Respiration in Plants — NEET Notes

Do plants breathe?

The answer is not quite as direct as it sounds. Yes — plants take in O₂ and give out CO₂, and like animals they need oxygen for respiration. But unlike animals, plants have no specialised respiratory organs, no lungs, no gills, no diaphragm. Gaseous exchange is handled by stomata in leaves and young stems, and by lenticels on the bark of woody trunks and roots. There are three structural reasons plants can get away with this. First, each plant part takes care of its own gas-exchange needs — there is little transport of gases between organs. Second, plants demand far less gas exchange than animals; roots, stems and even photosynthesising leaves respire at rates far lower than an active animal cell. Third, the diffusion distances inside a plant are short — living cells are organised in thin layers near the surface, while the bulky interior of stems and roots is mostly dead tissue providing only mechanical support. The loose packing of parenchyma cells creates an interconnected network of air spaces that every living cell can tap into.

Respiration itself is the controlled breaking of C–C bonds of complex organic molecules by oxidation inside the cell, releasing energy that is captured as ATP. The molecules that are oxidised are called respiratory substrates. Glucose is the favoured substrate, but fats, proteins and even organic acids can serve as respiratory fuels in certain situations. The crucial design feature is that glucose is not burnt in a single step — that would release all the energy as heat, which is useless to the cell. Instead, glucose is oxidised in a long series of small, enzyme-controlled steps, each one yielding just enough energy to be coupled to ATP synthesis. This is what makes respiration a slow combustion, not a fire.

C₆H₁₂O₆ + 6 O₂  →  6 CO₂ + 6 H₂O + Energy

The overall reaction — the energy is captured as ATP, not lost as heat

Glycolysis — the Embden-Meyerhof-Parnas pathway

Glycolysis takes its name from the Greek glycos (sugar) and lysis (splitting). The scheme was worked out by Gustav Embden, Otto Meyerhof and J. Parnas, and is therefore also called the EMP pathway. It is the universal starting point of respiration — present in every living organism, occurring in the cytoplasm of the cell, and running whether or not oxygen is available. In anaerobic organisms it is the only respiratory process; in aerobic organisms it is the first of three. In plants, the glucose for glycolysis comes from sucrose, which the enzyme invertase splits into glucose and fructose; both monosaccharides enter the pathway and are quickly converted by hexokinase into glucose-6-phosphate, then by phosphoglucoisomerase into fructose-6-phosphate.

Over ten enzyme-catalysed reactions, one molecule of glucose is partially oxidised into two molecules of pyruvic acid. ATP is consumed at two steps (hexokinase and phosphofructokinase) and generated at two steps per triose (BPGA → PGA, and PEP → pyruvate) — giving four ATP made, two ATP used, and a net gain of 2 ATP. One step also reduces NAD⁺ to NADH + H⁺ when 3-phosphoglyceraldehyde (PGAL) is oxidised to 1,3-bisphosphoglycerate (BPGA), so the pathway also produces 2 NADH per glucose. Pyruvate is the key end-product, and its fate depends on what oxygen the cell has access to.

Fermentation — the anaerobic fates of pyruvate

When oxygen is unavailable, the cell still has to keep glycolysis running, and to keep glycolysis running it must keep regenerating NAD⁺ (which is consumed at the PGAL step). The trick is to dump the electrons on pyruvate itself — pyruvate accepts the hydrogens from NADH and is reduced to either ethanol or lactic acid. This is fermentation — an incomplete oxidation of glucose under anaerobic conditions. Two industrial-scale variants exist.

Alcoholic fermentation is the route used by yeast (and by some plant cells under flooded or stagnant conditions). The enzyme pyruvic acid decarboxylase strips a CO₂ off pyruvate to make acetaldehyde, then alcohol dehydrogenase reduces acetaldehyde to ethanol — using the NADH from glycolysis. The end products are ethanol, CO₂ and 2 ATP net per glucose. Yeast poisons itself at about 13% ethanol, which is why naturally fermented beverages cap out around that figure; anything stronger needs distillation. Lactic acid fermentation is the route used by certain bacteria and by mammalian muscle cells under oxygen debt. The enzyme lactate dehydrogenase reduces pyruvate directly to lactic acid using NADH, regenerating NAD⁺ in one step. The end product is lactic acid and 2 ATP net — no CO₂ is released. Both fermentations are wasteful (less than seven per cent of the chemical energy of glucose is captured) and both are hazardous because the products themselves — alcohol or lactic acid — are toxic at high concentrations.

