Cellular Injury

From Anvita Health Wiki

Introduction

• General mechanisms of cell injury:

• reactive oxygen metabolites
• loss of calcium homeostasis

• activation of Ca+2-dependent proteases
• activation of Ca+2-dependent phospholipases
• activation of Ca+2-dependent ATPases
• activation of Ca+2-dependent endonucleases

• ATP depletion
• defects in membrane permeability
• genetic aberrations
• Sequence of events ( hypoxic & ischemic cellular injury):
• compromise of mitochondrial oxidative phosphorylation

• decreased cellular ATP

• failure of plasma-membrane Na+/K+ ATPase

• increased glycolysis

• diminished glycogen stores
• accumulation of lactic acid

• increased inorganic phosphate
• decreased creatine phosphate stores

• cellular edema

• dilation of the endoplasmic reticulum
• loss of cellular polarity

• ribosomal disruption

• detachment of ribosomes from endoplasmic reticulum
• dissociation of polysomes into monosomes

• formation of blebs
• loss of microvillae
• mitochondrial swelling
• injury to lysosomal membranes.
• The duration of ischemia require to produce irreversible cell injury varies with tissue:
• hepatocyte: 1-2 hours
• neuron: 3-5 minutes
• Morphologic changes:
• light microscopy

• cellular swelling
• fatty change

• electron microscopy

• plasma membrane alterations

• blebbing
• distortion of microvilli
• formation of myelin figures
• loosening of intercellular attachments
• alterations in the cytoskeleton

• mitochondrial changes

• swelling
• rarefaction
• appearance of small amorphous phospholipid-rich amorphous densities

• ribosomal disruption

• dilation of the endoplasmic reticulum
• detachment of ribosomes from endoplasmic reticulum
• dissociation of polysomes into monosomes

• nucleolar alterations

More General Terms

• injury

References

Cotran et al Robbins Pathologic Basis of Disease, 5th ed. W.B. Saunders Co, Philadelphia, PA 1994 pg 4-9

cellular injury