Cellular Physiology — MCQs

Cellular Physiology Indian Medical PG Practice Questions and MCQs

Question 151: Which of the following is not a phase in Meiosis?

A. Prophase
B. Telophase
C. Dyskinesis (Correct Answer)
D. Diakinesis

Explanation: **Explanation:** The correct answer is **Dyskinesis** because it is a clinical term referring to abnormal, involuntary movements (often associated with basal ganglia disorders or side effects of antipsychotic medications), rather than a stage of cell division. **Understanding the Phases of Meiosis:** Meiosis is a specialized form of cell division that reduces the chromosome number by half. It consists of two successive divisions: Meiosis I and Meiosis II. * **Prophase (Option A):** This is the longest and most complex phase. In Meiosis I, it is further divided into five sub-stages: Leptotene, Zygotene, Pachytene, Diplotene, and **Diakinesis**. * **Diakinesis (Option D):** This is the final stage of Prophase I. It is characterized by the terminalization of chiasmata, disappearance of the nucleolus, and breakdown of the nuclear envelope. It marks the transition into Metaphase I. * **Telophase (Option B):** This is the final stage of nuclear division where chromosomes reach opposite poles, the nuclear membrane reforms, and the cell prepares for cytokinesis. **High-Yield NEET-PG Pearls:** 1. **Pachytene:** The most high-yield sub-stage of Prophase I; this is where **crossing over** (genetic recombination) occurs via the enzyme **recombinase**. 2. **Zygotene:** Characterized by **synapsis** (pairing of homologous chromosomes) and the formation of the synaptonemal complex. 3. **Diplotene:** This is where the synaptonemal complex dissolves, and **chiasmata** become visible. In females, primary oocytes are arrested in this stage (specifically the Dictyotene stage) from birth until ovulation. 4. **Dyskinesis vs. Diakinesis:** Do not confuse these phonetically similar terms. Dyskinesis (e.g., Tardive Dyskinesis) is a neurological symptom, not a biological process of division.

Question 152: Which are the most common cells to exhibit ameboid locomotion in the human body?

A. RBC
B. WBC (Correct Answer)
C. Platelets
D. None of the above

Explanation: **Explanation:** **Ameboid locomotion** is a type of crawling-like movement characterized by the protrusion of **pseudopodia** (false feet). This process involves the continuous rearrangement of the actin cytoskeleton, where actin polymerization at the leading edge pushes the cell membrane forward. **Why WBCs are the correct answer:** White Blood Cells (WBCs), particularly **neutrophils and macrophages**, are the primary cells in the human body that utilize ameboid movement. This mechanism is essential for **chemotaxis**—the movement of cells toward a chemical stimulus (such as bacterial toxins or inflammatory cytokines). It allows WBCs to undergo **diapedesis** (squeezing through capillary walls) to reach the site of infection or tissue injury in the extravascular space. **Analysis of Incorrect Options:** * **A. RBCs:** Red Blood Cells are passive travelers within the circulatory system. They lack a nucleus and the complex cytoskeletal machinery required for independent locomotion. Their primary structural feature is flexibility (deformability) to pass through narrow capillaries, not active movement. * **C. Platelets:** While platelets can change shape and extend "filopodia" during activation and clot retraction, they do not exhibit true ameboid locomotion to migrate through tissues like WBCs. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Ameboid movement depends on **ATP**, **calcium ions**, and the interaction between **actin and myosin** filaments. * **Other cells:** Apart from WBCs, **fibroblasts** (during wound healing) and **embryonic cells** (during morphogenesis) also exhibit ameboid-like movement. * **Clinical Correlation:** Deficiencies in leukocyte adhesion or cytoskeletal remodeling (e.g., **LAD - Leukocyte Adhesion Deficiency**) result in impaired ameboid movement, leading to recurrent infections.

Question 153: A muscle cell has an intracellular sodium concentration of 14 mM and an extracellular sodium concentration of 140 mM. Assuming that 2.3 RT/F = 60 mV, what would the membrane potential be if the muscle cell membrane were permeable only to Na+?

