(a) Fatty acids regulate the nature of lipids, justify. 10 (b) Define coenzyme. Explain the role of coenzymes in the regulation…

(a) Fatty acids regulate the nature of lipids

The physical state of a lipid depends mainly on its fatty acid chains.

• Saturation: saturated chains (stearic acid, C18:0) are straight and pack tightly, so they have high melting points and make fats solid at room temperature. Unsaturated chains (oleic acid, C18:1) have cis double bonds that bend the chain, reduce packing and lower the melting point, so oils are liquid and membranes are more fluid.
• Chain length: longer chains have more hydrophobic contact and higher melting points; short chains lower them.
• Fluidity of membranes: the ratio of saturated to unsaturated acids, together with cholesterol, sets membrane fluidity, domain formation, enzyme activity and transport. Cold-adapted organisms raise the proportion of unsaturated acids (homeoviscous adaptation).
• Other properties: the acids decide whether the lipid is a fat or oil, its digestibility, rancidity and nutritional value (essential fatty acids give eicosanoids).

So the fatty acids determine the nature of the lipids.

(b) Coenzymes and regulation of metabolic reactions

A coenzyme is a small, heat-stable, non-protein organic molecule, often derived from a vitamin, that binds an enzyme temporarily and carries electrons, atoms or groups between reactions, being regenerated afterwards.

• NAD⁺/NADH (from niacin): NAD⁺ accepts hydride in dehydrogenase reactions (lactate, isocitrate, α-ketoglutarate dehydrogenases), and NADH passes electrons to the respiratory chain. A high NADH/NAD⁺ ratio slows these dehydrogenases and a low ratio speeds them, so the ratio links the cell's redox state to the rate of metabolism.
• FAD (from riboflavin) is bound to succinate dehydrogenase and passes electrons to the chain.
• Coenzyme A (pantothenic acid) carries acyl groups, and thiamine pyrophosphate helps decarboxylation.
• Control example: high NADH and acetyl-CoA activate pyruvate dehydrogenase kinase, which inhibits the pyruvate dehydrogenase complex.

(c) Respiratory regulation of acid–base balance

The lungs regulate pH by controlling the excretion of carbon dioxide, a volatile acid: CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻. The Henderson–Hasselbalch relation, pH = 6.1 + log[HCO₃⁻]/(0.03 × PCO₂), shows that pH depends on the bicarbonate to PCO₂ ratio. Normal arterial pH is 7.35–7.45.

• Acidosis: a rise in PCO₂ or H⁺ stimulates the central chemoreceptors (medulla) and peripheral chemoreceptors (carotid and aortic bodies), so ventilation increases, CO₂ is blown off and pH rises.
• Alkalosis: a fall in PCO₂ or H⁺ depresses ventilation, retaining CO₂ and lowering pH.
• The response begins within minutes but is only partial; the kidneys complete the correction over hours to days by adjusting H⁺ excretion and bicarbonate reabsorption.
• Respiratory acidosis (hypoventilation) and alkalosis (hyperventilation) arise when the lungs themselves are the cause.

(d) Rapidly acting synaptic transmitters

Rapidly acting transmitters are small molecules that bind ionotropic receptors, which are ligand-gated ion channels, and change the postsynaptic potential within milliseconds. Their action is stopped quickly by reuptake, enzymatic breakdown or diffusion.

• Acetylcholine: at the neuromuscular junction it binds nicotinic receptors, which open Na⁺ (and K⁺) channels, so a fast excitatory potential causes muscle contraction. It is broken down by acetylcholinesterase.
• Glutamate: the main excitatory transmitter of the central nervous system; AMPA (and NMDA) receptors open cation channels for fast excitation.
• GABA and glycine: the main inhibitory transmitters; their receptors are chloride channels, so the postsynaptic neuron is hyperpolarised or shunted. GABA acts in the brain and glycine in the spinal cord.
• Others include serotonin acting at the 5-HT₃ receptor.

They contrast with slow neuromodulators (dopamine, noradrenaline, neuropeptides), which act through metabotropic receptors, second messengers and longer-lasting changes.

(e) Sperm capacitation and its in vitro method in mammals

Capacitation is the final functional maturation of ejaculated sperm in the female genital tract, taking several hours. Cholesterol is lost from the sperm membrane, so it becomes more fluid; calcium and bicarbonate enter, cAMP and protein tyrosine phosphorylation rise, and the sperm becomes hyperactivated, so that it can undergo the acrosome reaction and fertilise the egg.

In vitro method: seminal plasma, which holds decapacitating factors, is removed by washing and centrifugation. Motile sperm are selected by the swim-up method or density-gradient (Percoll) centrifugation. They are then incubated at 37 °C in 5% CO₂ for some hours in a defined medium (such as TALP or HTF) containing bicarbonate, calcium, energy substrates such as pyruvate and glucose, and serum albumin, which takes up cholesterol. Heparin is added for bull sperm, and the calcium ionophore A23187 may induce the acrosome reaction. Capacitation is checked by hyperactivated motility and the chlortetracycline staining pattern, and the sperm are then used for IVF.