Why is oxidized LDL considered more atherogenic?
Which of the following enzymes is not involved in the urea cycle?
Urea & Kreb's cycle are linked at?
Which will activate carbamoyl phosphate synthase I?
Ochronosis is due to accumulation of ?
Organ that can utilize glucose, fatty acids and ketone bodies is:
Which of the following is not the source of cytosolic NADPH ?
Which amino acid requires ascorbic acid for its formation in the body?
What cofactor is required for the proper functioning of glucose-6-phosphate dehydrogenase?
Which of the following micronutrient deficiencies can lead to anemia?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 71: Why is oxidized LDL considered more atherogenic?
- A. Is not recognized by LDL receptors
- B. Is taken up by scavenger receptors (Correct Answer)
- C. Promotes inflammation in arterial walls
- D. Accumulates in macrophages
Explanation: ***Is taken up by scavenger receptors*** - **Oxidized LDL (oxLDL)** is taken up by **scavenger receptors (CD36, SR-A)** on macrophages, which have **no feedback regulation**. - Unlike native LDL receptors that downregulate when cells have sufficient cholesterol, **scavenger receptors continue unlimited uptake**, leading to foam cell formation. - This **unregulated uptake mechanism** is the key reason why oxLDL is **more atherogenic** than native LDL. - The result is lipid-laden macrophages forming **fatty streaks**, the initial lesions of **atherosclerosis**. *Is not recognized by LDL receptors* - While true that oxLDL has **reduced affinity** for native LDL receptors due to oxidative modification, this alone doesn't explain increased atherogenicity. - The critical factor is what happens instead—its uptake via an **alternative, unregulated pathway**. *Accumulates in macrophages* - This is a **consequence** of scavenger receptor uptake, not the primary mechanism. - Foam cell formation occurs **because** of unregulated scavenger receptor uptake, making this a downstream effect. *Promotes inflammation in arterial walls* - OxLDL does promote inflammation through multiple mechanisms (cytokine release, endothelial dysfunction). - However, this is a **secondary effect** that occurs after uptake and accumulation—not the primary reason for atherogenicity.
Question 72: Which of the following enzymes is not involved in the urea cycle?
- A. Arginase
- B. Argininosuccinate lyase
- C. CPS-II (Correct Answer)
- D. CPS-I
Explanation: ***CPS-II*** - Carbamoyl phosphate synthetase II is involved in **pyrimidine synthesis**, not the urea cycle. - It uses **glutamine** as a nitrogen donor and is located in the **cytosol**. *CPS-I* - Carbamoyl phosphate synthetase I is the **rate-limiting enzyme** of the urea cycle. - It catalyzes the formation of **carbamoyl phosphate** from **ammonia**, CO2, and ATP in the mitochondria. *Arginase* - Arginase is the **final enzyme** in the urea cycle, converting **arginine** to **ornithine** and **urea**. - This reaction occurs in the cytosol and releases urea for excretion. *Argininosuccinate lyase* - Argininosuccinate lyase catalyzes the cleavage of **argininosuccinate** into **fumarate** and **arginine**. - This is a key step in regenerating arginine for the final step of the urea cycle.
Question 73: Urea & Kreb's cycle are linked at?
- A. Arginine
- B. Ornithine
- C. Oxaloacetate
- D. Fumarate (Correct Answer)
Explanation: ***Fumarate*** - **Fumarate** is a key intermediate produced during the **urea cycle** when argininosuccinate is cleaved into arginine and fumarate. - This fumarate then enters the **Krebs cycle** (citric acid cycle) as an intermediate to be converted into malate and then oxaloacetate, thus linking the two cycles. *Arginine* - **Arginine** is an amino acid that participates in the urea cycle, serving as a precursor for the formation of urea. - While arginine is a part of the urea cycle, it does not directly enter the Krebs cycle or serve as its linking metabolite. *Ornithine* - **Ornithine** is another amino acid central to the urea cycle, being regenerated at the end of the cycle to combine with carbamoyl phosphate. - It is a carrier molecule for the nitrogen atoms, but it does not directly link to the Krebs cycle. *Oxaloacetate* - **Oxaloacetate** is a central intermediate in the Krebs cycle, and it can be a precursor for intermediates in the urea cycle (e.g., through aspartate). - However, it is not the direct molecule that links the two cycles in the direction of the urea cycle feeding into the Krebs cycle.
Question 74: Which will activate carbamoyl phosphate synthase I?