A. +80 mV
B. -60 mV
C. -80 mV
D. +60 mV (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right (The Nernst Equation)** The question asks for the equilibrium potential of sodium ($E_{Na}$), which is the membrane potential at which there is no net movement of sodium ions across the membrane. This is calculated using the **Nernst Equation**: $$E = \frac{2.3 RT}{zF} \times \log_{10} \frac{[\text{Ion}]_{\text{outside}}}{[\text{Ion}]_{\text{inside}}}$$ Given: * $2.3 RT/F = 60\text{ mV}$ * $z$ (valence of $Na^+$) = $+1$ * $[Na^+]_{\text{extracellular}} = 140\text{ mM}$ * $[Na^+]_{\text{intracellular}} = 14\text{ mM}$ Calculation: $$E_{Na} = 60 \times \log_{10} (140 / 14)$$ $$E_{Na} = 60 \times \log_{10} (10)$$ Since $\log_{10}(10) = 1$, the result is **$+60\text{ mV}$**. Because sodium is a cation moving from a higher concentration (outside) to a lower concentration (inside), it carries a positive charge into the cell, making the interior positive relative to the exterior. **2. Why the Incorrect Options are Wrong** * **Option A (+80 mV):** This value would require a concentration gradient of 100:1 (e.g., 140 mM outside vs 1.4 mM inside). * **Option B (-60 mV):** This is the correct magnitude but the wrong polarity. A negative potential would occur if the ion were an anion (like $Cl^-$) or if the concentration gradient were reversed. * **Option C (-80 mV):** This is close to the equilibrium potential for Potassium ($E_K \approx -90\text{ mV}$), where the concentration is higher inside the cell. **3. High-Yield Facts for NEET-PG** * **Resting Membrane Potential (RMP):** In most neurons, RMP is $\approx -70\text{ to } -90\text{ mV}$ because the membrane is far more permeable to $K^+$ than $Na^+$ at rest. * **Goldman-Hodgkin-Katz (GHK) Equation:** Unlike the Nernst equation (one ion), the GHK equation considers the permeability and concentration of all major ions ($Na^+$, $K^+$, $Cl^-$) to determine the actual RMP. * **Action Potential:** During the depolarization phase, the membrane potential moves toward $E_{Na}$ (+60 mV) but usually peaks at +35 to +40 mV because $Na^+$ channels inactivate quickly.

Question 154: Which cellular component is responsible for protein synthesis?

A. Smooth endoplasmic reticulum
B. Rough endoplasmic reticulum
C. Ribosomes (Correct Answer)
D. Mitochondria

Explanation: **Explanation:** **Correct Answer: C. Ribosomes** Ribosomes are the primary sites of **protein synthesis** (translation) in the cell. They are composed of ribosomal RNA (rRNA) and proteins. Their function is to translate the genetic code from messenger RNA (mRNA) into a specific sequence of amino acids to form polypeptide chains. **Analysis of Options:** * **A. Smooth Endoplasmic Reticulum (SER):** The SER is primarily involved in **lipid synthesis**, steroid hormone production (e.g., in the adrenals and gonads), and detoxification of drugs (via Cytochrome P450 enzymes). It lacks ribosomes on its surface. * **B. Rough Endoplasmic Reticulum (RER):** While the RER is heavily involved in protein synthesis, it is the **ribosomes attached to its surface** that perform the actual synthesis. The RER itself functions in the folding, modification, and transport of proteins destined for secretion or membrane insertion. * **D. Mitochondria:** Known as the "powerhouse of the cell," mitochondria are responsible for **ATP production** via oxidative phosphorylation. While they contain their own mDNA and specialized ribosomes (mitoribosomes), their primary global cellular role is energy metabolism. **High-Yield NEET-PG Pearls:** * **Ribosomal Subunits:** Eukaryotic ribosomes are **80S** (composed of 40S and 60S subunits), whereas prokaryotic and mitochondrial ribosomes are **70S** (30S and 50S). * **Antibiotic Target:** Many antibiotics (e.g., Aminoglycosides, Tetracyclines, Macrolides) work by selectively inhibiting bacterial 70S ribosomes. * **Free vs. Bound Ribosomes:** Free ribosomes synthesize proteins for internal cellular use (e.g., hemoglobin, enzymes), while RER-bound ribosomes synthesize proteins for secretion or lysosomes.

