Electron Transport Chain (ETC) and Oxidative Phosphorylation : Mnemonic

General concepts of ETC and Oxidative Phosphorylation:

mitochondria glucose catabolism

1. Occurs in cell cytosol: Glycolysis

2. Occurs in mytochondrial matrix: Kreb’s (TCA) cycle

3. Occurs in mitochondrial inner membrane: ETC – Stepwise movement of electrons from high energy to low energy that activates proton pump which transports proton from the mitochondrial matrix to mitochondrial inter-membrane and generate Proton gradient.

4. Occurs in mitochondrial intermembrane space: Creation of proton gradient

5. Occurs in mitochondrial inner membrane: Oxidative phosphorylation – This proton gradient generated from ETC is used by Oxidative Phosphorylation to generate ATP by phosphorylation of ADP to ATP.

6. Oxygen is the final electron acceptor: We breathe in oxygen with our lungs, transport it with red blood cells in our arteries to cells, and oxygen is ultimately used inside the mitochondria of every cell to accept electrons at the end of the electron transport chain to form water.

ATP produced from a molecule of glucose:

Each NADH yields 2.5 ATP and each FADH2 yields 1.5 ATP.

1. Glycolysis: 

  • 2 ATP
  • 2 NADH → 2 FADH2 (to ETC) = 3 ATP

2. Conversion of Pyruvate to Acetyl CoA:

  • 1 glucose forms 2 pyruvate
  • 2 NADH (to ETC) = 5 ATP

3. Kreb’s cycle: 2 Pyruvate from 1 glucose ~ 2 of each of following

  • ATP from GTP (1 site: Succinyl-CoA synthetase): 2 ATP
  • NADH (3 sites: Isocitrate dehydrogenase, Alpha-ketoglutarate dehydrogenase, Malate dehydrogenase): 6 NADH = 15 ATP
  • FADH2 (1 site: Succinate dehydrogenase): 2 FADH2 = 3 ATP

Total: (2+3) + (5) + (2+15+3) = 30 ATP

In contrast, total yield from 1 molecule of glycogen is 31 ATP:

  1. Glycogen is converted into glucose-1-phosphate (G1P)
  2. G1P is converted into glucose-6-phosphate (G6P) – this skips the 1st step of glycolysis catalized by Glucokinase/Hexokinase which uses 1 ATP

MNEMONIC: NADH Sends Bad (negative) charge And Formulate ATP

Complex I (NADH): NADH : CoQ oxidoreductase

  • NADH dehdrogenase
  • Ubiquinone (CoQ)

Complex II (Sends): Succinate : CoQ oxidoreductase

Complex III (Bad charge):

  • Cytochrome b/c1
  • Cytochrome c

Complex IV (And): Cytochrome a/a3 (Cytochrome oxidase)

Complex V (Formulate): F0F1 ATP synthase complex



electron transport chain

Complex I: NADH : CoQ oxidoreductase

  • NADH dehdrogenase: transfers 2 electrons from NADH to Ubiquinone (CoQ)
  • Ubiquinone (CoQ): Ubiquinone (QH2) is reduced to ubiquinol (free to diffuse within membranes)
  • 4 H+ ions move to intermembranous space

Complex II: Succinate : CoQ oxidoreductase

  • Succinate dehydrogenase (In TCA cycle): converts succinate to fumarate and produces FADH2 from FAD
  • Like in Complex I, FADH2 transfers 2 electrons to CoQ
  • Other electron donors from FADH2 are: Fatty Acyl CoA Dehydrogenase, Glycerol 3 Phosphate shuttle
  • It is not a proton pump

Complex III (Fe/heme protein):

  • Cytochrome b/c1: removes 2 electron from QH2 and transfers to 2 molecules of cytochrome C
  • Cytochrome c: water-soluble and located in outer mitochondrial membrane
  • Pumps 4 protons across membrane

Complex IV (Copper/heme protein): Cytochrome a/a3 (Cytochrome c oxidase)

