NEET-PG 2017 — Biochemistry

Q: A patient reports a change in colour of urine on air exposure. All are true about the condition shown below except:

Urine Benedict's test is negative. ***Urine Benedict's test is negative*** - This is FALSE - Benedict's test is actually **POSITIVE** in alkaptonuria because **homogentisic acid** is a reducing agent. - Homogentisic acid readily **reduces Benedict's reagent**, giving a positive test result in alkaptonuria patients. *Blackening of urine is accelerated on exposure to sunlight* - This is TRUE - **UV light** and sunlight accelerate the **oxidation of homogentisic acid** in urine. - The characteristic **dark discoloration** occurs more rapidly when exposed to light and air. *Alkaptone bodies are deposited in intervertebral disc* - This is TRUE - **Homogentisic acid (alkaptone bodies)** polymerizes to form **ochronotic pigment** deposits. - These deposits accumulate in **cartilage** including intervertebral discs, causing degenerative changes and spondylosis. *The condition is caused by deficiency of homogentisate 1,2-dioxygenase* - This is TRUE - Alkaptonuria is caused by deficiency of **homogentisate 1,2-dioxygenase** enzyme in the **tyrosine metabolic pathway**. - This enzyme deficiency leads to accumulation of **homogentisic acid** in blood and urine, causing the characteristic symptoms. [Practice more Biochemistry PYQs on OnCourse]

Q: All are correct about the amino acid marked as X, EXCEPT:

Ketogenic. ***Correct Answer: Ketogenic*** ✓ - Histidine is **purely glucogenic**, NOT ketogenic - Its carbon skeleton is converted to α-ketoglutarate (a TCA cycle intermediate), which can be used for gluconeogenesis - It does NOT produce acetyl-CoA or acetoacetate (ketone body precursors) - **This statement is FALSE, making it the correct answer for this EXCEPT question** *Incorrect: Maximum buffering action* - This statement is TRUE (so not the answer) - Histidine contains an **imidazole ring** with pKa ~6.0, close to physiological pH - Provides crucial **buffering capacity** in blood and tissues - Most effective amino acid buffer at physiological pH *Incorrect: Contributes to one carbon pool* - This statement is TRUE (so not the answer) - Histidine breakdown produces **Formimino glutamic acid (FIGLU)** - FIGLU donates its formimino group to **Tetrahydrofolate (THF)** - Contributes to the **one-carbon pool** essential for biosynthetic pathways *Incorrect: Excess amount leads to mental retardation* - This statement is TRUE (so not the answer) - **Histidinemia** results from histidase enzyme deficiency - Elevated histidine levels can be associated with **developmental delays and speech defects** in some cases - Though many affected individuals remain asymptomatic [Practice more Biochemistry PYQs on OnCourse]

Q: Name the plot dealing with kinetics of enzyme inhibition?

Dixon plot. ***Dixon plot*** - The **Dixon plot** is specifically used to determine the type of enzyme inhibition and to calculate the **inhibition constant (Ki)**. - It plots the reciprocal reaction velocity (1/V) against the **inhibitor concentration ([I])** at different substrate concentrations. *Donnan-Gibbs equation plot* - The **Donnan-Gibbs equation** describes the distribution of charged particles across a semi-permeable membrane at equilibrium. - It is irrelevant to enzyme kinetics or inhibition. *Lineweaver-Burk plot* - While the Lineweaver-Burk plot is used in enzyme kinetics to determine **Km** and **Vmax** and analyze inhibition, it plots **1/V against 1/[S]**. - The image provided, showing 1/V against [I], is characteristic of a Dixon plot, not a Lineweaver-Burk plot which plots 1/V against 1/[S]. *Hanes-Woolf plot* - The **Hanes-Woolf plot** is another linearization of the Michaelis-Menten equation, plotting **[S]/V against [S]**. - Like the Lineweaver-Burk plot, it is used for analyzing general enzyme kinetics but not specifically for determining Ki from varying inhibitor concentrations in the manner shown. [Practice more Biochemistry PYQs on OnCourse]