Question 155: What are residual bodies?

A. Mitochondria
B. Nucleus
C. Golgi apparatus
D. Lysosomes (Correct Answer)

Explanation: **Explanation:** **Residual bodies** are the final stage of the lysosomal digestive process. When lysosomes (specifically secondary lysosomes or phagolysosomes) break down cellular debris or foreign material via hydrolytic enzymes, some substances remain undigested. These membrane-bound vesicles containing undigested debris are termed **residual bodies**. In most cells, these are eliminated via exocytosis; however, in long-lived cells like neurons and cardiac muscles, they persist as **lipofuscin granules** (the "wear-and-tear" pigment). **Why other options are incorrect:** * **Mitochondria (A):** These are the "powerhouses" of the cell, primarily involved in ATP production through oxidative phosphorylation, not waste storage or digestion. * **Nucleus (B):** This is the genetic control center containing DNA. It does not participate in the cytoplasmic degradation of macromolecules. * **Golgi Apparatus (C):** This organelle is responsible for modifying, sorting, and packaging proteins. While it produces the primary lysosomes, it does not function as a residual body itself. **NEET-PG High-Yield Pearls:** * **Lipofuscin:** A brown-yellow pigment found in the residual bodies of aging cells. It is a hallmark of lipid peroxidation and cellular aging. * **Primary Lysosome:** A newly formed vesicle from the Golgi containing inactive enzymes. * **Secondary Lysosome:** Formed by the fusion of a primary lysosome with a phagosome/endosome; this is where active digestion occurs. * **Autophagy:** The process where lysosomes digest the cell's own damaged organelles, a critical mechanism during starvation and cellular remodeling.

Question 156: What is the mechanism of secretion of macromolecules by a cell through fusion with a vesicle?

A. Phagocytosis (Correct Answer)
B. Pinocytosis
C. Exocytosis
D. Endocytosis

Explanation: ### Explanation The correct mechanism for the secretion of macromolecules through vesicle fusion is **Exocytosis**. *(Note: There appears to be a discrepancy in the provided key; while Phagocytosis involves vesicles, it is an ingestive process. Exocytosis is the specific mechanism for secretion/export.)* #### 1. Why Exocytosis is the Correct Mechanism **Exocytosis** is the process by which a cell directs the contents of secretory vesicles out of the cell membrane. These membrane-bound vesicles move to the cell surface, fuse with the plasma membrane, and release their macromolecular contents (such as hormones, enzymes, or neurotransmitters) into the extracellular space. This process is often triggered by an increase in intracellular calcium ($Ca^{2+}$). #### 2. Analysis of Incorrect Options * **Phagocytosis (Option A):** Known as "cell eating," this is a form of **endocytosis** where the cell engulfs large solid particles (e.g., bacteria) into an internal vesicle called a phagosome. It is an intake mechanism, not a secretory one. * **Pinocytosis (Option B):** Known as "cell drinking," this involves the non-specific intake of extracellular fluid and small solutes via small vesicles. * **Endocytosis (Option D):** This is a general term for the transport of macromolecules **into** the cell. It encompasses phagocytosis, pinocytosis, and receptor-mediated endocytosis. #### 3. NEET-PG High-Yield Pearls * **SNARE Proteins:** The fusion of the vesicle with the plasma membrane is mediated by **v-SNAREs** (on the vesicle) and **t-SNAREs** (on the target membrane). * **Clathrin-Coated Pits:** Essential for receptor-mediated endocytosis (e.g., LDL cholesterol uptake). * **Transcytosis:** A combination of endocytosis and exocytosis used to move macromolecules across an entire cell layer (e.g., IgA secretion into breast milk). * **ATP Dependency:** All forms of vesicular transport (Exo/Endocytosis) are **active processes** requiring energy.

