Energetics of midvelocity emissions in peripheral heavy ion collisions at Fermi energies.

Peripheral and semiperipheral collisions have been studied in the system 93Nb+93Nb at 38A MeV. The evaporative and midvelocity components of the light charged particle and intermediate mass fragment emissions have been carefully disentangled. In this way it was possible to obtain the average amount not only of charge and mass, but also of energy, pertaining to the midvelocity emission, as a function of an impact parameter estimator. This emission has a very important role in the overall balance of the reaction, as it accounts for a large fraction of the emitted mass and for more than half of the dissipated energy. As such, it may give precious clues on the microscopic mechanism of energy transport from the interaction zone toward the target and projectile remnants.

O6-alkylguanines, dietary N-nitroso compounds, and their precursors in gastric cancer.

Several N-nitroso compounds, present in foods and beverages or formed in the stomach from their precursors, act as alkylating agents. By using a highly reliable technique (high-resolution gas chromatography-mass spectrometry with negative-ion chemical ionization and selected ion recording), we measured a series of specific O6-alkylguanines in snap-frozen paired stomach tissue samples (tumor and noninvolved mucosa) obtained at surgery from 24 gastric cancer patients identified in Florence, Italy. Samples of noninvolved mucosa had higher levels of total O6-alkylguanines and more frequently detectable levels (54%) than tumor samples (29.2%). O6-propylguanine and O6-methylguanine were the single adducts most frequently detected in noninvolved mucosa and tumor tissue, respectively. Tumor samples showed higher levels of total O6-alkylguanines in female patients (p = 0.03) and among those with a diffuse histological type (p = 0.06) or seronegative for Helicobacter pylori CagA antibodies (p = 0.06). Mean dietary nitrate intake was significantly higher in patients with detectable levels of adducts in tumor samples (p = 0.03). Estimated intakes of dimethylamine and N-nitrosodimethylamine correlated with total levels of O6-alkylguanines in noninvolved gastric mucosa. These findings, although based on a small series of cases, support a role for N-nitroso compounds from dietary sources in the etiology of gastric cancer.

Genetic toxicity of a mixture of fifteen pesticides commonly found in the Italian diet.

To determine the toxicological effects of complex mixtures of pesticides, we obtained data on 100 pesticide residues in common foods of central Italy. Fifteen pesticides were more regularly detected at higher levels (dithiocarbamates, benomyl/carbendazim, thiabendazole, diphenylamine, chlorthalonil, procymidone, fenarimol, chlorpropham, vinchlozolin, methidathion, chlorpyriphos-ethyl, parathion-methyl, parathion, chlorfenviphos, pirimiphos-ethyl). Using itemized data on daily food consumption in Italy, we calculated that the average exposure for an adult subject was 716 micrograms/day, ranging from 148 micrograms of dithiocarbamates to 1 microgram of pirimiphos-ethyl. We made a mixture of these 15 pesticides at concentrations proportional to the ratio determined in foods and tested it with the Salmonella-microsome assay, with and without metabolic activation with PCB-induced rat liver S9. No mutagenic activity was observed at concentrations up to 500 micrograms/plate. We also tested the same mixture at concentrations ranging from 0.1 to 20 micrograms/ml on human lymphocytes in vitro, and observed a slight but statistically significant increase in sister-chromatid exchanges at 1 microgram/ml. We also administered the mixture in corn oil by gavage to Wistar rats at doses of 1, 10, and 100 micrograms/kg. After 24 hr the ratio between bone marrow polychromatic and normochromatic lymphocytes (a sign of cellular toxicity) was decreased by the exposure, but we did not observe a significant increase in the frequency of micronuclei. We conclude that the pesticide mixture did not have appreciable genotoxic activity in the assays used.

Analysis of mutagenic activity in human urine after concentration on different resins and high-performance liquid chromatography.

Smokers' urine was tested for mutagenic activity on Salmonella typhimurium strain TA1538 with metabolic activation after adsorption on different resins and desorption with organic solvents. The amounts of XAD-2 were 1.25 and 5 g/100 ml urine, the amounts of alumina, cyanopropyl and C18 were all 5 g/100 ml and extrelut 80 g/100 ml. Adsorbed organic chemicals were eluted with acetone from XAD-2, with dichloromethane from extrelut and with a series of solvents from the other resins (hexane, toluene, dichloromethane and methanol). All columns gave similar results, with the exception of extrelut, which had poor recovery of mutagenic activity. Higher resin/urine ratios and sequences of columns gave better results. The organic eluates from XAD-2 columns loaded with the urine of patients treated with cyclophosphamide and melphalan were mutagenic on strain TA1535 with S9, and some mutagenic activity was also detectable in the aqueous eluate. Cisplatin was adsorbed on XAD-2, C18 and extrelut, but was eluted only from extrelut using dimethylformamide as a solvent. Smokers' urine was separated into several fractions with high-performance liquid chromatography, using C-18 columns with a series of solutions of 2.5 mM phosphoric acid and acetone or with a gradient of methanol. Several fractions containing dissolved organic compounds and no histidine were mutagenic with metabolic activation, but the overall mutagenic activity was still lower than the one detected with one-step chromatography on XAD-2. Using XAD-2 resins with a high ratio of resin to urine still seems to be the method of choice for studying urinary mutagenicity.

Pig plasma benzylamine oxidase: some considerations on the mechanism of the reaction.

The kinetics of benzaldehyde formation during the oxidation of benzylamine by pig plasma benzylamine oxidase have been studied at different pH values. It has been shown that the first step of the reaction catalyzed by this enzyme is the formation of a Schiff base between the amino group of the substrate and the aldehyde group of the enzyme. Present kinetic studies are consistent with this mechanism and demonstrate the existence of two steps which are alternatively rate-limiting one below pH 6.0, the other above this pH value. The rate-limiting step above pH 6.0 requires the participation of OH-. A mechanism of reaction has been proposed in which the release of products follows the sequence: hydrogen peroxide, aldehyde, ammonia.