ABSTRACT-Amylold is a 39-to 43-amino-add neurotoxic peptide that aggregtes to form the core of Ahemer disease-sociated senile (amyloid) plaques. No EPR Spectrscopy and Spin Trapping. 8APs were solubilized to 1.0 mg/ml by addition of buffer [150 mM phosphatebuffered saline at pH 7.4 (PBS) or Hepes at pH 7.4] to lyophilized powder. BSA was solubilized similarly, to concentrations of 1-62 mg/ml. Buffer used for spin trapping contained 50 mM N-tert-butyl-a-phenylnitrone (PBN) (Sigma or Aldrich). In studies designed to inhibit putative metalcatalyzed reactions, the chelator deferoxamine mesylate or EDTA (Sigma) was dissolved to 10 mM in PBS/PBN prior to peptide addition. In a further attempt to nullify buffer-borne metals, PBS/PBN was stirred overnight with Chelex 100, a nonspecific metal-chelating agent.Peptide solutions were aliquoted into a 300-A4 aqueous quartz EPR flat cell that was subsequently sealed at both ends and immersed in a 3rC water bath for 0-135 hr and removed periodically for EPR analysis. EPR spectra were acquired on a Bruker (Billerica, MA) 300 EPR spectrometer equipped with computerized data acquisition software. Instrumental parameters were microwave power = 20 mW, modulation amplitude = 0.% G, gain = 1 x i1W, and conversion time =

Oxygen free radicals and oxidative events have been implicated as playing a role in bringing about the changes in cellular function that occur during aging. Brain readily undergoes oxidative damage, so it is important to determine if aging-induced changes in brain may be associated with oxidative events. Previously we demonstrated that brain damage caused by an ischemia/reperfusion insult involved oxidative events. In addition, pretreatment with the spintrapping compound N-tert-butyl-a-phenylnitrone (PBN) diminished the increase in oxidized protein and the loss of glutamine synthetase (GS) activity that accompanied ischemia/reperfusion injury in brain. We report here that aged gerbils had a significantly higher level of oxidized protein as assessed by carbonyl residues and decreased GS and neutral protease activities as compared to young adult gerbils. We also found that chronic treatment with the spin-trapping compound PBN caused a decrease in the level of oxidized protein and an increase in both GS and neutral protease activity in aged Mongolian gerbil brain. In contrast to aged gerbils, PBN treatment of young adult gerbils had no significant effect on brain oxidized protein content or GS activity. Male gerbils, young adults (3 months of age) and retired breeders (15-18 months of age), were treated with PBN for 14 days with twice daily dosages of 32 mg/kg. If PBN administration was ceased after 2 weeks, the significantly decreased level of oxidized protein and increased GS and neutral protease activities in old gerbils changed in a monotonic fashion back to the levels observed in aged gerbils prior to PBN administration. We also report that old gerbils make more errors than young animals and that older gerbils treated with PBN made fewer errors in a radial arm maze test for temporal and spatial memory than the untreated aged controls. These data can be interpreted to indicate that oxidation of cellular proteins may be a critical determinant of brain function. Moreover, it also implies that there is an age-related increase in vulnerability of tissue to oxidation that can be modified by free radical trapping compounds.

Surfactant bilayers are proposed as two-dimensional solvents for the formation of ultrathin films from surfactant, monomer, and substrate systems. Results from polymerization of styrene in sodium dodecyl sulfate bilayers adsorbed on alumina show 75% and higher conversions of adsolubilized monomer to polymer after 25 min. Uniform films of 3.4-3.6-nm thickness were formed on aluminum oxide layers on glass slides for reaction times of 30-45 min. Under varying conditions film thicknesses of 13.0 nm were also obtainable.

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