Harvesting Chemical Energy PDF

Harvesting Chemical Energy Describe the processes involved in the generation of ATP from the breakdown of a glucose molecule Where do we get the glucose molecule from? Carbohydrates - broken down to simple sugars Proteins - broken down to amino acid Fats - broken down to simple fats Conversion of gl...

Harvesting Chemical Energy Describe the processes involved in the generation of ATP from the breakdown of a glucose molecule Where do we get the glucose molecule from? Carbohydrates - broken down to simple sugars Proteins - broken down to amino acid Fats - broken down to simple fats Conversion of glucose to ATP 1) 2) 3) 4) Glycolysis Pyruvate oxidation Citric acid cycle (or Krens cycle) Electron transport chain Where does cellular respiration (production of ATP) occur? The process occurs in the mitochondria. The main purpose of of generating ATP is for cellular work Including an overall description of the processes, where those processes occur and the net number of ATP molecules produced per glucose molecule broken down. A) Glycolysis Glycolysis, the initial step in glucose breakdown, occurs in the cytosol of cells. It’s like the opening act of a grand metabolic concert. Here’s a simplified version of what happens during glycolysis: 1. Glucose Splitting: ○ Glycolysis, which means “sugar splitting,” begins with a six-carbon glucose molecule. ○ This glucose is elegantly split into two three-carbon sugars: dihydroxyacetone phosphate (DHAP) and glyceraldehyde-3-phosphate (G3P). ○ These smaller sugars twirl and sway, preparing for their transformation. 2. Energy Investment and Payoff: ○ The performance unfolds in two acts: i. Energy Investment Phase: 1. The cell invests energy by using ATP. Two ATP molecules are spent during this phase. 2. The dancers (DHAP and G3P) undergo rearrangements, setting the stage for the next act. ii. Energy Payoff Phase: 1. Here’s where the magic happens! ATP is produced through substrate-level phosphorylation 2..NAD+ (our electron carrier) is reduced to NADH as electrons are released during glucose oxidation. 3. The net energy yield per glucose molecule: 2 ATP and 2 NADH. Carbon Choreography: a. All the carbon atoms from the original glucose find their place in the two pyruvate molecules. b. No carbon escapes as CO2 during glycolysis—it’s a tightly choreographed routine. Oxygen Optional: c. Glycolysis takes the stage regardless of whether oxygen (O2) is present. d. But if O2 joins the performance, the energy stored in pyruvate and NADH can be further extracted through pyruvate oxidation, the citric acid cycle, and oxidative phosphorylation. In summary, glycolysis invests a bit of ATP upfront but ultimately yields a net gain of two ATP and two NADH per glucose molecule. These energy-rich molecules will play crucial roles in subsequent stages of cellular respiration, like the citric acid cycle and oxidative phosphorylation B) Pyruvate oxidation Pyruvate’s Journey: In eukaryotic cells, when oxygen is available, pyruvate enters the mitochondrion. There, it undergoes a transformation akin to a backstage costume change. The multienzyme complex, pyruvate dehydrogenase, orchestrates three reactions: 1. Pyruvate’s carboxyl group is removed, releasing a carbon dioxide (CO₂) molecule. 2. The remaining two-carbon fragment binds to coenzyme A (CoA), forming acetyl CoA. 3. NADH is produced during this process. C) The Citric Acid Cycle (Krebs Cycle): ○ ○ This cycle functions as a metabolic furnace, further oxidizing organic fuel. Each turn of the cycle: ○ ○ ○ ○ Two carbons (in the form of an acetyl group) enter. Two different carbons leave as fully oxidized CO₂ molecules. The cycle generates one ATP per turn through substrate-level phosphorylation. Most of the chemical energy transfers to NAD+ and FAD during redox reactions. Reduced coenzymes, NADH and FADH₂, carry their cargo of high-energy electrons to the electron transport chain. The citric acid cycle is also known as the tricarboxylic acid cycle or the Krebs cycle, honoring scientist Hans Krebs. Understand the difference between substrate-level phosphorylation and oxidative phosphorylation and how the electron transfer chain builds a proton gradient across the inner mitochondrial membrane to generate ATP. D) Electron Transport Chain 1) Electron Transport Chain (ETC): ○ This intricate ensemble of proteins resides in the inner mitochondrial membrane. ○ Electrons embark on a journey, shuttling from NADH and FADH₂ (gifts from glycolysis and the citric acid cycle) to their final destination: oxygen. ○ As electrons flow, protons (H⁺) are pumped across the membrane, creating a proton gradient. ○ Oxygen, the prima donna, accepts electrons and joins protons to form water. ○ Without oxygen, this mesmerising dance halts, and ATP production ceases. 