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chemical injury

Monday 30 January 2006

Pathogenesis

Some chemicals can act directly by combining with some critical molecular component or cellular organelle. For example, in mercuric chloride poisoning, mercury binds to the sulfhydryl groups of the cell membrane and other proteins, causing increased membrane permeability and inhibition of ATPase-dependent transport.

In such instances, the greatest damage is usually to the cells that use, absorb, excrete, or concentrate the chemicals - in the case of mercuric chloride, the cells of the gastrointestinal tract and kidney (Chapter 9). Cyanide poisons mitochondrial cytochrome oxidase and blocks oxidative phosphorylation. Many antineoplastic chemotherapeutic agents and antibiotic drugs also induce cell damage by direct cytotoxic effects.

Most other chemicals are not biologically active but must be converted to reactive toxic metabolites, which then act on target cells. This modification is usually accomplished by the P-450 mixed function oxidases in the smooth endoplasmic reticulum of the liver and other organs.

Although these metabolites might cause membrane damage and cell injury by direct covalent binding to membrane protein and lipids, by far the most important mechanism of membrane injury involves the formation of reactive free radicals and subsequent lipid peroxidation.

See also

- Injuries

  • cellular injuries
  • tissular injuries