Q: Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

17-alpha-hydroxylase. ***17-alpha-hydroxylase*** - The diagram illustrates the synthesis of **vitamin D3**, which involves hydroxylation steps at positions C-25 in the liver and C-1 in the kidneys. These are catalyzed by **25-hydroxylase** and **1-alpha-hydroxylase**, respectively. - **17-alpha-hydroxylase** is involved in the synthesis of steroid hormones (like cortisol, androgens, and estrogens) from cholesterol, not in the synthesis or metabolism of vitamin D3; therefore, its absence would not be relevant to vitamin D synthesis. *3-beta-hydroxylase* - **3-beta-hydroxysteroid dehydrogenase** is crucial for the synthesis of all steroid hormones, converting delta-5-3-hydroxysteroids to delta-4-3-ketosteroids. - Its presence is essential for **steroidogenesis**, but it does not play a direct role in the specific hydroxylation steps for vitamin D activation. *21-hydroxylase* - **21-hydroxylase** is an enzyme involved in the synthesis of steroid hormones such as cortisol and aldosterone from progesterone and 17-hydroxyprogesterone. - Deficiency of this enzyme leads to **congenital adrenal hyperplasia**, a condition unrelated to vitamin D metabolism. *24-hydroxylase* - **24-hydroxylase** is responsible for the inactivation of vitamin D metabolites by adding a hydroxyl group at position C-24, leading to degradation. - This enzyme is part of the **catabolic pathway** to regulate vitamin D levels, rather than being a missing enzyme in the primary synthesis of active vitamin D. [Practice more Biochemistry PYQs on OnCourse]

Q: The following reaction occurs in which part of kidney?

Proximal convoluted tubule. **Proximal convoluted tubule** - The image shows the conversion of 25-hydroxycholecalciferol to **1,25 (OH)₂-D₃**, also known as calcitriol, via the enzyme **1α-hydroxylase**. - This critical hydroxylation reaction, occurring primarily in the **proximal convoluted tubule** cells of the kidney, produces the biologically active form of vitamin D. *Distal convoluted tubule* - The distal convoluted tubule is primarily involved in **fine-tuning** water and electrolyte reabsorption, influenced by hormones like aldosterone and antidiuretic hormone. - It does not contain the necessary enzymes, specifically **1α-hydroxylase**, for the final activation step of vitamin D. *Loop of Henle* - The loop of Henle's main function is to create a **medullary osmotic gradient** through countercurrent multiplication, crucial for concentrating urine. - It plays no significant role in the **hydroxylation of vitamin D** precursors. *Collecting duct* - The collecting duct is responsible for final adjustments to urine volume and concentration, largely under the influence of **antidiuretic hormone**. - It lacks the **enzymatic machinery** (1α-hydroxylase) required for the activation of vitamin D. [Practice more Biochemistry PYQs on OnCourse]

6 Previous Year Questions with Answers & Explanations

Questions

A patient reports a change in colour of urine on air exposure. All are true about the condition shown below except:

All are correct about the amino acid marked as X, EXCEPT:

Name the plot dealing with kinetics of enzyme inhibition?

Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

The following reaction occurs in which part of kidney?

Name the antigen marked as X determining blood group A.

NEET-PG 2017 - Biochemistry NEET-PG Practice Questions and MCQs

Question 1: A patient reports a change in colour of urine on air exposure. All are true about the condition shown below except:

A. Blackening of urine is accelerated on exposure to sunlight
B. Alkaptone bodies are deposited in intervertebral disc
C. Urine Benedict's test is negative (Correct Answer)
D. The condition is caused by deficiency of homogentisate 1,2-dioxygenase

