Protein refolding is carried out by?
Where does oxidative deamination primarily occur in the human body?
Which of the following is a plasma protein involved in blood clotting?
Which of the following statements BEST describes the net ATP production in glycolysis?
Which of the following substances does not inhibit glycolysis?
Which tissue cannot convert glucose 6-phosphate to free glucose due to lack of glucose-6-phosphatase?
Mutation in GLUT-2 causes which syndrome?
Which of the following is monoenoic acid ?
Which of the following fatty acids has the maximum number of carbon atoms?
Chylomicron remnants are associated with ?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 91: Protein refolding is carried out by?
- A. Valine
- B. Threonine
- C. Chaperone (Correct Answer)
- D. Aspartate
Explanation: ***Chaperone*** - **Chaperone proteins** assist in the proper folding of other proteins, particularly during stress conditions like heat shock, by preventing **aggregation** and promoting correct conformation. - They do not become part of the final functional protein but transiently bind during the folding process, thus facilitating **protein refolding** and assembly. *Valine* - **Valine** is an **essential amino acid** and a building block for proteins, but it does not play a direct role in protein refolding. - It contributes to the **hydrophobic core** of proteins due to its non-polar side chain, influencing protein structure but not managing the folding process. *Threonine* - **Threonine** is an **essential amino acid** with a polar side chain, often involved in **glycosylation** and phosphorylation, but not in the complex process of protein refolding. - Its hydroxyl group can participate in **hydrogen bonding**, influencing protein stability and interactions, but not acting as a folding catalyst. *Aspartate* - **Aspartate** is a **non-essential acidic amino acid** that can be involved in various metabolic pathways and is a component of proteins. - Its acidic side chain can form **salt bridges** and hydrogen bonds, contributing to the protein's overall charge and structure, but it does not actively oversee protein refolding.
Question 92: Where does oxidative deamination primarily occur in the human body?
- A. Cytoplasm of all cells
- B. Mitochondria of all cells
- C. Cytoplasm of liver cells
- D. Mitochondria of liver cells (Correct Answer)
Explanation: ***Mitochondria of liver cells*** - **Oxidative deamination**, particularly of glutamate, is a central process in **amino acid catabolism** and occurs predominantly in the **mitochondria of liver cells**. - This process is crucial for removing the **amino group (NH3)** from amino acids, forming ammonia, which is then detoxified into urea. *Cytoplasm of all cells* - While cells have cytoplasmic metabolic pathways, the primary enzyme for oxidative deamination, **glutamate dehydrogenase**, is located in the mitochondria. - The cytoplasm primarily handles glycolysis and various synthetic pathways, but not the bulk of oxidative deamination. *Mitochondria of all cells* - Although mitochondria are the site of oxidative metabolism in most cells, the **liver** is the main organ responsible for processing exogenous amino acids and their subsequent comprehensive deamination. - Other cells perform some amino acid metabolism, but not the large-scale oxidative deamination seen in the liver. *Cytoplasm of liver cells* - The cytoplasm of liver cells is involved in various metabolic processes, including gluconeogenesis and fatty acid synthesis. - However, the key enzymes for oxidative deamination are specifically compartmentalized within the **mitochondria** of these cells, not the cytoplasm.
Question 93: Which of the following is a plasma protein involved in blood clotting?
- A. Fibrinogen (Correct Answer)
- B. Lactate dehydrogenase (LDH)
- C. Aspartate aminotransferase (SGOT)
- D. Alanine aminotransferase (SGPT)
Explanation: ***Fibrinogen*** - **Fibrinogen** is a crucial plasma protein that is converted into **fibrin** during the coagulation cascade. - **Fibrin** then forms a meshwork, which is the structural basis of a **blood clot**. *Lactate dehydrogenase (LDH)* - **LDH** is an enzyme found in many tissues throughout the body and is involved in **cellular metabolism**, specifically the conversion of pyruvate to lactate. - Elevated levels of **LDH** can indicate tissue damage or disease but are not directly involved in blood clotting. *Aspartate aminotransferase (SGOT)* - **SGOT** (now commonly referred to as **AST**) is an enzyme primarily found in the **liver, heart, skeletal muscle, kidneys, brain, and red blood cells**. - High levels of **AST** are often indicative of **liver damage** or other organ injury, but it does not play a direct role in blood coagulation. *Alanine aminotransferase (SGPT)* - **SGPT** (now commonly referred to as **ALT**) is an enzyme predominantly found in the **liver**. - Elevated **ALT** levels are a sensitive marker for **liver cell damage** but are not involved in the blood clotting process.
Question 94: Which of the following statements BEST describes the net ATP production in glycolysis?
