Carbon Tetrachloride

Overview
Pathogenesis
  • Overview
    • CCl4 is converted into the free radical CCl3* by Cytochrome P450 enzymes in the liver. CCl3* results in lipid peroxidation of phospholipid membranes, yielding destruction of several critical sub-cellular structures.
  • Endoplasmic Reticulum
    • Destruction of the ER causes a decline in the liver's ability to synthesize proteins, especially apolipoproteins required for export of lipids from the liver. The consequent hepatic inability to export fats causes a centrilobular pattern of necrosis and steatosis.
  • Mitochondria
    • Mitochondrial injury severely reduces the capacity of the cell to produce ATP and thus maintain cellular energy-dependent processes. Furthermore, injured mitochondria tend to produce further free radicals, amplifying free radical cell injury.
  • Plasma Membrane:
    • Injury to the plasma membrane increases the cell's permeability to toxic ions such as calcium as described in cell injury biochemistry.