Biochemistry

A DNA has 11 base pairs per turn of its helix.

Piercidin A inhibits NADH-CoQ reductase (Complex I) to block electron flow from the latter to CoQ. So oxidations of substrates such as pyruvate, isocitrate, α-ketogluterate, malate and 3-hudroxybutyrate, whose electrons enter the respiratory chain through complex I are prevented.

4th and 5th carbon and 7th nitrogen come from glycine.

Difference in spatial orientation of groups on a single asymmetric carbon of a molecule having more than one asymmetric carbon. For example, glucose and galactose are 4 epimers of each other differing with respect to groups on C4.

Physiological concentration of ATP in cell inhibits Pfk-I allosterically and reduces its substrate affinity for fructose 6 phosphate. A 20% fall in ATP concentration rises the the rate of glycolysis 10-fold and Pfk activity to 50%. So low ATP/AMP ratio regulates the Pfk-I activity and thus, regulates glycolysis. Thus, Pfk-I is the enzyme for rate limiting step of glycolysis.

The initiator tRNA (tRNAimet) binds to the 5’ end of mRNA before binding of the small (40S) ribosomal subunit. The large ribosomal subunit in eukaryotes is 60S subunit, which binds to 5’mRNA after initiator tRNA, the 40S subunit and initiation factors bind to mRNA.

In complex III, electrons are transferred from ubiquinol (QH2) to cytochrome c by the enzyme cytochrome c reductase.

Since, the Bacteria has been transferred from N¹⁵ to N¹⁴ medium, the source of nitrogen for synthesis of DNA will be non radioactive. Now, the bacteria was grown in N¹⁵ medium after which it was grown for several generations in N¹⁴ medium. So, after centrifugation thick band will be formed in N¹⁴ zone and a thin band will be formed in the N¹⁵ zone as initially the DNA contained N¹⁵ nitrogen.

NADH is yielded in three steps- (a) oxidation of isocitrate to oxalosuccinate (b) oxidation of α-ketogluterate to succinyl CoA and (c) oxidation of malate to oxaloacetate. Thus, 3 NADH molecules are formed and CO₂ is produced during conversion of oxalosuccinate to α-ketogluterate and the latter to succinyl CoA. So in 1 cycle 3 NADH and 2 CO₂ are formed.

Riboflavin or vitamin B2 plays an important role in the production of energy in electron transport chain, the citric acid cycle and also in β-oxidation of fatty acid and it has no role in synthesis of neurotransmitter.

Attenuator produces terminator loop in presence of high tryptophan and anti terminator loop in presence of low tryptophan. The attenuator sequence is present within the leader sequence of the operon. In absence of leader sequence, there will be no attenuation. So, no attenuator loop will be formed and transcription of operon will increase.

In each β-oxidation cycle, 2 carbons are lessoned from a fatty acyl CoA for the production of 1 molecule of acetyl CoA. In this way a 16-carbon fatty acid is oxidized by reduction of 2 carbon atoms at each cycle and finally the last fatty acyl CoA is none other than an acetyl CoA.

Rate limiting enzyme for glycogenesis is glycogen synthase,urea is carbamoyl phosphate synthetase, TCA cycle is α-ketogluterate dehydrogenase, purine biosynthesis is glutamyl amido transferase and fatty acid synthesis is Acetyl CoA carboxylase.

Bicarbonate is the principal buffer of blood plasma. It consists of bicarbonate (HCO-3) and carbonic acid (H2CO3) as the base and acid members respectively. The bicarbonate buffer neutralizes stronger dietary and metabolic acids changing them to corresponding conjugate bases.

Glycogen synthase a is the active form of enzyme glycogen synthase.

The pH of buffer is 6.1 in plasma as it exists there in equilibrium with CO2.

Active glycogen synthase a is converted to inactive form glycogen synthase b by phosphorylation of its seven serine residues with ATP by different cAMP dependent protein kinase enzymes.

The ATP yield for every oxidation cycle is theoretically at maximum yield 17, as NADH produces 3 ATP, FADH2 produces 2 and a full rotation of the Citric Acid Cycle produces 12. In practice it is closer to 14 ATP for a full oxidation cycle as in practice the theoretical yield isn't attained, it's generally closer to 2.5 ATP per NADH molecule produced, 1.5 for each FADH2 Molecule produced and this equals to 10 per cycle of the TCA (according to the P/O ratio)Source ATP Total1 FADH2x 1.5 ATP = 1.5 ATP (Theoretically 2 ATP)1 NADHx 2.5 ATP = 2.5 ATP (Theoretically 3 ATP)1 acetyl CoAx 10 ATP = 10 ATP (Theoretically 12 ATP)TOTAL = 14 ATPFor a 16-carbon fatty acid, the number of ATPs generated:Source ATP Total7 FADH2 x 1.5 ATP = 10.5 ATP7 NADH x 2.5 ATP = 17.5 ATP8 acetyl CoA x 10 ATP = 80 ATP. Activation = -2 ATPNET = 106 ATPIn the first step of β-oxidation, the acyl CoA produced from a 16-C saturated fatty acid is transferred to mitochondria by carnitine carriers at the cost of 2 ATPs. So the net energy yield is 106 ATPs at the end of one complete β-oxidation of a 16-C fatty acid.

Cycloheximide inhibits initiation of protein synthesis, puromycin inhibits protein synthesis by resembling an amino acid attached to terminal adenosine of t-RNA, chloramphenicol is an antibiotic that inhibits bacterial protein synthesis by blocking the translation elongation and tetracyclin is also an antibiotic that inhibits bacterial protein synthesis by blocking the a-site on ribosome.

The attenuator sequence is present within leader sequence.