Question 157: Who proposed the fluid mosaic model of membrane structure?

A. Singer and Nicolson (Correct Answer)
B. Danielli
C. Overton
D. Gorter

Explanation: **Explanation:** The **Fluid Mosaic Model**, proposed by **S.J. Singer and Garth L. Nicolson in 1972**, is the currently accepted model of the cell membrane. It describes the membrane as a "quaternary structure" where proteins are embedded like a mosaic in a fluid lipid bilayer. The "fluidity" is provided by the lateral movement of lipids and proteins, while the "mosaic" refers to the diverse arrangement of integral and peripheral proteins. **Analysis of Options:** * **Singer and Nicolson (Correct):** They revolutionized cell biology by proving that the membrane is a dynamic, semi-fluid structure rather than a static, solid layer. * **Danielli (and Davson):** Proposed the **"Sandwich Model"** (1935), suggesting a lipid bilayer coated on both sides by a layer of globular proteins. This model failed to explain the transmembrane nature of many proteins. * **Overton:** Known for **Overton’s Rule** (1890s); he observed that lipid-soluble substances enter cells more rapidly, concluding that the membrane is composed of lipids. * **Gorter (and Grendel):** In 1925, they correctly deduced that the cell membrane is a **lipid bilayer** by measuring the surface area of lipids extracted from red blood cells. **High-Yield Clinical Pearls for NEET-PG:** * **Membrane Fluidity:** Regulated by **cholesterol** (acts as a temperature buffer) and the ratio of saturated to unsaturated fatty acids. * **Asymmetry:** The membrane is asymmetrical; **glycolipids and glycoproteins** are always found on the outer leaflet (extracellular side). * **Flippases/Floppases:** These enzymes maintain membrane asymmetry by moving phospholipids between the inner and outer leaflets (an ATP-dependent process). * **Lipid Rafts:** Specialized microdomains rich in cholesterol and sphingolipids involved in cell signaling.

Question 158: Sorting of protein molecules is performed in?

A. Mitochondria
B. Golgi apparatus (Correct Answer)
C. Nucleosome
D. Endosome

Explanation: **Explanation:** The **Golgi apparatus** is often referred to as the "Post Office" or "Shipping Center" of the cell. Its primary function is the post-translational modification, packaging, and **sorting of proteins** received from the Rough Endoplasmic Reticulum (RER). Proteins are tagged with specific signals (like Mannose-6-Phosphate) in the Golgi, which determines their final destination: secretion, the plasma membrane, or lysosomes. **Analysis of Options:** * **Mitochondria (A):** Known as the "Powerhouse" of the cell, its primary role is ATP production via oxidative phosphorylation. While it contains its own DNA and ribosomes, it is not a sorting hub for cellular proteins. * **Nucleosome (C):** This is a structural unit of eukaryotic chromosomes consisting of DNA coiled around histone proteins. It is involved in DNA packaging, not protein sorting. * **Endosome (D):** These are membrane-bound vesicles involved in endocytosis. They act as sorting stations for internalized material (recycling back to the membrane or sending to lysosomes), but they do not perform the primary sorting of newly synthesized proteins. **High-Yield NEET-PG Pearls:** * **Cis-Golgi:** Receives vesicles from the RER. * **Trans-Golgi Network (TGN):** The actual site where sorting and exit occur. * **I-Cell Disease:** A clinical correlation where a deficiency in the enzyme N-acetylglucosaminyl-1-phosphotransferase leads to a failure to tag proteins with **Mannose-6-Phosphate**. Consequently, enzymes are secreted extracellularly rather than being sorted to lysosomes, leading to inclusion bodies. * **COP-II** vesicles transport proteins from RER to Golgi (Anterograde), while **COP-I** handles Retrograde transport.

Question 159: Which of the following cell organelles is rich in catalases?

