Write your answer in about 150 words for each of the following : 10×5=50 (a) Fatty acids regulate the nature of lipids, justify…

(a) Fatty acids are determinants of lipid behaviour because their saturation and chain length set packing, melting point and phase state. Although head groups and sterols modify membranes, acyl chain composition sets the baseline physical state. Saturated chains are straight and pack tightly, raising melting temperature and making lipids more solid; stearic acid, a saturated 18-carbon acid, contributes to rigid, high-melting membranes. Unsaturated chains contain cis double bonds that introduce kinks, reduce van der Waals contacts, lower melting point and increase fluidity; oleic acid, a monounsaturated 18-carbon acid, keeps phospholipid bilayers more mobile. Longer chains increase hydrophobic interactions and raise melting point, while shorter chains lower it. In membranes, the saturated to unsaturated ratio controls fluidity, domain formation, enzyme activity and transport. Thus, when an organism changes diet or temperature, it alters fatty acid composition to maintain membrane function, which justifies the statement that fatty acids regulate the nature of lipids.

(b) A coenzyme is a small non-protein organic cofactor that binds transiently to an enzyme and participates directly in electron, atom or group transfer, becoming regenerated in the reaction. Many coenzymes are vitamins or their derivatives. NAD+ and NADH are central mitochondrial dehydrogenase coenzymes: NAD+ accepts hydride from substrates such as lactate, isocitrate and alpha-ketoglutarate, and NADH donates electrons to respiratory chain complexes. The NADH/NAD+ ratio therefore signals the cellular redox state and directly controls the rate of dehydrogenases; high NADH slows oxidative decarboxylation, while high NAD+ favours it. FAD is tightly bound to succinate dehydrogenase, where it accepts electrons from succinate to form fumarate and passes them to ubiquinone, linking the citric acid cycle to the electron transport chain. Coenzyme availability thus regulates metabolic flux. For example, high NADH and acetyl-CoA favour pyruvate dehydrogenase kinase activity, which phosphorylates and inhibits pyruvate dehydrogenase, preventing unnecessary entry of pyruvate into the cycle.

(c) The respiratory system regulates acid-base balance mainly by controlling excretion of carbon dioxide, a volatile acid. Carbon dioxide and water form carbonic acid, which dissociates to hydrogen ion and bicarbonate, so changing ventilation changes hydrogen ion concentration. The Henderson-Hasselbalch relation is pH = 6.1 + log10([HCO3-] mmol/L / (0.03 x PaCO2 mm Hg)), where PaCO2 is measured in mm Hg. Normal arterial pH is 7.35 to 7.45. When PaCO2 rises, as in hypoventilation or airway obstruction, carbon dioxide retention lowers pH; central and peripheral chemoreceptors stimulate ventilation, increasing CO2 elimination and restoring pH. Hypoxia also stimulates peripheral chemoreceptors, while hypercapnia is the dominant respiratory acid-base stimulus. Renal compensation follows over hours to days by retaining bicarbonate or excreting acid. In veterinary practice, respiratory acidosis may occur in obstructed animals, while metabolic acidosis in ruminant acidosis is managed by correcting the cause and, only when severe, by bicarbonate therapy.

(d) Rapidly acting synaptic transmitters at chemical synapses are small molecules that bind ionotropic receptors, opening ion channels directly and producing millisecond changes in postsynaptic membrane potential. Acetylcholine is a classic example: at the neuromuscular junction it binds nicotinic receptors, opens sodium channels, and causes fast excitatory postsynaptic potentials and muscle contraction. Glutamate is the main excitatory transmitter in most central nervous system neurons; binding AMPA receptors opens sodium and sometimes calcium channels, producing fast excitation. GABA is the main inhibitory transmitter; GABA-A receptors are chloride channels, so GABA-A activation typically hyperpolarises or shunts the postsynaptic cell, producing fast inhibition. These ionotropic actions are brief because the transmitter is rapidly removed by reuptake, diffusion or enzymatic breakdown, as with acetylcholinesterase. They differ from slow neuromodulators such as dopamine, serotonin or neuropeptides, which usually act through metabotropic receptors, second messengers and longer-lasting changes in excitability, synaptic strength or gene expression.

(e) Sperm capacitation is the post-ejaculatory maturation of mammalian sperm in the female reproductive tract, involving membrane cholesterol loss, protein tyrosine phosphorylation, calcium changes and motility changes, which enable the acrosome reaction and fertilisation. In vitro capacitation mimics this by first removing seminal plasma and immotile sperm. Swim-up allows progressively motile sperm to migrate into a fresh medium, while Percoll or density gradient centrifugation separates motile sperm from debris and leukocytes. The selected sperm are then incubated in capacitating media such as TALP or HTF, usually with bovine serum albumin, at 37 degrees C in 5 percent CO2, for several hours. After capacitation, the acrosome reaction is assessed or induced using calcium ionophore A23187 or heparin; these agents trigger the acrosome reaction and are not themselves capacitating agents. Applied in assisted reproduction and cryopreservation of Indian Murrah buffalo semen, it shows capacitation is a controlled maturation step essential for fertilisation.