- A. N-acetyl glutamate (Correct Answer)
- B. ATP
- C. Acetyl-CoA
- D. Ornithine
Explanation: **N-acetyl glutamate** - **N-acetyl glutamate** is an **allosteric activator** of **carbamoyl phosphate synthase I (CPS I)**, which is the mitochondrial enzyme that catalyzes the first committed step of the **urea cycle**. - Its synthesis is stimulated by high levels of **arginine**, linking nitrogen load to urea production. *Acetyl-CoA* - Acetyl-CoA is a common **substrate** and **product** in various metabolic pathways, but it is not a direct activator of CPS I. - It is a precursor for the synthesis of **N-acetyl glutamate**, but does not activate CPS I directly. *Ornithine* - **Ornithine** is a key intermediate of the **urea cycle**, but it does not directly activate CPS I. - It combines with carbamoyl phosphate (the product of CPS I) in the second step of the urea cycle to form citrulline. *ATP* - **ATP** is a **substrate** used by CPS I to provide energy for the synthesis of carbamoyl phosphate. - While essential for the reaction, ATP itself does not act as an allosteric activator of the enzyme.
Question 75: Ochronosis is due to accumulation of ?
- A. Homogentisic acid (Correct Answer)
- B. Phenylpyruvate
- C. Xanthurenate
- D. Glyoxylate
Explanation: ***Homogentisic acid*** - Ochronosis is a condition caused by the excessive accumulation of **homogentisic acid** in connective tissues. - This accumulation occurs due to a deficiency of the enzyme **homogentisate 1,2-dioxygenase** (HGD), which is responsible for breaking down homogentisic acid in the tyrosine degradation pathway. *Phenylpyruvate* - **Phenylpyruvate** accumulates in **phenylketonuria (PKU)**, a different metabolic disorder where there's a deficiency in phenylalanine hydroxylase. - PKU leads to intellectual disability and other neurological problems, not the characteristic pigmentation and arthritis of ochronosis. *Xanthurenate* - **Xanthurenate** is an abnormal metabolite of tryptophan metabolism that can accumulate in **vitamin B6 deficiency**. - Its accumulation is associated with increased urinary excretion and is not directly implicated in the pathology of ochronosis. *Glyoxylate* - **Glyoxylate** is involved in various metabolic pathways, and its accumulation (or accumulation of its metabolic products like oxalate) is associated with **primary hyperoxaluria**. - Primary hyperoxaluria leads to kidney stones and kidney failure, a condition distinct from ochronosis.
Question 76: Organ that can utilize glucose, fatty acids and ketone bodies is:
- A. Liver
- B. Brain
- C. Skeletal muscle (Correct Answer)
- D. RBC
Explanation: ***Skeletal muscle*** - Skeletal muscle is highly adaptable and can utilize **glucose**, **fatty acids (FAs)**, and **ketone bodies** as fuel sources, especially during prolonged exercise or starvation. - Its metabolic flexibility allows it to switch between these substrates depending on their availability and the body's energy demands. *Liver* - The liver is central to metabolism but primarily **produces ketone bodies** from fatty acids rather than utilizing them as a major fuel source for its own energy needs. - While it uses glucose and FAs, its role in ketone body metabolism is largely synthetic. *Brain* - The brain preferentially uses **glucose** as its primary fuel. - During prolonged starvation, it can adapt to utilize **ketone bodies** as an alternative fuel source, but it does not significantly use fatty acids directly. *RBC* - Red blood cells (RBCs) lack mitochondria and therefore rely exclusively on **anaerobic glycolysis** for energy, metabolizing only **glucose**. - They cannot utilize fatty acids or ketone bodies.
Question 77: Which of the following is not the source of cytosolic NADPH ?
- A. Malic enzyme
- B. G6PD
- C. Isocitrate dehydrogenase
- D. ATP citrate lyase (Correct Answer)
Explanation: ***ATP citrate lyase*** - **ATP citrate lyase** is an enzyme involved in the synthesis of **acetyl-CoA** from citrate in the cytosol, which is then used for **fatty acid synthesis**. It does not generate NADPH. - While the **acetyl-CoA** produced is used in pathways that require NADPH, ATP citrate lyase itself does not directly produce NADPH. *Isocitrate dehydrogenase* - Cytosolic **isocitrate dehydrogenase** catalyzes the oxidative decarboxylation of **isocitrate** to alpha-ketoglutarate, producing **NADPH**. - This reaction is an important source of **cytosolic NADPH**, especially in non-photosynthetic tissues. *Malic enzyme* - **Malic enzyme** catalyzes the oxidative decarboxylation of **malate** to pyruvate, simultaneously reducing **NADP+ to NADPH**. - This enzyme is a significant source of **cytosolic NADPH** in various tissues, contributing to fatty acid synthesis and other reductive processes. *G6PD* - **Glucose-6-phosphate dehydrogenase (G6PD)** is the rate-limiting enzyme in the **pentose phosphate pathway** (PPP). - It catalyzes the first step of the PPP, converting **glucose-6-phosphate** to 6-phosphogluconolactone and producing **NADPH** as a crucial coenzyme.