- A. Glycolysis produces 2 molecules of pyruvate
- B. Glycolysis produces a net gain of 2 ATP per glucose molecule (Correct Answer)
- C. Hexokinase consumes ATP during glycolysis
- D. Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules
Explanation: ***Glycolysis produces a net gain of 2 ATP per glucose molecule*** - In the initial "investment" phase of glycolysis, **2 ATP molecules are consumed** to phosphorylate glucose. - In the subsequent "payoff" phase, **4 ATP molecules are produced** through substrate-level phosphorylation, resulting in a net gain of 2 ATP. *Glycolysis produces 2 molecules of pyruvate* - While glycolysis does produce **2 molecules of pyruvate** from one glucose molecule, this statement describes the end product of the pathway, not the net ATP production. - Pyruvate is a crucial product that can be further metabolized in aerobic or anaerobic conditions, but it does not directly represent the energy yield in terms of ATP. *Hexokinase consumes ATP during glycolysis* - **Hexokinase** is indeed the enzyme that catalyzes the first ATP-consuming step in glycolysis, phosphorylating glucose to glucose-6-phosphate. - However, this statement describes only one aspect of ATP utilization within the pathway and does not account for the total ATP produced or the overall net gain. *Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules* - **Aldolase** is a key enzyme in glycolysis responsible for cleaving **fructose-1,6-bisphosphate** into dihydroxyacetone phosphate and glyceraldehyde-3-phosphate. - This step is part of the preparatory phase of glycolysis but does not directly describe the net ATP production.
Question 95: Which of the following substances does not inhibit glycolysis?
- A. Fluoride
- B. Arsenite
- C. Iodoacetate
- D. Fluoroacetate (Correct Answer)
Explanation: ***Fluoroacetate*** - **Fluoroacetate** is not a direct inhibitor of glycolysis. Instead, it is metabolized to **fluorocitrate**, which then acts as an inhibitor of **aconitase** in the **Krebs cycle (TCA cycle)**, thereby affecting cellular respiration at a later stage. - Its primary role in metabolic inhibition is within the **mitochondria**, impacting energy production via the TCA cycle rather than the glycolytic pathway. *Fluoride* - **Fluoride** is a known inhibitor of **enolase**, an enzyme in the penultimate step of glycolysis. - It forms a complex with **magnesium** and **phosphate** to block the active site of enolase, preventing the conversion of 2-phosphoglycerate to phosphoenolpyruvate. *Arsenite* - **Arsenite** inhibits glycolysis by targeting enzymes containing **sulfhydryl (–SH) groups**, particularly **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**, a critical enzyme in the glycolytic pathway. - It also inhibits the **pyruvate dehydrogenase complex** (linking glycolysis to the TCA cycle) and TCA cycle enzymes like **α-ketoglutarate dehydrogenase**, thereby affecting multiple stages of cellular respiration. *Iodoacetate* - **Iodoacetate** is a potent inhibitor of the enzyme **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**. - It specifically alkylates the **cysteine residue** at the active site of GAPDH, preventing the conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate, thereby blocking glycolysis.
Question 96: Which tissue cannot convert glucose 6-phosphate to free glucose due to lack of glucose-6-phosphatase?
- A. Liver
- B. Kidney
- C. Adipose tissue
- D. Muscle (Correct Answer)
Explanation: ***Muscle*** - Muscle tissue lacks the enzyme **glucose-6-phosphatase**, which is essential for hydrolyzing glucose 6-phosphate back to **free glucose**. - Therefore, glucose 6-phosphate in muscle is primarily used for **glycolysis** (energy production) or stored as glycogen for local use. *Liver* - The liver contains **glucose-6-phosphatase**, allowing it to convert **glucose 6-phosphate** to **free glucose**. - This capability is crucial for maintaining **blood glucose homeostasis** and releasing glucose into circulation. *Adipose tissue* - Adipose tissue, like muscle, **lacks glucose-6-phosphatase** and cannot convert glucose 6-phosphate back to free glucose. - Glucose 6-phosphate in adipose tissue is primarily channeled into **fatty acid synthesis** and storage. *Kidney* - The kidney, particularly the renal cortex, possesses **glucose-6-phosphatase** and can convert glucose 6-phosphate to **free glucose**. - This contributes to **gluconeogenesis** and release of glucose into the blood, especially during fasting.
Question 97: Mutation in GLUT-2 causes which syndrome?