Aerobic respiration — pyruvate enters the mitochondrion

When oxygen is available, the cell stops dumping electrons on pyruvate and instead sends pyruvate into the mitochondrion for complete oxidation. Two crucial events define aerobic respiration: the complete oxidation of pyruvate, with all six carbons of the original glucose leaving as CO₂, and the passing of the electrons removed (as hydrogens) onto molecular O₂ at the end of an electron transport chain, with ATP synthesis coupled to that electron flow. The first event happens in the matrix of the mitochondrion; the second on the inner mitochondrial membrane.

Before the Krebs cycle begins, pyruvate must be prepared. The link reaction — oxidative decarboxylation by the multi-enzyme complex pyruvate dehydrogenase — happens once pyruvate has crossed into the matrix. One CO₂ is released, NAD⁺ is reduced to NADH, and the remaining 2-carbon acetyl group is loaded onto Coenzyme A to form acetyl-CoA. Because each glucose yields two pyruvates, the link reaction runs twice per glucose, producing 2 acetyl-CoA, 2 CO₂ and 2 NADH.

Pyruvate + CoA + NAD⁺  →  Acetyl-CoA + CO₂ + NADH

The link reaction — catalysed by pyruvate dehydrogenase, in the mitochondrial matrix

The Krebs cycle (TCA / citric acid cycle)

Acetyl-CoA now enters a cyclic pathway named after Hans Krebs, who first elucidated it. It is also called the tricarboxylic acid (TCA) cycle because its first intermediate, citric acid, has three carboxyl groups; or simply the citric acid cycle. The cycle begins with the condensation of acetyl-CoA with oxaloacetic acid (OAA) and water to yield citric acid — a reaction catalysed by citrate synthase, with CoA released. Citrate is then isomerised to isocitrate. Two successive oxidative decarboxylations follow: isocitrate → α-ketoglutarate (releasing CO₂ and reducing NAD⁺ to NADH), and α-ketoglutarate → succinyl-CoA (again releasing CO₂ and reducing NAD⁺). Succinyl-CoA is then converted to succinic acid with the production of 1 GTP by substrate-level phosphorylation — GTP is later converted to ATP. Succinic acid is oxidised to fumaric acid, reducing FAD⁺ to FADH₂ — this is the only FAD-reducing step in the cycle. Fumaric acid is hydrated to malic acid, which is oxidised to regenerate OAA, producing one more NADH. OAA then condenses with a fresh acetyl-CoA and the cycle starts again.

The Electron Transport System (ETS)

Glycolysis and the Krebs cycle have done the carbon work — the six carbons of glucose are now spent, lost as six molecules of CO₂. But the energy of glucose has been transferred to 10 NADH + 2 FADH₂ per glucose (2 from glycolysis, 2 from the link reaction, 6 from the Krebs cycle, plus 2 FADH₂ from Krebs). The job of the electron transport system is to extract that energy, transferring electrons from NADH and FADH₂ down a chain of carriers — and using the energy released to pump protons across the inner mitochondrial membrane. The ETS lives in the inner mitochondrial membrane and consists of five complexes.

Electrons enter the chain in two ways. NADH docks at Complex I and is oxidised; its electrons travel I → ubiquinone → III → cytochrome c → IV → O₂. FADH₂ is generated inside Complex II (succinate dehydrogenase, the only TCA enzyme embedded in the membrane), so its electrons skip Complex I and enter the chain at ubiquinone — II → ubiquinone → III → cytochrome c → IV → O₂. That single bypass is the reason FADH₂ powers fewer proton pumps than NADH, and therefore yields less ATP.