Question 78: Which amino acid requires ascorbic acid for its formation in the body?
- A. Lysine
- B. Hydroxyproline (Correct Answer)
- C. Cysteine
- D. Proline
Explanation: ***Hydroxyproline*** - **Ascorbic acid (Vitamin C)** is an essential cofactor for **prolyl hydroxylase** and **lysyl hydroxylase** enzymes - These enzymes catalyze the **post-translational hydroxylation** of proline and lysine residues within collagen chains to form hydroxyproline and hydroxylysine - This hydroxylation is crucial for **stabilization of the collagen triple helix** structure - Hydroxyproline is formed by **modification of proline after incorporation into collagen**, not as a free amino acid - **Scurvy** (Vitamin C deficiency) results in defective collagen due to inadequate hydroxyproline formation *Lysine* - Lysine is an **essential amino acid** obtained from diet - Does not require ascorbic acid for its synthesis or formation - While lysine residues in collagen can be hydroxylated (forming hydroxylysine), the question asks about the amino acid whose formation requires Vitamin C *Cysteine* - Cysteine is a **sulfur-containing amino acid** synthesized from methionine via transsulfuration pathway - Its synthesis does not involve ascorbic acid *Proline* - Proline is a **non-essential amino acid** synthesized from glutamate - **Proline synthesis does not require ascorbic acid** - Proline serves as the precursor that gets hydroxylated to hydroxyproline within collagen
Question 79: What cofactor is required for the proper functioning of glucose-6-phosphate dehydrogenase?
- A. NAD
- B. NADP (Correct Answer)
- C. FAD
- D. FMN
Explanation: ***NADP*** - **NADP+** (nicotinamide adenine dinucleotide phosphate) acts as the **electron acceptor** in the **glucose-6-phosphate dehydrogenase (G6PD)** reaction, becoming **NADPH**. - **NADPH** is crucial for maintaining the **redox balance** in cells, particularly in red blood cells, by reducing **oxidative stress**. *NAD* - **NAD+** (nicotinamide adenine dinucleotide) is a primary cofactor for many **dehydrogenase reactions** in catabolic pathways like **glycolysis** and the **Krebs cycle**. - It primarily functions as an electron acceptor in pathways that generate **ATP**, distinct from the role of **NADPH** in reductive biosynthesis and antioxidant defense. *FAD* - **FAD** (flavin adenine dinucleotide) is a coenzyme derived from **riboflavin (vitamin B2)** that is involved in various redox reactions, often in the form of **flavoproteins**. - Enzymes like **succinate dehydrogenase** in the electron transport chain utilize **FAD** as an electron acceptor, which is not the case for G6PD. *FMN* - **FMN** (flavin mononucleotide) is another coenzyme derived from **riboflavin**, structurally similar to FAD but lacking the additional adenosine monophosphate. - It participates in electron transfer reactions, particularly within **complex I** of the **electron transport chain**, but is not a cofactor for G6PD.
Question 80: Which of the following micronutrient deficiencies can lead to anemia?
- A. Molybdenum
- B. Copper (Correct Answer)
- C. Fluorine
- D. Selenium
Explanation: ***Copper*** - **Copper** is essential for **iron metabolism** and red blood cell formation; its deficiency can lead to **sideroblastic anemia** (often with microcytic or normocytic features) that may be accompanied by neutropenia. - Copper is required for **ceruloplasmin** function, which is necessary for iron mobilization from stores and incorporation into hemoglobin. - It also plays a role in the function of **superoxide dismutase** and **cytochrome c oxidase**, enzymes involved in antioxidant defense and energy production. *Molybdenum* - **Molybdenum** is a cofactor for several enzymes, including **xanthine oxidase** and **sulfite oxidase**, crucial for purine metabolism and detoxification. - While essential, its deficiency does not typically lead to **anemia** in humans. *Selenium* - **Selenium** is a component of selenoproteins, such as **glutathione peroxidase**, which protect cells from oxidative damage. - Deficiency is associated with conditions like **Keshan disease** (cardiomyopathy) but not primary anemia. *Fluorine* - **Fluorine** (as fluoride) is primarily known for its role in **bone and tooth mineralization**, protecting against dental caries. - It does not directly participate in **hematopoiesis** or iron metabolism, and its deficiency is not linked to anemia.