- A. Dandy walker syndrome
- B. Beckwith-Wiedemann syndrome
- C. Menke's disease
- D. Fanconi-Bickel syndrome (Correct Answer)
Explanation: ***Fanconi-Bickel syndrome*** - This syndrome is caused by a **mutation in the GLUT-2 gene**, leading to dysfunctional glucose transport in the liver, kidneys, and intestines. - Key features include **hepatorenal glycogen accumulation**, **renal tubulopathy** (Fanconi syndrome), and **impaired glucose and galactose utilization**. *Dandy-Walker syndrome* - This is a **congenital brain malformation** involving the cerebellum and fourth ventricle. - It is often associated with hydrocephalus, but not directly linked to glucose transporter defects. *Beckwith-Wiedemann syndrome* - This is an **overgrowth disorder** characterized by a high risk of childhood cancer and congenital anomalies. - It is primarily caused by genetic abnormalities on **chromosome 11p15.5** and is unrelated to GLUT-2 mutations. *Menke's disease* - This is a rare X-linked recessive disorder of **copper metabolism**, leading to severe neurological degeneration. - It results from mutations in the **ATP7A gene**, which encodes a copper-transporting ATPase.
Question 98: Which of the following is monoenoic acid ?
- A. Linoleic acid
- B. Oleic acid (Correct Answer)
- C. Linolenic acid
- D. Arachidonic acid
Explanation: ***Oleic acid*** - **Oleic acid** is a **monounsaturated fatty acid** (MUFA), meaning it has **one double bond** in its hydrocarbon chain. - Its presence in many natural fats and oils makes it a significant component of the human diet. *Arachidonic acid* - **Arachidonic acid** is a **polyunsaturated fatty acid** (PUFA) containing **four double bonds**. - It is a precursor for **eicosanoids**, including prostaglandins and leukotrienes, involved in inflammation and other physiological processes. *Linoleic acid* - **Linoleic acid** is an **essential omega-6 polyunsaturated fatty acid** with **two double bonds**. - It is crucial for human health and serves as a precursor for other fatty acids like arachidonic acid. *Linolenic acid* - **Linolenic acid** refers to two essential fatty acids: **alpha-linolenic acid (ALA)**, an omega-3 fatty acid with **three double bonds**, and **gamma-linolenic acid (GLA)**, an omega-6 fatty acid also with three double bonds. - Both are **polyunsaturated fatty acids** with multiple double bonds.
Question 99: Which of the following fatty acids has the maximum number of carbon atoms?
- A. Oleic acid
- B. Linolenic acid
- C. Arachidonic acid
- D. Cervonic acid (Correct Answer)
Explanation: **Cervonic acid** - **Cervonic acid**, also known as **docosahexaenoic acid (DHA)**, is a long-chain omega-3 fatty acid with **22 carbon atoms** and 6 double bonds (22:6). - It is a primary structural component of the brain and retina and is the longest fatty acid among the options provided. *Oleic acid* - **Oleic acid** is a monounsaturated fatty acid with **18 carbon atoms** and one double bond (18:1). - It is a common fatty acid found in many animal fats and vegetable oils, but it has fewer carbon atoms than cervonic acid. *Linolenic acid* - **Linolenic acid** refers to two essential fatty acids: alpha-linolenic acid (ALA) and gamma-linolenic acid (GLA). Both have **18 carbon atoms**. - Alpha-linolenic acid (ALA) is an omega-3 fatty acid with 3 double bonds (18:3), while gamma-linolenic acid (GLA) is an omega-6 fatty acid with 3 double bonds (18:3), neither of which has more carbon atoms than cervonic acid. *Arachidonic acid* - **Arachidonic acid** is an omega-6 fatty acid with **20 carbon atoms** and four double bonds (20:4). - It is a precursor to eicosanoids and is longer than oleic and linolenic acids but shorter than cervonic acid.
Question 100: Chylomicron remnants are associated with ?
- A. Apo-C
- B. Apo-A
- C. Apo-E (Correct Answer)
- D. Apo-B100
Explanation: ***Apo-E*** - **Apolipoprotein E (Apo-E)** is a crucial apolipoprotein on the surface of chylomicron remnants, acting as a **ligand for the LDL receptor-related protein 1 (LRP1)** in the liver. - This binding facilitates the **hepatic uptake and clearance** of chylomicron remnants from circulation. *Apo-A* - **Apo-AI** is the primary apolipoprotein of **HDL** and plays a key role in reverse cholesterol transport by activating **lecithin-cholesterol acyltransferase (LCAT)**. - While chylomicrons *acquire* some Apo-AI from HDL, it is not the primary apolipoprotein defining their remnants' hepatic clearance. *Apo-C* - **Apo-CII** is a vital activator of **lipoprotein lipase (LPL)**, which metabolizes triglycerides in chylomicrons and VLDL. - **Apo-CIII** inhibits LPL and hinders receptor-mediated uptake, but **Apo-E** is the key for remnant recognition and uptake, not Apo-C in general. *Apo-B100* - **Apo-B100** is the main structural apolipoprotein of **LDL** and **VLDL**, serving as the ligand for the LDL receptor, mediating their hepatic uptake. - While chylomicrons have **Apo-B48**, which is a truncated form of Apo-B100, Apo-B100 itself is not found on chylomicron remnants.