A. Mitochondria
B. Ribosome
C. Peroxisome (Correct Answer)
D. Cell membrane

Explanation: ### Explanation **Correct Option: C. Peroxisome** Peroxisomes (also known as microbodies) are membrane-bound organelles that contain a variety of oxidative enzymes. The hallmark enzyme of the peroxisome is **Catalase**. * **Mechanism:** Peroxisomes utilize molecular oxygen to oxidize organic molecules, a process that produces hydrogen peroxide ($H_2O_2$) as a toxic byproduct. * **Role of Catalase:** Catalase specifically decomposes $H_2O_2$ into water and oxygen ($2H_2O_2 \rightarrow 2H_2O + O_2$), thereby protecting the cell from oxidative damage. This is vital for functions like long-chain fatty acid oxidation ($\beta$-oxidation) and detoxification of alcohol in the liver. **Incorrect Options:** * **A. Mitochondria:** Known as the "powerhouse of the cell," they are primarily involved in ATP production via the Electron Transport Chain and Krebs cycle. While they handle oxidative stress, they are not the primary site for catalase. * **B. Ribosome:** These are non-membranous organelles responsible for protein synthesis (translation). They do not contain oxidative enzymes. * **D. Cell membrane:** This is a phospholipid bilayer that regulates the transport of substances in and out of the cell; it lacks enzymatic machinery like catalase. **High-Yield Clinical Pearls for NEET-PG:** * **Zellweger Syndrome:** A rare congenital disorder caused by the absence of functional peroxisomes, leading to the accumulation of very-long-chain fatty acids (VLCFAs). * **$\beta$-oxidation:** While mitochondria oxidize short and medium-chain fatty acids, **peroxisomes** are the exclusive site for the initial oxidation of **Very-Long-Chain Fatty Acids (VLCFA)**. * **Marker Enzyme:** Catalase is considered the biochemical marker for identifying peroxisomes in subcellular fractionation.

Question 160: Proteins synthesized in the rough endoplasmic reticulum will first travel to which cellular organelle?

A. Mitochondria
B. Cytosol
C. Golgi body (Correct Answer)
D. Lysosome

Explanation: ### Explanation The correct answer is **C. Golgi body**. **Underlying Concept:** This question tests the understanding of the **Secretory Pathway** (Anterograde transport). Proteins destined for secretion, membrane integration, or lysosomal enzymes are synthesized by ribosomes on the **Rough Endoplasmic Reticulum (RER)**. Once synthesized, these proteins are packaged into **COPII-coated transport vesicles**, which bud off from the ER and travel directly to the **cis-Golgi network**. The Golgi body acts as the "post office" of the cell, where proteins undergo post-translational modifications (like glycosylation and sulfation) and sorting. **Analysis of Incorrect Options:** * **A. Mitochondria:** Most mitochondrial proteins are synthesized by free ribosomes in the cytosol or within the mitochondria themselves. They do not pass through the RER-Golgi pathway. * **B. Cytosol:** Proteins synthesized on the RER are sequestered within the ER lumen or membrane; they do not return to the cytosol. Proteins found in the cytosol are synthesized by **free ribosomes**. * **D. Lysosome:** While many RER-synthesized proteins are destined for the lysosome, they must **first** pass through the Golgi body to receive the **Mannose-6-Phosphate (M6P)** tag, which targets them specifically to the lysosome. **High-Yield Clinical Pearls for NEET-PG:** * **I-Cell Disease:** Caused by a deficiency in N-acetylglucosaminyl-1-phosphotransferase. This leads to a failure of the Golgi to add the M6P tag, causing lysosomal enzymes to be secreted extracellularly rather than delivered to lysosomes. * **Vesicular Transport:** * **COPII:** Anterograde transport (ER → Golgi). * **COPI:** Retrograde transport (Golgi → ER). * **Clathrin:** Trans-Golgi → Lysosomes; Plasma membrane → Endosomes (Receptor-mediated endocytosis).

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Cell Membrane Structure and Function

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Membrane Transport Proteins

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Cellular Energetics and Metabolism

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Mitochondrial Function

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Cell Volume Regulation

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Cellular Responses to Stress

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Calcium Signaling

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Cell Cycle and Regulation

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Cellular Aging

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Apoptosis and Cell Death

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