Explanation: ***Urine Benedict's test is negative*** - This is FALSE - Benedict's test is actually **POSITIVE** in alkaptonuria because **homogentisic acid** is a reducing agent. - Homogentisic acid readily **reduces Benedict's reagent**, giving a positive test result in alkaptonuria patients. *Blackening of urine is accelerated on exposure to sunlight* - This is TRUE - **UV light** and sunlight accelerate the **oxidation of homogentisic acid** in urine. - The characteristic **dark discoloration** occurs more rapidly when exposed to light and air. *Alkaptone bodies are deposited in intervertebral disc* - This is TRUE - **Homogentisic acid (alkaptone bodies)** polymerizes to form **ochronotic pigment** deposits. - These deposits accumulate in **cartilage** including intervertebral discs, causing degenerative changes and spondylosis. *The condition is caused by deficiency of homogentisate 1,2-dioxygenase* - This is TRUE - Alkaptonuria is caused by deficiency of **homogentisate 1,2-dioxygenase** enzyme in the **tyrosine metabolic pathway**. - This enzyme deficiency leads to accumulation of **homogentisic acid** in blood and urine, causing the characteristic symptoms.

Question 2: All are correct about the amino acid marked as X, EXCEPT:

A. Maximum buffering action
B. Ketogenic (Correct Answer)
C. Contributes to one carbon pool
D. Excess amount leads to mental retardation

Explanation: ***Correct Answer: Ketogenic*** ✓ - Histidine is **purely glucogenic**, NOT ketogenic - Its carbon skeleton is converted to α-ketoglutarate (a TCA cycle intermediate), which can be used for gluconeogenesis - It does NOT produce acetyl-CoA or acetoacetate (ketone body precursors) - **This statement is FALSE, making it the correct answer for this EXCEPT question** *Incorrect: Maximum buffering action* - This statement is TRUE (so not the answer) - Histidine contains an **imidazole ring** with pKa ~6.0, close to physiological pH - Provides crucial **buffering capacity** in blood and tissues - Most effective amino acid buffer at physiological pH *Incorrect: Contributes to one carbon pool* - This statement is TRUE (so not the answer) - Histidine breakdown produces **Formimino glutamic acid (FIGLU)** - FIGLU donates its formimino group to **Tetrahydrofolate (THF)** - Contributes to the **one-carbon pool** essential for biosynthetic pathways *Incorrect: Excess amount leads to mental retardation* - This statement is TRUE (so not the answer) - **Histidinemia** results from histidase enzyme deficiency - Elevated histidine levels can be associated with **developmental delays and speech defects** in some cases - Though many affected individuals remain asymptomatic

Question 3: Name the plot dealing with kinetics of enzyme inhibition?

A. Donnan-Gibbs equation plot
B. Lineweaver-Burk plot
C. Dixon plot (Correct Answer)
D. Hanes-Woolf plot

Explanation: ***Dixon plot*** - The **Dixon plot** is specifically used to determine the type of enzyme inhibition and to calculate the **inhibition constant (Ki)**. - It plots the reciprocal reaction velocity (1/V) against the **inhibitor concentration ([I])** at different substrate concentrations. *Donnan-Gibbs equation plot* - The **Donnan-Gibbs equation** describes the distribution of charged particles across a semi-permeable membrane at equilibrium. - It is irrelevant to enzyme kinetics or inhibition. *Lineweaver-Burk plot* - While the Lineweaver-Burk plot is used in enzyme kinetics to determine **Km** and **Vmax** and analyze inhibition, it plots **1/V against 1/[S]**. - The image provided, showing 1/V against [I], is characteristic of a Dixon plot, not a Lineweaver-Burk plot which plots 1/V against 1/[S]. *Hanes-Woolf plot* - The **Hanes-Woolf plot** is another linearization of the Michaelis-Menten equation, plotting **[S]/V against [S]**. - Like the Lineweaver-Burk plot, it is used for analyzing general enzyme kinetics but not specifically for determining Ki from varying inhibitor concentrations in the manner shown.

