title: Critical pH level of lye (NaOH) for esophageal injury.
abstract: OBJECTIVE
  Lye (NaOH) ingestion in humans often results in alkaline damage to the esophagus, but knowledge about this process is limited. Here, we explore the effects of lye on esophageal epithelial structure and function using rabbit esophageal epithelium as a model of lye ingestion.
  
  
  METHODS
  Rabbit esophageal epithelium was mounted in Ussing chambers so that the electrical potential difference (PD), short-circuit current (I (sc)), and transepithelial resistance (R (T)) could be monitored before, during, and after mucosal exposure to lye (NaOH) at pHs ranging from 7.4 to 12.1. Histopathology and dextran fluxes were also performed and correlated with the electrical data.
  
  
  RESULTS
  Mucosal exposure to lye at pHs <11.5 had no damaging effects on the esophagus. However, at pHs >or=11.5, damage was both time- and pH-dependent, as noted by increases in PD and I (sc), and declines in R (T). Further, the electrical changes were paralleled morphologically by epithelial liquefaction necrosis and increases in dextran flux. Also, by pretreating tissues with ouabain, the early lye-induced rise in PD and I (sc) was shown to result from a combination of increased active (sodium) transport and passive (sodium) diffusion which indicates that, even early on, the damaging effects of lye include changes in both apical cell membranes and tight junctions of this epithelium.
  
  
  CONCLUSIONS
  Lye (NaOH) injury to the esophageal epithelium is both pH- and time-dependent, but requires a minimum pH of 11.5. At pHs >or=11.5, lye produces liquefaction necrosis, an injury that involves both cellular and junctional barriers, and which markedly increases epithelial permeability to ions and uncharged molecules. Based on these results, non-industrial cleaning products in the home are likely to be safer if they have a concentration of lye below pH 11.5.
authors.affiliation: Department of Gastroenterology, Marmara University School of Medicine, Istanbul, Turkey. ozlenatug@hotmail.com
authors.forename: Ozlen
authors.initials: O
authors.lastname: Atug
authors.forename: Ahmet
authors.initials: A
authors.lastname: Dobrucali
authors.forename: Roy Charles
authors.initials: RC
authors.lastname: Orlando
mesh_terms: D000818:Animals; D002424:Caustics / Q000633:toxicity*; D002462:Cell Membrane / Q000187:drug effects / Q000473:pathology; D004058:Diffusion; D017097:Electric Impedance; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004935:Esophageal Diseases / Q000139:chemically induced* / Q000473:pathology; D004947:Esophagus / Q000187:drug effects* / Q000293:injuries / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials; D009092:Mucous Membrane / Q000187:drug effects / Q000473:pathology; D009336:Necrosis; D010042:Ouabain / Q000494:pharmacology; D010539:Permeability; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D012972:Sodium Hydroxide / Q000633:toxicity*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism; D019108:Tight Junctions / Q000187:drug effects / Q000473:pathology; D013997:Time Factors
chemical_list: D002424:Caustics; D004791:Enzyme Inhibitors; D012972:Sodium Hydroxide; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase