In which stage of cell division is chromosomal study best carried out?
Who invented the technique for identifying individuals by their DNA?
Acute intermittent porphyria is due to deficiency of?
What is the primary metal ion found in myoglobin?
Which of the following is a tripeptide?
Which of the following is the shortest peptide?
Where does omega oxidation of fatty acids occur?
Which of the following is not affected in Abetalipoproteinemia ?
What is the metabolic abnormality associated with Zellweger syndrome?
Which of the following substances is not derived from tyrosine?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 131: In which stage of cell division is chromosomal study best carried out?
- A. Metaphase (Correct Answer)
- B. Telophase
- C. Anaphase
- D. Prophase
Explanation: ***Metaphase*** - During **metaphase**, chromosomes are maximally condensed and align at the cell's equatorial plate, making them easily visible and distinguishable under a microscope. - This arrangement allows for clear visualization of **chromosome number**, **size**, and **morphology**, which is crucial for genetic analysis. *Prophase* - In **prophase**, chromosomes begin to condense, but they are still diffuse and not fully compact, making detailed study difficult. - The nuclear envelope is also still present for most of prophase, obstructing a clear view of the chromosomes. *Telophase* - During **telophase**, chromosomes decondense and arrive at opposite poles, becoming less distinct and harder to analyze individually. - New nuclear envelopes form around the separated chromosomes, further obscuring their view for detailed study. *Anaphase* - In **anaphase**, sister chromatids separate and move towards opposite poles, but they are in motion and not aligned, making them difficult to capture and analyze individually. - The separated chromatids are also stretched and elongated, which makes their morphological assessment challenging.
Question 132: Who invented the technique for identifying individuals by their DNA?
- A. Shapiro
- B. Lewis
- C. Jeffreys (Correct Answer)
- D. Pasteur
Explanation: ***Jeffreys*** - **Alec Jeffreys** developed the technique of **DNA fingerprinting** in 1984, which revolutionized forensic science and paternity testing. - His method involved analyzing **variable number tandem repeats (VNTRs)** in DNA to create a unique profile for each individual. *Shapiro* - **Robert Shapiro** is a legal figure, famously associated with the O. J. Simpson murder trial, not directly with the invention of DNA identification techniques. - While he was involved in cases where DNA evidence was used, he did not contribute to its scientific development. *Lewis* - **Edward B. Lewis** was a Nobel Prize-winning geneticist known for his work on **developmental genetics** in *Drosophila melanogaster*, not for DNA identification techniques. - His research focused on gene clusters and their role in embryonic development. *Pasteur* - **Louis Pasteur** was a pioneering microbiologist and chemist, famous for his discoveries related to **vaccination**, microbial fermentation, and pasteurization. - His work predates the discovery and application of DNA for individual identification by over a century.
Question 133: Acute intermittent porphyria is due to deficiency of?
- A. Porphobilinogen deaminase (Correct Answer)
- B. Uroporphyrinogen III synthase
- C. Ferrochelatase
- D. ALA synthase
Explanation: ***Porphobilinogen deaminase*** - **Acute intermittent porphyria (AIP)** results from a deficiency in **porphobilinogen deaminase** (also known as hydroxymethylbilane synthase). - This enzyme deficiency leads to the accumulation of **aminolevulinic acid (ALA)** and **porphobilinogen (PBG)**, which are neurotoxic and cause the characteristic symptoms of AIP. *Uroporphyrinogen III synthase* - A deficiency in **uroporphyrinogen III synthase** causes **congenital erythropoietic porphyria (Günther disease)**, which is characterized by severe photosensitivity and hemolytic anemia. - This enzyme defect leads to the accumulation of uroporphyrinogen I and coproporphyrinogen I, not the ALA and PBG associated with AIP. *Ferrochelatase* - Deficiency in **ferrochelatase** causes **erythropoietic protoporphyria (EPP)**, which presents with photosensitivity and chronic liver disease due to the accumulation of **protoporphyrin**. - This condition does not cause the acute neurological attacks seen in AIP. *ALA synthase* - **ALA synthase** is the **rate-limiting enzyme** in heme synthesis; while its activity is crucial, a congenital *deficiency* is not the cause of AIP. - Instead, the *upregulation* of ALA synthase activity in AIP (due to the PBG deaminase block) contributes to the accumulation of ALA and PBG.
Question 134: What is the primary metal ion found in myoglobin?