Question 4: Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

A. 3-beta-hydroxylase
B. 17-alpha-hydroxylase (Correct Answer)
C. 21-hydroxylase
D. 24-hydroxylase

Explanation: ***17-alpha-hydroxylase*** - The diagram illustrates the synthesis of **vitamin D3**, which involves hydroxylation steps at positions C-25 in the liver and C-1 in the kidneys. These are catalyzed by **25-hydroxylase** and **1-alpha-hydroxylase**, respectively. - **17-alpha-hydroxylase** is involved in the synthesis of steroid hormones (like cortisol, androgens, and estrogens) from cholesterol, not in the synthesis or metabolism of vitamin D3; therefore, its absence would not be relevant to vitamin D synthesis. *3-beta-hydroxylase* - **3-beta-hydroxysteroid dehydrogenase** is crucial for the synthesis of all steroid hormones, converting delta-5-3-hydroxysteroids to delta-4-3-ketosteroids. - Its presence is essential for **steroidogenesis**, but it does not play a direct role in the specific hydroxylation steps for vitamin D activation. *21-hydroxylase* - **21-hydroxylase** is an enzyme involved in the synthesis of steroid hormones such as cortisol and aldosterone from progesterone and 17-hydroxyprogesterone. - Deficiency of this enzyme leads to **congenital adrenal hyperplasia**, a condition unrelated to vitamin D metabolism. *24-hydroxylase* - **24-hydroxylase** is responsible for the inactivation of vitamin D metabolites by adding a hydroxyl group at position C-24, leading to degradation. - This enzyme is part of the **catabolic pathway** to regulate vitamin D levels, rather than being a missing enzyme in the primary synthesis of active vitamin D.

Question 5: The following reaction occurs in which part of kidney?

A. Proximal convoluted tubule (Correct Answer)
B. Distal convoluted tubule
C. Loop of Henle
D. Collecting duct

Explanation: **Proximal convoluted tubule** - The image shows the conversion of 25-hydroxycholecalciferol to **1,25 (OH)₂-D₃**, also known as calcitriol, via the enzyme **1α-hydroxylase**. - This critical hydroxylation reaction, occurring primarily in the **proximal convoluted tubule** cells of the kidney, produces the biologically active form of vitamin D. *Distal convoluted tubule* - The distal convoluted tubule is primarily involved in **fine-tuning** water and electrolyte reabsorption, influenced by hormones like aldosterone and antidiuretic hormone. - It does not contain the necessary enzymes, specifically **1α-hydroxylase**, for the final activation step of vitamin D. *Loop of Henle* - The loop of Henle's main function is to create a **medullary osmotic gradient** through countercurrent multiplication, crucial for concentrating urine. - It plays no significant role in the **hydroxylation of vitamin D** precursors. *Collecting duct* - The collecting duct is responsible for final adjustments to urine volume and concentration, largely under the influence of **antidiuretic hormone**. - It lacks the **enzymatic machinery** (1α-hydroxylase) required for the activation of vitamin D.

Question 6: Name the antigen marked as X determining blood group A.

A. N-Acetyl-Glucosamine
B. Dermatan sulphate
C. Keratan sulfate
D. N-Acetyl-Galactosamine (Correct Answer)

Explanation: ***N-Acetyl-Galactosamine*** - Blood group A antigens are formed by the addition of **N-acetylgalactosamine** to the H antigen precursor molecule on the surface of red blood cells. - This sugar modification is catalyzed by the **A transferase enzyme**, which is specific for N-acetylgalactosamine. *N-Acetyl-Glucosamine* - While N-acetylglucosamine is a component of many glycans, it is not the terminal sugar that defines the **blood group A antigen**. - **N-acetylglucosamine** is a key building block for the H antigen and other blood group precursors, but not the specific modifying sugar for A. *Dermatan sulphate* - **Dermatan sulfate** is a **glycosaminoglycan** primarily found in connective tissues, skin, and blood vessels. - It plays a role in wound healing and coagulation, but is not involved in **ABO blood group determination**. *Keratan sulfate* - **Keratan sulfate** is another **glycosaminoglycan** found in cartilage, cornea, and bone. - It contributes to tissue hydration and structural integrity, but it is not part of the **ABO blood group antigens**.