Biochemistry
7 questionsGlcNAc-P-P-oligosaccharide is -
Which of the following proteins is primarily responsible for marking other proteins for degradation?
Abnormal proteins which are bound to ubiquitin are degraded in -
Which of the following statements is true regarding the functions of cAMP and cGMP?
Prolyl hydroxylase requires which cofactor?
What type of bond is involved in the side chain linkage of proteoglycans?
Which of the following is not a free radical?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 331: GlcNAc-P-P-oligosaccharide is -
- A. Proteoglycan
- B. Glycoprotein (Correct Answer)
- C. Collagen
- D. Phospholipid
Explanation: ***Glycoprotein*** - **GlcNAc-P-P-oligosaccharide** refers to the **N-linked oligosaccharide precursor** that is synthesized on a **dolichol pyrophosphate** carrier (`-P-P`). This complex is characteristic of the initial stages of **N-linked glycosylation**, a process that forms glycoproteins. - **N-acetylglucosamine (GlcNAc)** is a crucial sugar residue found at the reducing end of this precursor, linking it to the dolichol carrier. *Proteoglycan* - Proteoglycans consist of a **core protein** covalently attached to long, unbranched **glycosaminoglycan (GAG)** chains, such as chondroitin sulfate or heparin. - While they contain sugar units, their structure and synthesis pathway are distinct from the GlcNAc-P-P-oligosaccharide described, which is specific to N-linked glycoprotein synthesis. *Collagen* - **Collagen** is a fibrous protein, primarily composed of a triple helix of polypeptide chains rich in **glycine, proline, and hydroxyproline**. - Although collagen undergoes some post-translational modifications like **glycosylation**, it does not involve the GlcNAc-P-P-oligosaccharide precursor in its typical synthesis. *Phospholipid* - **Phospholipids** are a major component of cell membranes, composed of a **hydrophilic head** (containing a phosphate group) and two **hydrophobic fatty acid tails**. - They are lipids and do not contain carbohydrate structures like GlcNAc-P-P-oligosaccharide.
Question 332: Which of the following proteins is primarily responsible for marking other proteins for degradation?
- A. Ubiquitin (Correct Answer)
- B. RNAse
- C. Zymase
- D. Chaperone
Explanation: **Ubiquitin** - **Ubiquitin** is a small regulatory protein that marks proteins for degradation by targeting them to the **proteasome**. - The ubiquitination process involves a cascade of enzymes (E1, E2, E3) that sequentially attach ubiquitin to the target protein, forming a **polyubiquitin chain**. *RNAse* - **RNAse** (Ribonuclease) is an enzyme that catalyzes the degradation of **RNA into smaller components**. - Its primary function is in **RNA processing** and turnover, not protein degradation. *Zymase* - **Zymase** is a complex of enzymes that catalyzes the **fermentation of sugar into ethanol and carbon dioxide**. - It is commonly found in yeast and is essential for **alcoholic fermentation**, with no role in protein degradation. *Chaperone* - **Chaperone proteins** assist in the **folding of newly synthesized proteins** and the refolding of misfolded or denatured proteins. - Their role is to ensure proper protein structure and function, preventing aggregation, rather than marking proteins for destruction.
Question 333: Abnormal proteins which are bound to ubiquitin are degraded in -
- A. Proteasomes (Correct Answer)
- B. Golgi apparatus
- C. Smooth ER
- D. Lysosomes
Explanation: ***Proteasomes*** - **Proteasomes** are multi-subunit protein complexes responsible for degrading **ubiquitin-tagged proteins**. - This degradation is a tightly regulated process essential for cell cycle control, gene expression, and immune response. *Golgi apparatus* - The **Golgi apparatus** primarily functions in modifying, sorting, and packaging proteins and lipids synthesized in the Endoplasmic Reticulum. - It does not directly participate in the degradation of **ubiquitin-bound proteins**. *Smooth ER* - The **smooth endoplasmic reticulum (SER)** is involved in lipid synthesis, detoxification of drugs and poisons, and storage of calcium ions. - It lacks ribosomes and is not directly implicated in the degradation of misfolded proteins tagged with ubiquitin. *Lysosomes* - **Lysosomes** are organelles containing various hydrolytic enzymes that break down waste materials and cellular debris, as well as foreign invaders like bacteria. - While they degrade proteins, they primarily target **extracellular proteins** taken up by endocytosis or cellular components via **autophagy**, not specifically ubiquitin-bound proteins.
Question 334: Which of the following statements is true regarding the functions of cAMP and cGMP?
- A. All of the above statements are true
- B. They act on membrane receptors.
- C. They are both second messengers. (Correct Answer)
- D. They act by post-translational modification.