- A. Iron (Correct Answer)
- B. Copper
- C. Selenium
- D. Zinc
Explanation: ***Iron*** - **Iron** is the central metal ion in the **heme group** of myoglobin. - It is responsible for **binding oxygen** reversibly, which is myoglobin's primary function in muscle tissue. *Copper* - **Copper** is a component of several enzymes, such as **cytochrome c oxidase** and **superoxide dismutase**, but not myoglobin. - It plays a role in **electron transport** and connective tissue formation. *Selenium* - **Selenium** is an essential trace element that functions as a component of **glutathione peroxidase**, an antioxidant enzyme. - It is not found in the structure of myoglobin. *Zinc* - **Zinc** is a critical component of many enzymes, including **carbonic anhydrase** and **DNA polymerase**. - It is involved in **immune function** and wound healing, but not in oxygen transport by myoglobin.
Question 135: Which of the following is a tripeptide?
- A. Glutathione (Correct Answer)
- B. Angiotensin
- C. Glucagon
- D. Oxytocin
Explanation: ***Glutathione*** - **Glutathione** is a tripeptide composed of three amino acids: **glutamate**, **cysteine**, and **glycine**. - It plays a crucial role as an **antioxidant** in the body, protecting cells from damage by **free radicals**. *Angiotensin* - **Angiotensin** is a peptide hormone that causes **vasoconstriction** and an increase in **blood pressure**. - It is an **oligopeptide** (typically 8-10 amino acids) rather than a tripeptide. *Glucagon* - **Glucagon** is a peptide hormone produced by the **alpha cells** of the pancreas that raises **blood glucose levels**. - It is a **29-amino acid** polypeptide, much larger than a tripeptide. *Oxytocin* - **Oxytocin** is a hormone involved in social bonding and sexual reproduction, best known for its role in **childbirth** and **lactation**. - It is a **nonapeptide**, meaning it consists of nine amino acids.
Question 136: Which of the following is the shortest peptide?
- A. Oxytocin
- B. Vasopressin
- C. Angiotensin III (Correct Answer)
- D. Angiotensin II
Explanation: ***Angiotensin III*** - **Angiotensin III** is a **heptapeptide**, meaning it consists of **7 amino acids**. - It is formed by the removal of the N-terminal aspartate from Angiotensin II (8 amino acids), making it the shortest peptide among the options. - It has similar but weaker actions compared to Angiotensin II in regulating blood pressure and aldosterone secretion. *Oxytocin* - **Oxytocin** is a **nonapeptide**, composed of **9 amino acids**. - It plays a role in uterine contractions during labor and milk ejection during lactation. *Vasopressin* - **Vasopressin**, also known as **antidiuretic hormone (ADH)**, is a **nonapeptide** (**9 amino acids**). - Its primary functions are water reabsorption in the kidneys and vasoconstriction. *Angiotensin II* - **Angiotensin II** is an **octapeptide**, containing **8 amino acids**. - It is a potent vasoconstrictor and stimulates aldosterone secretion, playing a key role in blood pressure regulation.
Question 137: Where does omega oxidation of fatty acids occur?
- A. Endoplasmic Reticulum (Correct Answer)
- B. Cytosol
- C. Mitochondria
- D. None of the options
Explanation: ***Endoplasmic Reticulum*** - **Omega oxidation** of fatty acids occurs in the **endoplasmic reticulum (microsomes)** of liver and kidney cells. - This pathway involves **hydroxylation of the terminal omega carbon** by **cytochrome P450 enzymes** located in the smooth ER. - The omega carbon is then oxidized to a **carboxyl group**, forming a **dicarboxylic acid**. - This is a **minor pathway** that becomes important when **beta-oxidation is impaired** or for metabolism of **medium-chain fatty acids**. *Cytosol* - The cytosol is involved in **fatty acid synthesis**, not omega oxidation. - While some later steps of fatty acid metabolism occur in the cytosol, the initial hydroxylation step of omega oxidation requires ER-localized cytochrome P450 enzymes. *Mitochondria* - **Mitochondria** are the primary site for **beta-oxidation** of fatty acids, not omega oxidation. - Beta-oxidation sequentially removes **two-carbon units from the carboxyl end**, which is distinct from omega oxidation. - The dicarboxylic acids produced by omega oxidation may subsequently undergo beta-oxidation in mitochondria. *None of the options* - This option is incorrect because the endoplasmic reticulum is the correct cellular location for omega oxidation. - The ER contains the necessary cytochrome P450 enzymes for the hydroxylation reaction that initiates this pathway.
