Helicobacter pylori is a gram negative spiral bacterium, which is colonized in human gastric mucosa. This organism was first reported in Australia, 1983. Now H. pylori has been recognized to cause chronic active gastritis, and is a major factor in the pathogenesis of duodenal ulcer and gastric ulcer. It was also reported that its infection is a risk factor for both MALT (mucosa associated lymphoid tissue) lymphoma and gastric adenocarcinoma. H. pylori has many virulence factors. Urease is one of the most important colonization and virulence factors studied. Ammonia made by urease protects the organisms from gastric low pH, and is toxigenic to gastric epithelial cells. Vacuolating toxin and CagA proteins are thought to be pathogenic agents especially for causing gastric and duodenal ulcers. Neutrophil reactions against the bacteria, and the abnormal immunological reactions are also considered to cause the damage of gastric epithelial cells, although the detailed pathogenic mechanisms are still not clear. In developing countries, infection by H. pylori is established in childhood, and the organisms can be identified in the mouth and feces, indicating its infection through water. The infected organisms can be eradicated by administration with proton pump inhibitor and one or two antibiotics. This may provide an useful therapeutic means to the patients especially with recurrent ulceration and MALT lymphoma.

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(E)-4-Hydroxy-2-nonenal (HNE) is a major breakdown product of lipid peroxides formed from n-6 fatty acids. This aldehyde has high reactivity towards nucleophilic groups of proteins or nucleic acids, and exerts significant deleterious effects on cell functions and viability. While, HNE in vivo is rapidly metabolized to 4-hydroxy nonenoic acid, 1, 4-dihydroxynonene and HNE-glutathione conjugate by enzymatic systems, but the metabolism is depressed in aging and various pathological conditions. HNE may, therefore, play a key role in the initiation and development of oxidative damage in biological system. This review outlines the formation and metabolism of HNE including our proposed mechansim on the toxic effect of the HNE-glutathione conjugate.

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The thermal properties of a characteristic pyrolyzed product from the smoking of methamphetamine (MA) with tobacco, N-cyanomethylmethamphetamine (CMMA), in a free form and a hydrochloric salt (HCl salt) were investigated by thermogravimetry (TG)-differential thermal analysis and TG-mass spectrometry in comparison with those of MA and its hydrochloride (MA·HCl). The stability of CMMA·HCl in water, physiological saline and plasma was investigated by gas chromatography (GC), GC-mass spectrometry and nuclear magnetic resonance spectrometry. CMMA was stable when heated in a base form, but not in a HCl salt form, whereas MA was stable when heated in either form. CMMA began to vaporize without any decomposition at a temperature (80°C) higher than MA did (30°C). CMMA·HCl, in contrast, decomposed with a weight loss at over 100°C, although MA·HCl began to decrease appreciably at a higher temperature than its fusion point (174°C). CMMA and CMMA·HCl stored as a pure form or in organic solvents in a refrigerator did not decompose over a 12 month period. However, CMMA·HCl was primarily unstable in any aqueous medium of water, physiological saline or plasma. The lower concentration of CMMA·HCl in the aqueous medium and the higher temperature of the medium appreciably accelerated its decomposition rate. Even if stored at 4°C, CMMA·HCl in plasma at 0.01 mg/ml decreased to 65% of initial value after 2 h, and when stored at 37°C, it had completely decomposed after 2 h. Our results, however, indicated that treatment of CMMA as a free base form at a temperature lower than 4°C and within 30 min after defrosting minimized its decomposition in an aqueous medium. It was demonstrated that CMMA·HCl in aqueous media decomposed largely to MA, CH₂O and HCN.

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The formation of methylglyoxal in rat liver microsomes by reduced nicotinamide adenine dinucleotide phosphate-dependent lipid peroxidation and its binding to proteins were studied. Methylglyoxal in the microsomes of rat liver after enzymic lipid peroxidation was identified as its fluorescent derivative, 2-(2-benzimidazolyl)-3-methyl-quinoxaline, by gas chromatographymass spectrometric determination. The contents of both thiobarbituric acid reactive substances and methylglyoxal showed time-dependent increases until 80 min after the start of lipid peroxidation. The production of thiobarbituric acid reactive substances and methylglyoxal in microsomes by lipid peroxidation was supressed by heat treatment (24.3 and 26.3%, respectively) and by the addition of catalase (EC 1.11.1.6) (28.5 and 67.1%) or superoxide dismutase (EC 1.15.1.1) (74.3 and 49.9%). Methylglyoxal, formed in microsomes by the peroxidation, existed in the high molecular weight fractions of the reaction mixture, which were separated by gel filtration chromatography with a Sephadex G-25 column. These results suggest that methylglyoxal derived by enzymic lipid peroxidation in rat liver microsomes binds readily to microsomal proteins.

