Energy Generation in Mitochondria and Prokaryotes PDF

Energy Generation in Mitochondria (and Prokaryotes) Chapter 14 Learning Outcomes:  Structure of mitochondria  ATP, the energy currency of the cell can be obtained by 2 mechanisms: substrate-level and oxidative phosphorylation.  Cells obtain most of their energ...

Energy Generation in Mitochondria (and Prokaryotes) Chapter 14 Learning Outcomes:  Structure of mitochondria  ATP, the energy currency of the cell can be obtained by 2 mechanisms: substrate-level and oxidative phosphorylation.  Cells obtain most of their energy by a membrane-based mechanism (oxidative phosphorylation)  Mitochondrial disorders o Genetic disorders due to mitochondrial mutations Mitochondria are present in nearly all eukaryotic cells Mitochondria are dynamic in shape, location, number, and function Mitochondria are located near sites of high ATP utilization The number of mitochondria can vary with the energy needs of the cell Mitochondria produce many key metabolites via the citric acid cycle The Movement of Electrons Is Coupled to the Pumping of Protons The electrochemical gradient across the membrane generates a proton motive force which pulls the H+ back into the matrix ATP synthase in action (Chapter 4 slide 20) In mitochondria, what is the final electron acceptor in the electron transport chain?  Carbon dioxide (CO2)  Water (H2O)  NADH and FADH2  Oxygen ✅ (O22) Uncoupling agents can short-circuit the electron transport In brown fat cells, a carrier protein in the inner membrane allows protons to move down their electrochemical gradient, circumventing ATP synthase. Thus, most of the energy from the oxidation of fat is dissipated as heat rather than being converted into ATP. As a result, these cells oxidize their fat stores at a rapid rate and produce much more heat than ATP. Tissues containing brown fat serve as biological heating pads, helping to revive hibernating animals and to protect sensitive areas of newborn human babies (such as the backs of their necks) from the cold. What happens if oxidative phosphorylation malfunctions? Impairment of oxidative phosphorylation often, but not always, causes lactic acidosis, particularly affecting the central nervous system, retina, and muscle. Tissues with a high energy demand (eg, brain, nerves, retina, skeletal and cardiac muscle) are particularly vulnerable to defects in oxidative phosphorylation. The most common clinical manifestations are Seizures Hypotonia = abnormally low level of muscle tone Ophthalmoplegia= paralysis of muscles within or surrounding the eye Stroke-like episodes Muscle weakness Severe constipation Cardiomyopathy= chronic disease of heart muscle