2. Electron Flow and Proton Pumping: ○ Electrons leap from one protein to another, like notes in a symphony. ○ At each transfer, electrons surrender a bit of energy. ○ This energy fuels proton pumps, moving H⁺ ions from the matrix to the intermembrane space. ○ The proton gradient builds—an electrochemical masterpiece. 3. Aerobic Overture: ○ Oxygen orchestrates the finale, accepting electrons and completing the chain. ○ The proton gradient powers ATP synthesis via chemiosmosis. ○ ATP synthase, our conductor, spins, producing abundant ATP. 4. Hydrogen Ions’ Rush: ○ In the intermembrane space of the mitochondrion, a concentration gradient builds up. ○ H⁺ ions, like eager dancers, rush down this gradient. ○ Their journey through ATP synthase sets the stage for ATP production. 5. ATP Synthase Turbine: ○ Picture ATP synthase as a delicate turbine, poised to spin. ○ As H⁺ ions flow through ATP synthase, it rotates—a mesmerizing pirouette. ○ This rotation enables the phosphorylation of ADP, transforming it into ATP. ○ Each spin of the turbine generates ATP, like musical notes in a symphony. 6. The Grand Finale: ○ For every glucose molecule, this elegant dance produces 26 or 28 ATP. ○ Oxygen, our silent conductor, orchestrates this process—an aerobic masterpiece. Chemiosmosis: ○ ○ ○ ○ ○ Picture ATP synthase as a delicate turbine, poised to spin. H⁺ ions, like eager dancers, rush down the proton gradient. Their journey through ATP synthase sets the stage for ATP production. As ATP synthase spins, it elegantly phosphorylates ADP, creating ATP. This efficient process produces the bulk of ATP—much more than substrate phosphorylation. Oxidative Phosphorylation: ○ This process occurs in the inner mitochondrial membrane. ○ It’s like a high-energy relay race: NADH and FADH₂, produced during glycolysis and the citric acid cycle, carry electrons. These electrons flow through a series of protein complexes in the electron transport chain (ETC). As electrons move, protons (H⁺) are pumped across the membrane, creating a proton gradient. The final complex, ATP synthase, harnesses this gradient to generate ATP. ○ In summary, NADH and FADH₂ donate electrons, and the ETC pumps protons, leading to ATP synthesis. Substrate Phosphorylation: ○ This simpler method directly transfers a phosphate group from a substrate to ADP. ○ Glycolysis and the citric acid cycle participate in substrate phosphorylation: During glycolysis, substrate-level phosphorylation produces ATP. In the citric acid cycle, one ATP is generated per turn via the same process. Absolutely! Our cellular energy factories are versatile—they don’t rely solely on glucose. Let’s explore how other molecules contribute to the ATP dance: 1. Fats (Lipids): ○ Lipids, such as triglycerides, store abundant energy. ○ Before they hit the metabolic stage, they’re broken down into glycerol and fatty acids. ○ Glycerol enters glycolysis, while fatty acids undergo beta-oxidation and enter the citric acid cycle. ○ The result? NADH, FADH₂, and ATP—all fuel for our cellular engines. 2. Proteins: ○ Proteins, our cellular architects, can also yield energy. ○ First, they’re disassembled into amino acids. ○ These amino acids take different routes: Some enter glycolysis or the citric acid cycle directly. Others contribute to the synthesis of intermediates. ○ The energy-rich products include ATP and NADH. 3. Complex Carbohydrates: ○ Starches and glycogen, our carbohydrate storage vaults, release energy. ○ They’re broken down into monosaccharides (like glucose). ○ These monomers join the glycolysis party or enter the citric acid cycle. ○ The outcome? More ATP, NADH, and FADH₂. 4. Monomers’ Dance: ○ Each monomer—whether from fats, proteins, or complex carbs—has its own backstage pass. ○ They enter glycolysis or the citric acid cycle at different checkpoints. ○ Together, they harmonise, fueling the grand ATP production. Glycolysis regulation, where phosphofructokinase-1 (PFK1) takes center stage as the “gatekeeper.” Imagine a metabolic theater where ATP, AMP, and citrate play pivotal roles. 1. Phosphofructokinase-1 (PFK1): ○ This enzyme catalyzes the third step in glycolysis, where fructose 6-phosphate transforms into fructose 1,6-bisphosphate. ○ It’s a crucial checkpoint because this reaction is the first irreversible step of glycolysis. ○ PFK1 is like the bouncer at the nightclub—it decides whether glucose gets past the velvet rope. ○ The presence of different hexokinase enzymes in different cell types adds complexity. These isozymes allow differential control over hexose phosphorylation. ○ PFK1 can use multiple hexoses as substrates, including mannose, fructose, and 2-deoxyglucose. 