Parietal cell necrosis is a relatively uncommon, direct toxic effect of certain pharmaceutical agents. The coupling of this effect in rodents in two instances to systemic phospholipidosis, and a series of mechanistic studies undertaken to evaluate thepathogenesis of the cytotoxicity are discussed. Hypotheses potentially accounting for this unusual constellation of changes are considered. The demonstrated role of cationic amphiphilicity and surface-active properties in the pathogenesis of parietal cell necrosis, and how they may be employed in cell-free systems to counter-screen this liability are presented.
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