Short, high-concentration peaks of the atmospheric pollutant ozone (O 3 ) cause the formation of cell death lesions on the leaves of sensitive plants. Numerous similarities between the plant responses to O 3 and pathogens suggest that O 3 triggers hypersensitive response-like programmed cell death (PCD). We examined O 3 and superoxide-induced cell death in the O 3 -sensitive radical-induced cell death1 (rcd1) mutant. Dying cells in O 3 -exposed rcd1 exhibited several of the typical morphological characteristics of the hypersensitive response and PCD. Double-mutant analyses indicated a requirement for salicylic acid and the function of the cyclic nucleotide-gated ion channel AtCNGC2 in cell death. Furthermore, a requirement for ATPases, kinases, transcription, Ca 21 flux, caspase-like proteolytic activity, and also one or more phenylmethylsulfonyl fluoridesensitive protease activities was shown for the development of cell death lesions in rcd1. Furthermore, mitogen-activated protein kinases showed differential activation patterns in rcd1 and Columbia. Taken together, these results directly demonstrate the induction of PCD by O 3 .

Dysfunction and downregulation of dad (defending against death) has been linked to programmed cell death (PCD) in animals and plants. As DAD is an essential subunit of the oligosaccharyltransferase that is located in the ER membrane, the results have raised the possibility that downregulation of N-linked glycosylation could be involved in the regulation of PCD. Here we show that the 16 kDa subunit of phytepsin, a vacuolar proteinase, is normally processed and glycosylated at the onset of DNA fragmentation in germinating barley scutella. Two cDNA clones encoding dad (dad1, dad2), and one cDNA encoding another subunit of the same oligosaccharyltransferase complex (ost1) were isolated from barley. Northern analysis of germinating scutella show that the expression of only dad1 is declining before onset of DNA fragmentation. In contrast to this, the expression of both dad2 and ost1 increase before onset of DNA fragmentation.

Metirman JH, Kuittinen T, Kangas M, Tuisku T: Buffering effect of antacids in the mouth -a new treatment of dental erosioti? ScandJ Dent Res 1988: 96: 412 7.Abstract -Antacids are drugs of choice in the treatmeiU of reflux esophagitis and peptic ulcer disease, where acid regurgitation may cause dental erosion. Since there are no specific preventive measures or effective treatment for erosions, the present study was made to asse.ss whetlier the keeping of antacids in the mouth before swallowing would be beneficial with regard to their effect on mouth pH, after acidic challenge. Fi\'e healthy subjects formed the test panel. After meastiring tlie acid binding capacity of al] the antacid preparations in the Finnish market, the two most effective were selected for testing, one in emulsion form (Novaluzid), the other a tablet (Link). Acid regurgitation was mimicked by consuming a low-pH (3.2} drink immediately before the antacid. Control series were made with the acidic drink only. Both the antacids were found to counteract totally the pH fall caused by the drink, when measured as changes in the tongue surface pH. The Novaluzid preparation was more effective than the Link preparation but the difference was not significant. It may be anticipated that patients, suffering from acid regurgitations would benefit if they are counseled to keep their antacids in the mouth for a while before swallowing.