2. Regulation of PFK1: ○ Inhibition: Citrate (a product of the citric acid cycle) and ATP act as stern bouncers, inhibiting PFK1. When cellular energy is abundant, these molecules signal PFK1 to slow down the glycolytic party. ○ Stimulation: AMP (adenosine monophosphate) plays the role of an enthusiastic promoter. When ATP is rapidly consumed (like during intense exercise), AMP accumulates. AMP activates PFK1, encouraging more glucose to enter glycolysis. In summary, PFK1 dances between inhibition and stimulation, ensuring that glycolysis proceeds efficiently based on cellular energy needs. It’s a metabolic tango where ATP, AMP, and citrate lead the steps! Be able to describe the roles of insulin and glucagon in the body, and how these contribute to blood sugar levels. Insulin and glucagon, two key players in maintaining blood sugar balance. Imagine them as a dynamic duo, orchestrating a delicate dance within your body. 1. Insulin: ○ Produced by beta cells in the Islets of Langerhans (located in the pancreas). ○ Function: Insulin acts as a traffic controller, ensuring that glucose (blood sugar) is efficiently utilized. ○ When blood glucose levels rise (after a meal), insulin: Signals cells throughout your body to absorb glucose from your bloodstream. Promotes glucose uptake into cells for energy production or storage (especially in the liver). 2. Glucagon: ○ Produced by alpha cells in the Islets of Langerhans (also in the pancreas). ○ Function: Glucagon plays the role of an emergency responder. ○ When blood glucose levels drop (between meals or during fasting), glucagon: Signals your liver and muscle cells to convert stored glycogen back into glucose. Releases this glucose into your bloodstream, ensuring that your other cells have a steady supply of energy. Describe the fundamental pathology of Diabetes Mellitus. Diabetes Mellitus: A metabolic condition where the body’s ability to produce or respond to insulin is impaired. This results in abnormal carbohydrate metabolism and elevated blood glucose levels. Let’s explore further: 1. No Glucose in Cells: ○ When insulin isn’t functioning properly, glucose struggles to enter cells. ○ Without glucose, cells lack their primary source of ATP (energy). ○ Glycogen, the stored form of glucose, remains untapped for harder times. 2. Diabetes Mellitus: ○ It’s like a disrupted orchestra—where insulin, the conductor, faces challenges. ○ Type 1 diabetes: The body’s immune system attacks insulin-producing cells in the pancreas. ○ Type 2 diabetes: Cells become resistant to insulin, leading to elevated blood sugar levels. ○ Chronic high blood sugar can harm blood vessels, nerves, and organs. 3. Symptoms: ○ Being very thirsty. ○ Urinating often. ○ Feeling much more tired than usual. ○ Blurry vision. ○ Unintentional weight loss. 4. Management: ○ Lifestyle changes (diet, exercise). ○ Medications (oral or insulin injections). ○ Regular monitoring of blood sugar levels. 1. symptoms of Diabetes: ○ Increased Hunger: Elevated blood sugar levels lead to cellular hunger. Despite having excess glucose in the bloodstream, cells struggle to utilize it effectively. ○ Significant Weight Loss: When glucose can’t enter cells due to insulin deficiency or resistance, the body turns to alternative energy sources (such as fat and muscle). This results in unintended weight loss. 2. Pathological Consequences: ○ Altered Blood Volume and Osmolarity: High blood sugar levels cause osmotic imbalances. Water moves from cells into the bloodstream, leading to increased blood volume and altered osmolarity. This can strain blood vessels, kidneys, and other organs. ○ Long-Term Effects: Chronic high blood sugar can harm blood vessels, nerves, and immune systems. Complications include cardiovascular disease, kidney damage, neuropathy, and impaired wound healing. Type 1 Diabetes (Insulin-Dependent): ○ ○ ○ ○ ○ Cause: i. Autoimmune: The immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. ii. Genetic and Environmental Factors: While the exact cause isn’t fully understood, genetics and exposure to viruses may play a role. Onset: i. Usually occurs early in life, often during childhood or adolescence. Characteristics: i. No insulin production: Beta cells are destroyed, leading to insulin deficiency. ii. Requires insulin replacement: People with Type 1 diabetes need external insulin to regulate blood sugar. Prevalence: i. Affects 5–10% of diabetics. Image: i. !Type 1 Diabetes Type 2 Diabetes (Non-Insulin-Dependent): ○ ○ ○ ○ ○ Cause: i. Insulin Resistance: Cells become less responsive to insulin. ii. Lifestyle Factors: Obesity, lack of exercise, and other environmental factors contribute. iii. Genetics: Genetic predisposition plays a role. Onset: i. Usually occurs in adults, especially those over 40. Characteristics: i. Insulin Resistance: Cells don’t effectively use insulin. ii. Pancreas compensates: Initially produces more insulin. iii. Later stages: Insulin production may decrease. Linked to Other Pathologies: i. Often associated with other health conditions, including obesity. Prevalence: i. >90% of diabetics have Type 2 diabetes.