Toxicity

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Across
  1. 3. Metabolic signal that links ATP consumption at the cellular level to increased whole-body ventilation.
  2. 5. Inner-membrane protein complex that oxidizes NADH, initiates proton pumping, and is commonly impaired in mitochondrial myopathies.
  3. 7. Final step of aerobic respiration where electrons, protons, and molecular oxygen combine to prevent upstream redox backup.
  4. 9. Unique inner-mitochondrial enzyme that participates directly in the TCA cycle while simultaneously donating electrons to the electron transport chain.
  5. 11. Clinical intervention that reduces hyperthermia by limiting sustained skeletal muscle contraction rather than correcting mitochondrial dysfunction.
  6. 13. Shuttle that preserves cytosolic reducing equivalents as NADH rather than converting them to FADH₂.
  7. 16. Carbon-containing gas that binds heme iron, interferes with electron transport, and shifts the oxyhemoglobin dissociation curve.
  8. 17. Clinical state in which mitochondrial oxygen consumption is increased, ATP production is inefficient, and heat generation predominates.
  9. 18. Lipophilic electron carrier whose deficiency is theorized (but not proven) to contribute to statin-associated myopathy.
Down
  1. 1. Electrochemical force composed of charge separation and proton concentration difference that stores energy for ATP synthesis.
  2. 2. Cellular condition in which rising ADP accelerates oxygen consumption by increasing electron transport flux.
  3. 4. Inner mitochondrial membrane property that is essential for coupling electron transport to ATP synthesis.
  4. 6. Toxin that produces cellular hypoxia despite adequate oxygen delivery by preventing its role as a terminal electron acceptor.
  5. 8. Protein expressed in neonatal adipose tissue that allows controlled proton leak to generate heat without ATP.
  6. 10. Weight-loss compound causes extreme hyperthermia, tachypnea, and diaphoresis despite preserved oxygenation; mechanism involves dissipation of the proton gradient.
  7. 12. Metabolic consequence of ETC blockade characterized by increased lactate due to impaired NAD⁺ regeneration.
  8. 14. The mitochondrial compartment that becomes relatively negative during active electron transport.
  9. 15. Physiologic mechanism in which energy from fuel oxidation is intentionally diverted away from ATP generation.