  • Removes 4 electrons from 4 molecules of Cytochrome c and trasfers to O2 [In hypoxia, rate of ETC and ATP production decreases, which leads to increase in glycolysis (anaerobic in the abscence of oxygen) leading to lactic acidosis]
  • Produces 2 molecules of H2O (water)
  • Pumps 4 protons across membrane

4 “C”s of Complex 4

  • Cytochrome oxidase
  • Copper/heme protein
  • Carbon monoxide inhibits it
  • Cyanide inhibits it

Complex V: F0F1 ATP synthase complex

  • F0 component: Proton flows back to mitochondrial matrix from intermembrane space producing energy
  • F1 component: Energy produced is used to phosphorylate ADP using Pi


  • 1 NADH = 2.5 ATP
  • 1 FADH2 = 1.5 ATP



Inhibitors of any step result in:

  1. Decreased oxygen consumption
  2. Increased intracellular NADH/NAD and FADH2/FAD ratio
  3. Decreased ATP

Mnemonic: CRAP Tightens Muscle And Produces Muscle ACHe

Complex I inhibitors: CRAP

  • Chlorpromazine
  • Rotenone (Fish poison, pesticide – Remember “one” in the last)
  • Amobarbital/Amytal (Barbiturate)
  • Piercidin A

Doxorubicin inhibits CoQ

Complex II inhibitors: Tightens Muscle

  • Thenoyltrifluoroacetone (TTA)
  • Malonate

Complex III inhibitors: AND Produces Muscle

  • Antimycin A (Antifungal)
  • Napthoquinone
  • Dimercaprol (ABC)
  • Phenformin
  • Myxothiazole

Complex IV inhibitors: ACH

Remember, All complex IV inhibitors end with “-ide”

  • Azide
  • Carbon monoxide, Cyanide
  • Hydrogen sulphide

Cyanide poisoning: Thiosulfate forms thiocyanate which is less toxic and excreted by kidneys; Nitrites convert hemoglobin to methemoglobin (which binds cyanide in blood before reaching to tissues) – must be given shortly after exposure

Carbon monoxide poisoning: Headache, nausea, tachycardia, tachypnea, cherry-red lips and cheeks, respiratory depression and coma (treated with oxygen)

Complex V inhibitor:

  • Oligomycin (antibiotic)

ATP/ADP translocase inhibitor:

  • Atractyloside (plant toxin)



Uncouplers uncouples ETC and oxidative phosphorylation by decreasing the proton gradient causing:

  • Decreased ATP synthesis
  • Increased oxygen consumption
  • Increased oxidation of NADH

Because the rate of ETC increases, with no ATP synthsis, energy is released as heat. Important uncouplers are:

  1. 2,4 – Dinitrophenol (2,4-DNP)
  2. Aspirin (and other salicylates)
  3. Brown adipose tissue (thermogenin/natural uncoupling protein – kidneys, neck, breastplate, scapula in newborns)

Mnemonic: Uncouplers are BAD

  • Brown fat
  • Aspirin
  • Dinitrophenol



Mutations in mitochondrial DNA affect highly aerobic tissues (nerve, muscle) and is characterized by:

  1. Maternal inheritance
  2. Metabolic (Lactic) acidosis
  3. Massive proliferation of mitochondria in muslce (ragged red fibers)

Mnemonic: 3 “M“s of Mitochondrial DNA Mutation

1. MELAS (Mitochondrial Encephalopathy, Lactic Acidosis, Stroke): Mutation in Complex I

2. LHON (Leber’s Hereditary Optic Neuropathy – Loss of Central vision): Mutation in Cytochrome reductase

3. Kearns-Sayre Syndrome (short stature, external ophthalmoplegia, pigmentary retinopathy, ataxia, cardiac conduction defects): Mutation in Complex II

4. Leigh disease (lactic acidemia, developmental delay, seizure, extraocular palsies, hypotonia; fatal by age 2): Mutation in Complex IV


Abnormal signal in the basal ganglia, basal ganglia calcification, cerebral and cerebellar atrophy, bilateral striatal necrosis, cerebellar hypoplasia, infarcts, leukoencephalopathy
Lactic acidosis, elevated lactate/pyruvate ratio in blood and CSF, elevated alanine in blood and CSF, elevated CK, myoglobinuria

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