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Maltol is a food additive used worldwide, while it enhances the brain toxicity of aluminum (Al). Al injected with maltol is primarily transferred to the liver and so it may also cause hepatic injury. Kojic acid is used as a food additive in Japan and is structurally related to maltol. Therefore, the hepatotoxicity of Al with maltol was compared to that of Al with kojic acid in mice. Al injected intravenously with maltol in a 1 : 4 molar ratio at a dose of 0.25 mmol Al/kg caused an increase in the plasma activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) despite lower hepatic Al concentration than those found after administration in a 1 : 2 molar ratio and with Al only. At the same time, hepatic phosphorus and sulfur (S) levels decreased. The decrease in the S level was ascribed to that in the taurine content. The increase in urinary taurine was also observed. Al alone, maltol alone, or Al : kojic acid at a ratio of 1 : 4 did not alter the plasma activities of AST and ALT or the hepatic element levels. These findings may suggest that tris (maltolato) aluminum (III) (Al (maltol)₃) is a hepatotoxin.

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To assess the LC/MS methods for the determination of these compounds in biological materials positive ion mass spectra were measured for benzodiazepines and their metabolites by thermospray-liquid chromatography/mass spectrometry (TSP-LC/MS) and atomospheric pressure chemical ionization-liquid chromatography/mass spectrometry (APCI-LC/MS). In both TSP-LC/MS and APCI-LC/MS, LC analyses were performed on a TSKgel octyl-80Ts in the solvent system of methanol-ammonium acetate at a flow rate of 1.0 ml/min. TSP mass spectra showed only a [M+H]⁺ ion for most of compounds, while APCI mass spectra showed [M+H]⁺ and some fragment ions. The analysis of these compounds with TSP gave better detection limits than with APCI by scan mode, and gave the same results for detection limits as with APCI by selected ion monitoring (SIM). The data, described in this paper, should serve as a basis for the qualitative and quantitative analyses of benzodiazepines and their metabolites in biological samples.

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A difference in adsorption characteristics of β-carotene between one component (β-carotene) and two components (β-carotene and constant concentration of triolein) in n-hexane solution was investigated in order to elucidate the inhibition effect of triolein on β-carotene adsorption by attapulgites and sepiolites. The adsorption rate of triolein was faster than that of β-carotene in the two components hexane solution. The amount of β-carotene adsorbed per minitue at the very beginning of adsorption decreased to approximately 1/2-1/3 of that in the one component hexane solution. A decrease in the amount of triolein desorbed in hexane suggests that small number of adsorbed triolein were covered with β-carotene adsorption and that the rest of adsorbed triolein was independent of adsorption sites of β-carotene on adsorbent. Adsorption isotherms of β-carotene in the two components hexane solution were a typical Langmuir type in which the plot of adsorbed amount against the residual concentration gives a flat curve. Triolein adsorption capacity of adsorbent was proportional to the decrease in the amount of adsorbed β-carotene and this fact indicates that one molecule triolein adsorption inhibits 0.84 molecule β-carotene adsorption.

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A versatile analytical method using liquid-liquid extraction and GC/MS for nicotine and cotinine in the urine was developed. Concentrations of nicotine and cotinine in the urine from 5 non-smokers and 6 smokers were analyzed by this method. The levels of nicotine and cotinine in the urine of smokers were 17-2200 ng/ml and 120-3200 ng/ml, respectively. On the contrary, their levels in the urine of non-smokers were below the detection limit except persons accepting passive smoking. The variations of the concentrations of nicotine and cotinine and that of mutagenic activity after smoking were similar and reached maxima at 3-6 h after smoking.

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Dichloromethane levels in wastewater discharged from chemical laboratories were measured. The average concentrations of this compound in wastewater untreated and treated by a chemical wastewater treatment plant were 0.17 and 0.07 mg/l, respectively. Using a vacuum pump instead of aspirator to evaporate this solvent in the laboratories effectively reduced the amount of dichloromethane in wastewater. Furthermore, the removal efficiency of dichloromethane in the treatment plant of chemical wastewater by use of activated carbon adsorption and coagulation precipitation processes was investigated. The results of monitoring for one year showed that the removal efficiency of dichloromethane from wastewater in the treatment plant was on the average 67.4%. Our experiments showed that the prolongation of reaction time of activated carbon adsorption to 30 min sufficiently improved the removal efficiency of dichloromethane. Activated carbon adsorption process was very effective to remove this compound, but coagulation precipitation process was not effective.

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