Explanation: ***They are both second messengers.*** - **cAMP (cyclic adenosine monophosphate)** and **cGMP (cyclic guanosine monophosphate)** are crucial intracellular signaling molecules. - They relay signals from **first messengers** (like hormones or neurotransmitters) received at the cell surface to intracellular targets, thus acting as second messengers. *They act on membrane receptors.* - **cAMP** and **cGMP** are *produced* in response to activation of **membrane receptors** by first messengers, but they themselves do not act directly on these receptors. - Their action is primarily *intracellular*, binding to and activating various enzymes and proteins like **protein kinases**. *All of the above statements are true* - This statement is incorrect because the claim that they act on membrane receptors is false. - Only one of the statements provided is accurate regarding the functions of cAMP and cGMP. *They act by post-translational modification.* - While cAMP and cGMP can lead to **post-translational modification** (e.g., phosphorylation by protein kinases A and G), they are not themselves the direct modifiers. - They act as **allosteric regulators** of enzymes, which then catalyze the modifications.
Question 335: Prolyl hydroxylase requires which cofactor?
- A. Vitamin C (Correct Answer)
- B. Iron (Fe²⁺)
- C. Molybdenum
- D. Vitamin K1
Explanation: ***Vitamin C*** - **Prolyl hydroxylase** is an enzyme critical for the hydroxylation of proline residues during **collagen synthesis**. - **Vitamin C** (ascorbic acid) acts as an essential **cofactor**, reducing the ferric iron of the enzyme back to its ferrous state after each catalytic cycle, enabling continued activity. - The enzyme requires both **iron (Fe²⁺)** as a metal cofactor and **vitamin C** to maintain the iron in its reduced state. *Iron (Fe²⁺)* - While **iron** is indeed required by prolyl hydroxylase as a **metal cofactor**, the question asks for the cofactor, which specifically refers to **vitamin C**. - Iron functions as part of the enzyme's active site, but vitamin C is the reducing agent that keeps iron functional. - Vitamin C deficiency (scurvy) leads to defective collagen synthesis despite adequate iron. *Molybdenum* - **Molybdenum** is a cofactor for several human enzymes, including **xanthine oxidase** and **sulfite oxidase**. - However, it plays no direct role in the activity of prolyl hydroxylase. *Vitamin K1* - **Vitamin K1** is a crucial cofactor for **gamma-glutamyl carboxylase**, an enzyme involved in the carboxylation of glutamic acid residues in clotting factors. - It is not involved in the hydroxylation of proline by prolyl hydroxylase.
Question 336: What type of bond is involved in the side chain linkage of proteoglycans?
- A. Covalent (Correct Answer)
- B. Hydrogen bond
- C. Electrostatic bond
- D. Van-der Waal's force
Explanation: ***Covalent*** - Proteoglycans are formed by **glycosaminoglycan (GAG)** chains that are covalently linked to a protein core. - Specifically, an **O-glycosidic bond** forms between a xylose residue on the GAG chain and a serine residue on the core protein. *Hydrogen bond* - **Hydrogen bonds** are weaker intermolecular forces that stabilize protein secondary structures and interactions between water molecules. - They are not strong enough to form the primary structural linkage between the GAG chains and the core protein in proteoglycans. *Electrostatic bond* - **Electrostatic bonds**, or ionic bonds, involve attraction between oppositely charged ions. While proteoglycans have many charged groups, these bonds are not the primary linkage connecting the GAG chains to the protein core. - They contribute to the overall structure and interactions of proteoglycans with other molecules but do not form the main side chain linkage. *Van-der Waal's force* - **Van der Waals forces** are weak, short-range intermolecular forces that arise from temporary fluctuations in electron distribution. - These forces play a role in tertiary and quaternary protein structure and molecular packing, but they are far too weak to establish the covalent attachments of GAG chains to the proteoglycan core protein.
Question 337: Which of the following is not a free radical?
- A. Superoxide anion
- B. Hydrogen peroxide (H2O2) (Correct Answer)
- C. Nitric oxide (NO·)
- D. Hydroxyl radical (.OH)
Explanation: ***Hydrogen peroxide (H₂O₂)*** - **Hydrogen peroxide** is a **reactive oxygen species (ROS)** but is not a free radical because it has **no unpaired electrons** in its outermost shell. - While it can be converted into the highly reactive hydroxyl radical via the **Fenton reaction**, it is stable enough to be transported across membranes. *Superoxide anion (O₂⁻)* - The **superoxide anion (O₂⁻)** is a free radical because it has an **unpaired electron** in its outer shell. - It is one of the primary **reactive oxygen species** formed during cellular metabolism and can damage cellular components. *Nitric oxide (NO·)* - **Nitric oxide** is an important **free radical** with a single **unpaired electron** in its molecular structure. - It functions as a vital signaling molecule in vascular biology, regulating blood pressure and neurotransmission, despite being a free radical. *Hydroxyl radical (·OH)* - The **hydroxyl radical (·OH)** is one of the most reactive and damaging **free radicals** in biological systems. - It has a single **unpaired electron**, making it highly unstable and able to react indiscriminately with virtually all types of biomolecules.
