INICET Biochemistry Previous Year Questions (2017–2026)

The correct answer is 1, 2, 3, and 4 - all four pairings are correctly matched.

Cysteine is an UNCHARGED amino acid (its thiol side chain carries no charge at physiological pH). Proline is NONPOLAR (its cyclic side chain is hydrophobic). Histidine and Lysine are both BASIC amino acids (along with arginine), carrying a positive charge. Since every statement is correct, the answer is all of them.

A student may hesitate over cysteine, since some texts call it weakly polar. But the claim here is only that it is UNCHARGED, which is true regardless of the polar versus nonpolar debate. Histidine is sometimes overlooked as basic, yet it is one of the three basic amino acids. So no pairing is wrong, and the correct option is 1, 2, 3, and 4.

Incorrect Options (each omits a correct pairing):

• 1 and 2 only: Omits the correct basic pairings (Histidine and Lysine).
• 3 and 4 only: Omits the correct uncharged (Cysteine) and nonpolar (Proline) pairings.
• 2 and 3 only: Omits the correct Cysteine and Lysine pairings.

High-Yield Facts:

• Basic amino acids: Histidine, Arginine, Lysine (mnemonic HAL).
• Acidic amino acids: Aspartate and Glutamate.
• Polar uncharged: Cysteine, Serine, Threonine, Asparagine, Glutamine, Tyrosine.
• Nonpolar: Proline, Glycine, Alanine, Valine, Leucine, Isoleucine, Methionine.

Figure: Amino acid properties Venn diagram. Charged and positive amino acids (H, K, R) are basic. Cysteine (C) is polar uncharged, and proline (P) lies in the hydrophobic group.

The correct answer is Decreased ATP, increased oxygen consumption, increased heat.

An uncoupler (such as 2,4-dinitrophenol, salicylates, or thermogenin) makes the inner mitochondrial membrane leaky to protons, dissipating the proton gradient. ATP synthase can no longer use the gradient, so ATP production falls. Freed from the back-pressure of the gradient, the electron transport chain runs FASTER, so oxygen consumption rises, and the energy that would have made ATP is released as heat (hyperthermia).

The closest distractor is the option with DECREASED oxygen consumption, which is the pattern of an ETC INHIBITOR (such as cyanide or rotenone), where the chain stops and oxygen use falls. An uncoupler is the opposite for oxygen: the chain speeds up, so oxygen consumption INCREASES while ATP still falls. Options that keep ATP high are wrong because uncoupling always stops net ATP synthesis.

Incorrect Options:

• Increased ATP, decreased oxygen consumption, increased heat: ATP cannot rise during uncoupling, and oxygen consumption increases, not decreases.
• Decreased ATP, decreased oxygen consumption, decreased heat: This is the ETC-inhibitor pattern (cyanide). An uncoupler increases oxygen consumption and heat.
• Increased ATP, increased oxygen consumption, decreased heat: ATP falls (not rises) and heat increases (not decreases) with uncoupling.

High-Yield Facts:

• Uncouplers: 2,4-DNP, salicylates (overdose), and thermogenin (UCP1) in brown fat.
• Uncoupler effect: ATP DOWN, oxygen consumption UP, heat UP.
• ETC inhibitors (cyanide, rotenone): oxygen consumption DOWN, ATP stops.
• Brown fat thermogenin drives non-shivering thermogenesis.

Figure 1: Normal oxidative phosphorylation. The ETC pumps protons and ATP synthase uses the gradient to make ATP. An uncoupler dissipates this gradient.

Figure 2: Coupling of the proton gradient to ATP synthesis. Uncouplers let protons leak back, so the chain runs on but ATP is not made and heat is released.

The correct answer is Peroxisomal biogenesis defect.

Coarse facies, hypotonia, and seizures in an infant with elevated very long-chain fatty acids (VLCFA) is the classic picture of Zellweger syndrome (cerebrohepatorenal syndrome). VLCFA are beta-oxidized in peroxisomes, not mitochondria. Mutations in PEX genes impair peroxisome biogenesis, so functional peroxisomes are absent and VLCFA accumulate. This is the most severe peroxisome biogenesis disorder.

The closest distractor is lysosomal hydrolase deficiency, because lysosomal storage diseases (such as Hurler) also cause COARSE FACIES. However, lysosomal disorders do NOT elevate VLCFA. The raised VLCFA specifically points to a PEROXISOMAL defect, since peroxisomes carry out VLCFA beta-oxidation. Mitochondrial beta-oxidation handles shorter chains and does not raise VLCFA.

Incorrect Options:

• Mitochondrial beta oxidation defect: Handles medium and long chains (causing hypoketotic hypoglycemia), not VLCFA, which are peroxisomal.
• Lysosomal hydrolase deficiency: Causes storage diseases with coarse facies, but not elevated VLCFA.
• Endoplasmic reticulum defect: Not associated with VLCFA accumulation or this clinical picture.

High-Yield Facts:

• Elevated VLCFA = peroxisomal disorder (Zellweger spectrum, X-linked ALD).
• Zellweger = PEX gene mutation, peroxisome biogenesis failure.
• Peroxisomes beta-oxidize VLCFA and branched-chain (phytanic) fatty acids.
• Features: coarse facies, hypotonia, seizures, hepatomegaly.

Figure 1: Zellweger (cerebrohepatorenal) syndrome - craniofacial dysmorphism with hypotonia, from a peroxisome biogenesis defect.

Figure 2: Peroxisomes (green puncta). In Zellweger syndrome, PEX mutations prevent functional peroxisome assembly, so VLCFA are not beta-oxidized.