Question 138: Which of the following is not affected in Abetalipoproteinemia ?
- A. LDL
- B. HDL (Correct Answer)
- C. IDL
- D. VLDL
Explanation: ***HDL*** - **Abetalipoproteinemia** is caused by a defect in the **microsomal triglyceride transfer protein (MTP)**, which is essential for the assembly and secretion of **chylomicrons**, **VLDL**, and subsequently **LDL** and **IDL**. - **HDL synthesis** and secretion occur independently of MTP, as nascent HDL particles are formed in the plasma from lipids and apolipoproteins (primarily apoA-I) released from other lipoproteins and cells. *LDL* - **LDL** is critically affected in abetalipoproteinemia because it is a metabolic product of **VLDL**. - Since **VLDL** production is severely impaired due to the MTP defect, there is a profound deficiency of **LDL** in the plasma. *VLDL* - **VLDL** production is severely impaired in abetalipoproteinemia because **microsomal triglyceride transfer protein (MTP)** is required for its assembly and secretion from the liver. - The inability to load triglycerides onto apoB leads to very low or absent plasma **VLDL** levels. *IDL* - **IDL** is an intermediate lipoprotein in the metabolism of **VLDL** to **LDL**. - Given that both **VLDL** and **LDL** are severely deficient in abetalipoproteinemia, **IDL** levels are also consequently very low or absent.
Question 139: What is the metabolic abnormality associated with Zellweger syndrome?
- A. Accumulation of long-chain fatty acids
- B. Accumulation of short-chain fatty acids
- C. Accumulation of very long-chain fatty acids (Correct Answer)
- D. Accumulation of medium-chain fatty acids
Explanation: ***Accumulation of very long-chain fatty acids*** - **Zellweger syndrome** is a peroxisomal biogenesis disorder, meaning that peroxisomes, which are responsible for the **beta-oxidation** of very long-chain fatty acids (VLCFAs), are absent or dysfunctional. - The inability to break down **VLCFAs** leads to their accumulation in various tissues, causing significant neurological and systemic dysfunction. *Accumulation of long-chain fatty acids* - While peroxisomes can contribute to the metabolism of some **long-chain fatty acids (LCFAs)**, their primary role in this context is with **VLCFAs**. - **Mitochondria** are the main organelles responsible for the beta-oxidation of most LCFAs. *Accumulation of short-chain fatty acids* - **Short-chain fatty acids (SCFAs)** are primarily produced by gut bacteria and are metabolized in the mitochondria and other cellular compartments. - Their accumulation is not characteristic of **Zellweger syndrome**. *Accumulation of medium-chain fatty acids* - **Medium-chain fatty acids (MCFAs)** are primarily metabolized in the **mitochondria** and do not typically accumulate in Zellweger syndrome. - Disorders affecting MCFA metabolism usually point to different enzyme deficiencies, such as **MCAD deficiency.**
Question 140: Which of the following substances is not derived from tyrosine?
- A. Thyroxine
- B. Melanin
- C. Nicotinic acid (Correct Answer)
- D. Dopamine
Explanation: ***Nicotinic acid*** - **Nicotinic acid** (niacin, vitamin B3) is synthesized from **tryptophan** in the body, not tyrosine. - It plays a crucial role in metabolism as a precursor for NAD+ and NADH, which are involved in various enzymatic reactions. *Thyroxine* - **Thyroxine** (T4), a thyroid hormone, is derived from the amino acid **tyrosine**. - **Iodine** is incorporated into tyrosine residues on thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT), which then couple to form T4 (and T3). *Melanin* - **Melanin**, the pigment responsible for skin, hair, and eye color, is synthesized from **tyrosine** through a pathway involving the enzyme **tyrosinase**. - This process involves the hydroxylation of tyrosine to 3,4-dihydroxyphenylalanine (DOPA) and subsequent oxidation reactions. *Dopamine* - **Dopamine**, an important neurotransmitter, is synthesized from **tyrosine** in a two-step process in the brain and adrenal medulla. - Tyrosine is first hydroxylated to DOPA by **tyrosine hydroxylase**, and then DOPA is decarboxylated to dopamine by DOPA decarboxylase.