Physiology
3 questionsWhat is the normal transpulmonary pressure during quiet breathing?
Damage to pneumotaxic center along with vagus nerve causes which type of respiration?
What is the total surface area of the respiratory membrane in a healthy adult human?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 331: What is the normal transpulmonary pressure during quiet breathing?
- A. 0 to + 1 cm H2O
- B. 0 to -1 cm H2O
- C. +5 to +8 cm H2O (Correct Answer)
- D. - 8 to - 5 cm H2O
Explanation: ***+5 to +8 cm H2O*** - Transpulmonary pressure (P_tp) is the **difference between alveolar pressure and pleural pressure** (P_alv - P_pl). - During quiet breathing at **functional residual capacity (FRC)**, alveolar pressure is **0 cm H2O** (atmospheric) while pleural pressure is approximately **-5 cm H2O**, giving P_tp = **+5 cm H2O**. - At end-inspiration during quiet breathing, pleural pressure becomes more negative (**-8 cm H2O**) while alveolar pressure remains near atmospheric, resulting in P_tp ≈ **+8 cm H2O**. - This positive transpulmonary pressure gradient is essential to **keep the lungs inflated** against elastic recoil and prevent **atelectasis**. *0 to +1 cm H2O* - This pressure is far too low to maintain lung inflation against elastic recoil forces. - Normal transpulmonary pressure must be several cm H2O positive to counterbalance the lung's tendency to collapse. - This value would result in **near-complete lung collapse**. *0 to -1 cm H2O* - A negative or zero transpulmonary pressure would mean pleural pressure equals or exceeds alveolar pressure. - This condition would cause **immediate lung collapse (pneumothorax)** as there would be no pressure gradient to keep the lungs expanded. *-8 to -5 cm H2O* - This range represents **pleural pressure**, not transpulmonary pressure. - Pleural pressure is indeed -5 to -8 cm H2O during quiet breathing, but transpulmonary pressure is calculated as the difference between alveolar and pleural pressures. - Confusing pleural pressure with transpulmonary pressure is a common error.
Question 332: Damage to pneumotaxic center along with vagus nerve causes which type of respiration?
- A. Cheyne-Stokes breathing
- B. Deep and slow breathing
- C. Shallow and rapid breathing
- D. Apneustic breathing (Correct Answer)
Explanation: ***Apneustic breathing*** - Damage to the **pneumotaxic center** prevents the normal inhibition of inspiration, leading to **prolonged inspiratory gasps**. - **Vagal nerve damage** further removes the inhibitory feedback from the lungs, exacerbating the inspiratory "holds" characteristic of apneustic breathing. *Cheyne-Stokes breathing* - This pattern is characterized by a **crescendo-decrescendo pattern** of breathing, interspersed with periods of **apnea**. - It is often associated with conditions like **heart failure**, stroke, or severe neurological damage, not specifically the pneumotaxic center and vagus nerve. *Deep and slow breathing* - This pattern can be seen in conditions like **Kussmaul breathing** (due to metabolic acidosis) or as a compensatory mechanism. - It does not directly result from the combined damage of the **pneumotaxic center** and the **vagus nerve**. *Shallow and rapid breathing* - This pattern is commonly seen in restrictive lung diseases, anxiety, or pain, where tidal volume is decreased and respiratory rate increased. - It does not reflect the **prolonged inspiration** that would result from a compromised pneumotaxic center and vagal input.
Question 333: What is the total surface area of the respiratory membrane in a healthy adult human?
- A. 30 m2
- B. 50 m2
- C. 75 m2 (Correct Answer)
- D. 100 m2
Explanation: ***75 m²*** - The **total surface area** of the respiratory membrane in a healthy adult human is approximately **70-80 m²**, with 75 m² being the most accurate estimate among the given options. - This large surface area is primarily attributed to the presence of approximately **300-500 million alveoli**, which are crucial for efficient gas exchange. - Modern measurements using **stereological techniques** have refined earlier estimates and established this range as the current standard. *100 m²* - This value represents an **older estimate** that has been revised downward with more accurate measurement techniques. - While historically cited in older textbooks, current physiological data supports a **smaller surface area** of approximately 70-80 m². *30 m²* - This value is significantly **underestimated** for the total respiratory membrane surface area. - Such a small surface area would result in highly **inefficient gas exchange**, leading to severe respiratory compromise and inability to meet metabolic demands. *50 m²* - While larger than 30 m², this is still an **underestimation** of the full respiratory membrane surface area. - It does not adequately account for the extensive and intricate branching of the **respiratory bronchioles** and the vast number of alveolar sacs.