Oxidative phosphorylation & chemiosmosis

The flow of electrons down the ETS is not directly coupled to ATP synthesis. Instead, the energy released at Complexes I, III and IV is used to pump protons (H⁺) from the matrix into the intermembrane space. The inner membrane is impermeable to H⁺, so protons accumulate there, generating both a chemical gradient (pH difference) and an electrical gradient (charge difference) — collectively, the proton-motive force. Protons can only flow back into the matrix through one channel: the F₀ stalk of ATP synthase (Complex V). As they pass through, they cause the F₀ rotor to spin; the rotation is mechanically coupled to the F₁ headpiece, which catalyses ADP + Pᵢ → ATP. For each ATP produced, 4 H⁺ pass through F₀ from the intermembrane space to the matrix down the electrochemical gradient. This whole mechanism — coupling redox energy via a proton gradient to ATP synthesis — is Peter Mitchell's chemiosmotic hypothesis, and the process is called oxidative phosphorylation because the energy comes from oxidation, not from light.

The role of oxygen in this whole symphony is small but absolutely essential: O₂ is the final hydrogen and electron acceptor at Complex IV. It "pulls" the electrons down the chain by being reduced to water. Without O₂ to receive the electrons at the end, the chain stalls, NADH and FADH₂ cannot be reoxidised, and within seconds the Krebs cycle and even glycolysis grind to a halt. This is the deep reason aerobic organisms cannot survive without oxygen — not because oxygen is involved at many steps, but because it sits at the very bottom of the only exit.

The respiratory balance sheet

The respiratory balance sheet is the bookkeeping exercise — adding up every ATP from every step. NCERT itself flags that the calculation rests on four assumptions: a strictly sequential pathway, that glycolytic NADH actually reaches the mitochondrion and gets fully oxidised, that no intermediates are siphoned off for biosynthesis, and that only glucose is being respired. In a real cell these assumptions break down, so the balance sheet is theoretical — but it is essential for NEET. The convention used in NCERT is 3 ATP per NADH and 2 ATP per FADH₂.

Amphibolic pathway — catabolism meets anabolism

Glucose is the favoured substrate, and all carbohydrates are converted to glucose before entering the pathway at glycolysis. But other substrates can also be respired — and the entry points are exactly where you would expect from the chemistry. Fats are first broken down to glycerol and fatty acids; glycerol joins the glycolytic pathway after conversion to PGAL, while fatty acids are degraded by β-oxidation into acetyl-CoA and enter the Krebs cycle at the citrate synthase step. Proteins are first cleaved by proteases into amino acids; each amino acid, after deamination, joins the respiratory pathway at the point dictated by its carbon skeleton — sometimes as pyruvate, sometimes as acetyl-CoA, sometimes as α-ketoglutarate, sometimes as OAA.

But the very same compounds are withdrawn from the respiratory pathway when the cell needs to synthesise fatty acids, amino acids or other biomolecules. Acetyl-CoA leaves the cycle to build fatty acids; α-ketoglutarate leaves to build glutamate and other amino acids; OAA leaves to build aspartate. Breaking down is catabolism; building up is anabolism. Because the respiratory pathway feeds both, it is best described as an amphibolic pathway (from Greek amphi, both) — not a purely catabolic one. NCERT explicitly demands this language.

Catabolism + anabolism = amphibolism

Why respiration is more than a pathway of breakdown

Respiratory quotient (RQ)

The respiratory quotient (RQ) — also called the respiratory ratio — is the ratio of the volume of CO₂ evolved to the volume of O₂ consumed during respiration. Mathematically:

RQ = volume of CO₂ evolved / volume of O₂ consumed

A diagnostic for what substrate is being burnt

The value depends on the chemical composition of the substrate. Carbohydrates, when completely oxidised, give an RQ of exactly 1.0 — equal volumes of CO₂ produced and O₂ consumed (C₆H₁₂O₆ + 6 O₂ → 6 CO₂ + 6 H₂O). Fats are richer in hydrogen than carbohydrates, so more O₂ is needed to oxidise them relative to the CO₂ produced — the RQ of tripalmitin (a fat) works out to 0.7 (2 C₅₁H₉₈O₆ + 145 O₂ → 102 CO₂ + 98 H₂O). Proteins sit between, with an RQ of about 0.9. Organic acids, being already partially oxidised, give an RQ greater than 1.0. In real plants, respiratory substrates are usually mixed — pure proteins or pure fats are almost never used alone, so observed RQ values typically sit somewhere between these benchmarks.