Ketonic oxidation products of cyclobarbital.

Chemical or biochemical oxidation of cyclobarbital yielded 5-(3-oxo-1-cyclohexen-1-yl)-5-ethyl -2,4,6,- (1H,3H,5H)-pyrimidinetrione, and photochemical oxidation gave 5-(6-oxo-1-cyclohexen-1-yl)-5-ethyl-2,4,6-(1H,3H,3H)-pyrimidinetrione. These compounds were isolated and purified by TLC, and their structures were determined by UV, IR, NMR, and mass spectral data; the crystalline structure was determined by X-ray diffraction.     

Occurrence of lipid oxidation products in foods

Lipid oxidation products are ubiquitous in foods, although much variation exists in the levels present. Although these levels are generally low, the problem of lipid oxidation severely compromises the quality of some foods and limits the shelf-life of others. Lipid oxidation represents a key barrier in the development of new food products and processes, especially convenience items and processes required to manufacture them. Deleterious changes in foods caused by lipid oxidation include loss of flavour, development of off-flavours, loss of colour, nutrient value and functionally, and the accumulation of compounds which may be detrimental to the health of consumers. All foods that contain lipids are susceptible to oxidation but especially affected are foods which are dehydrated, subjected to high temperatures or cooked and subsequently stored, e.g. dehydrated eggs, cheeses and meats, foods fried in frying oils, and cooked (uncured) meats. Specific examples of compounds which are of health concern include lipid peroxides and the free radicals involved in their formation and propagation, malonaldehyde, and several cholesterol oxidation products. Coronary artery disease (CAD) may be in part caused by the consumption of lipid oxidation products.     

人尿制品乙肝表面抗原(HBsAg)的检测

目的建立尿激酶、乌司他丁及尤瑞克林等3种人尿制品乙肝表面抗原(HBsAg)的检测方法。方法采用ELISA法对尿激酶、乌司他丁、尤瑞克林进行了HBsAg的检测。结果尿激酶原料药及注射用尿激酶、乌司他丁原料药及注射用乌司他丁、注射用尤瑞克林HBsAg均为阴性。结论该法简单、安全,可作为尿激酶、乌司他丁及尤瑞克林的常规HBsAg检测方法。     

Effect of oxidation and extent of oxidation on biologically active PACs in asphalt products

Recent studies have reported divergent results in rodent cancer assays using fume condensates from a variety of asphalt products. This paper presents results of a study investigating the role of oxidation, or extent of oxidation, on these findings. Five straight run asphalts, made from widely used crude oils, were used as inputs to both production scale and laboratory oxidation units and processed to a range of softening points used in common roofing products. For each of the five asphalts studied, the oxidation reaction significantly decreased measures of polycyclic aromatic compounds (PACs) that have been linked, previously and in analyses included in this study, to tumor induction in rodent bioassays. Mutagenicity index determined by the modified Ames assay was reduced between 41% and 50% from the input asphalt to the final oxidized product. A fluorescence method tuned to a subset of PAC compounds that have been associated with carcinogenic behavior in mouse bioassays was reduced between 39% and 71%. The decrease was largest in the first quarter of the oxidation reaction. These findings indicate that oxidation, by itself, was not a likely factor in the tumor induction seen in the previous studies. Rather, other factors such as the conditions of fume generation and crude source (coupled with possible differences in distillation endpoints) were more likely to have determined the outcomes. Analyses of previously published data, presented in this paper, suggest that the modified Ames and fluorescence assays are valuable screening tools for use in future health-related asphalt research.     

Effect of oxidation and extent of oxidation on biologically active PACs in asphalt products

Recent studies have reported divergent results in rodent cancer assays using fume condensates from a variety of asphalt products. This paper presents results of a study investigating the role of oxidation, or extent of oxidation, on these findings. Five straight run asphalts, made from widely used crude oils, were used as inputs to both production scale and laboratory oxidation units and processed to a range of softening points used in common roofing products. For each of the five asphalts studied, the oxidation reaction significantly decreased measures of polycyclic aromatic compounds (PACs) that have been linked, previously and in analyses included in this study, to tumor induction in rodent bioassays. Mutagenicity index determined by the modified Ames assay was reduced between 41% and 50% from the input asphalt to the final oxidized product. A fluorescence method tuned to a subset of PAC compounds that have been associated with carcinogenic behavior in mouse bioassays was reduced between 39% and 71%. The decrease was largest in the first quarter of the oxidation reaction. These findings indicate that oxidation, by itself, was not a likely factor in the tumor induction seen in the previous studies. Rather, other factors such as the conditions of fume generation and crude source (coupled with possible differences in distillation endpoints) were more likely to have determined the outcomes. Analyses of previously published data, presented in this paper, suggest that the modified Ames and fluorescence assays are valuable screening tools for use in future health-related asphalt research.     

The cytotoxic and mutagenic properties of cholesterol oxidation products

The oxidation of cholesterol proceeds as part of the lipid peroxidation process in membranes. Several oxidation products characteristic of a free-radical mechanism are formed and some can serve as indices of the nature and extent of cholesterol oxidation and of lipid peroxidation in general. Among the most typical oxidation products of lipid peroxide-dependent propagation reactions are the enantiomeric 5,6-epoxides and 7-ketocholestanol. Small amounts of these compounds may persist in tissues experiencing lipid peroxidation at a low but steady flux of free-radical reactions. Supporting evidence includes the routine detection of small quantities of cholesterol epoxides in tissues of normal animals, and the increase of these epoxides under conditions of oxidant stress or antioxidant deficiency. Conversion of cholesterol epoxides to cholestane triol is expected in cells possessing cholesterol epoxide hydrolase. All of these oxidation products possess remarkable cytotoxicity (at least part of which may be due to effects on the cell membrane) causing an increase in intracellular calcium. The cholesterol epoxides are also weakly mutagenic, although the mechanism for this mutagenicity remains to be clarified. In contrast, the other lipid epoxides normally encountered in tissues (chiefly fatty acid epoxides) are not mutagenic, and are much less toxic than the oxysterols described. The cytotoxicity of several oxysterols may be due to a number of mechanisms. That only the epoxides are mutagenic suggests that genotoxicity is a function of their electrophilic reactivity. This is not consistently apparent with the other compounds examined.     

Determination of cobalt in pharmaceutical products

The aim of this paper is to determine the content of cobalt in pharmaceutical products (B(12) vitamin powder, B(12) ampoules, Centrum, Spectrum ABC and Optima Forte) by spectrometric (FAAS, GFAAS and ICP-AES) and electrometric (AdSV) analytical techniques. The samples (approximately 0.5g) were treated with a mixture of 6mL HNO(3) and 1mL H(2)O(2) in the microwave oven. Due to the matrix effects the method of standard addition is preferred. The validity of the methods was tested by recovery studies of standard addition and results were found to be satisfactory.