diabetes, contributing to vascular and organ damage. - While AGEs play a role in the broader aging process, they are not the primary underlying genetic defect or direct etiology of Werner syndrome, which is a **DNA repair disorder**. *Decreased lipid peroxidation* - **Lipid peroxidation** is a process by which **free radicals** attack lipids, leading to cellular damage and is often associated with oxidative stress and aging. - A **decrease in lipid peroxidation** would generally be considered protective against aging-related damage, which is the opposite of what is seen in Werner syndrome, where there's an accelerated aging phenotype and increased cellular stress.
Question 18: Apolipoprotein B-48 is made by which process?
- A. DNA editing
- B. RNA editing (Correct Answer)
- C. RNA alternate splicing
- D. RNA interference
Explanation: ***RNA editing*** - Apolipoprotein B-48 is synthesized from ApoB-100 mRNA through a process called **RNA editing** (specifically ApoB mRNA editing) - This involves a **cytidine deaminase enzyme (APOBEC-1)** that converts cytidine to uridine at position 6666, changing a glutamine codon (CAA) to a premature stop codon (UAA) in the small intestine - This results in a truncated protein that is 48% the length of ApoB-100 - ApoB-48 is produced in the **intestine**, while ApoB-100 (unedited) is produced in the **liver** *DNA editing* - DNA editing refers to permanent modifications in the DNA sequence itself - The ApoB gene remains unchanged; only the mRNA transcript is edited in intestinal cells - This is not the mechanism for producing ApoB-48 *RNA alternate splicing* - Alternative splicing involves selecting different combinations of exons from pre-mRNA to produce multiple mRNA isoforms - This process creates different protein variants through exon inclusion/exclusion - ApoB-48 production does not involve alternative splicing but rather direct nucleotide modification (C to U) within the coding sequence *RNA interference* - RNA interference (RNAi) is a biological process involving small RNA molecules (siRNA, miRNA) that silence gene expression - RNAi typically degrades mRNA or blocks translation - This process is not involved in generating a truncated protein like ApoB-48 from the same mRNA transcript
Question 19: A child was fed on a staple diet of maize for a long time. Which of the following vitamin may get deficient in his body?
- A. Thiamine (Vitamin B1)
- B. Vitamin B6 (Pyridoxine)
- C. Cobalamin (Vitamin B12)
- D. Niacin (Vitamin B3) (Correct Answer)
Explanation: ***Niacin (Vitamin B3)*** - Maize is deficient in tryptophan (an amino acid that can be converted to **niacin**) and contains niacin in a bound form (**niacytin**) that is not bioavailable. - A staple diet of maize without adequate supplementation can lead to **pellagra**, characterized by the classic triad of dermatitis, diarrhea, and dementia (3 D's). - This is particularly common in populations relying heavily on untreated maize as a staple food. *Thiamine (Vitamin B1)* - While polishing rice can remove thiamine, maize itself is not primarily associated with **thiamine deficiency** as a staple. - **Beriberi** (thiamine deficiency) presents with neurological and cardiovascular symptoms (wet and dry beriberi), distinct from pellagra. *Vitamin B6 (Pyridoxine)* - Deficiency of **pyridoxine** is uncommon with maize-based diets unless there are other contributing factors like drug interactions (e.g., isoniazid). - Symptoms include peripheral neuropathy, seborrheic dermatitis, and sideroblastic anemia, which are not directly linked to a maize staple diet. *Cobalamin (Vitamin B12)* - **Vitamin B12** is found primarily in animal products, so a vegetarian or vegan diet poses a risk for deficiency, not specifically a maize-based diet. - Deficiency leads to megaloblastic anemia and neurological damage (subacute combined degeneration), unrelated to maize's nutritional profile.
Question 20: Which of the following is true about non-competitive inhibition?
- A. Km increases, Vmax remains same
- B. Km decreases, Vmax increases
- C. Km increases, Vmax increases
- D. Km remains same, Vmax decreases (Correct Answer)
Explanation: ***Km remains same, Vmax decreases*** - In **non-competitive inhibition**, the inhibitor binds to an allosteric site on the enzyme, altering its conformation, thereby **reducing its catalytic efficiency**. - This binding does not affect the **enzyme's affinity for the substrate (Km remains the same)**, but it **reduces the maximum reaction rate (Vmax decreases)** because fewer enzyme molecules are able to perform catalysis per unit time. *Km increases, Vmax remains same* - This describes **competitive inhibition**, where the inhibitor competes with the substrate for the enzyme's active site. - While it **increases the apparent Km** (more substrate needed to reach half Vmax), **Vmax remains unchanged** as high substrate concentrations can overcome the inhibition. *Km decreases, Vmax increases* - This scenario would imply an activation rather than inhibition, where both enzyme affinity and catalytic efficiency are enhanced. - This is not characteristic of any standard **enzyme inhibition mechanism**. *Km increases, Vmax increases* - This combination is not observed in any typical **enzyme inhibition pattern**. - An increase in **Vmax** implies enhanced catalytic activity, while an increase in **Km** suggests reduced substrate affinity, which are contradictory effects for a single inhibitor.