Mechanisms of Cell Injury: Hypoxia, Free Radicals, Toxins
Start with the big picture
The lesson traces hypoxic injury from reduced oxidative phosphorylation and ATP depletion to pump failure, cellular swelling, lactic acidosis, and calcium-activated damage. It distinguishes ischemia from hypoxemia and outlines how reperfusion may add oxidative and inflammatory stress. It then examines reactive oxygen species: their sources, effects on lipids, proteins, and DNA, and the antioxidant defenses that limit them. Chemical injury is organized into direct-acting toxins and toxins that require CYP450 bioactivation, with examples such as cyanide, mercury, carbon tetrachloride, and acetaminophen. Together, these mechanisms clarify how different insults converge on membrane, mitochondrial, and other cellular injury.
What you'll learn
- Trace how hypoxia-driven ATP depletion disrupts cellular ion balance and metabolism.
- Identify changes associated with progression toward irreversible cell injury.
- Distinguish ischemic injury from hypoxemia and describe added stress from reperfusion.
- Explain how reactive oxygen species damage cellular components and how antioxidants counter them.
- Compare direct-acting toxins with toxins requiring metabolic bioactivation.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
