Cell death is an irreversible loss of structure and function. Cells die primarily by one of two major mechanisms, that is, by necrosis or apoptosis (Arends and Wyllie, 1991; Walker et al, 1988; Wyllie et al., 1980). Cell death by necrosis occurs as a result of a marked toxic or physical insult. For many years, cell death had been synonymous with necrosis and felt to be a result of massive 186tissue damage and widespread cell injury, often following exposure to high concentrations of chemicals. In necrosis, there occurs an irreversible increase in the permeability of mitochondrial and plasma membranes, resulting in the cells being stained by vital dyes such as trypan blue. In vivo, necrosis often affects groups of cells, and an inflammatory reaction is commonly observed. The histological appearance of necrosis is well documented, and there is good agreement of its ultrastructural features in a wide range of cells. At an early stage, when the mitochondria generally swell, autophagocytosis may increase. Mitochondrial matrix densities are often observed in necrotic cells committed to die. This is often accompanied by irregular dense clumping of chromatin, progressive dissolution of ribosomes, and focal disruption of plasma and organelle membranes. At later stages of necrosis, karyolysis is observed.