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J T Bernert

Publications and source records attributed to J T Bernert.

At least 37 records · Page 2Linked to original sources
PubMed1991

Manufacturing processes at two French rapeseed oil companies: possible relationships to toxic oil syndrome in Spain.

The toxic oil syndrome (TOS) epidemic that occurred in Spain in spring 1981 has been associated with the consumption of rapeseed oil that was denatured with aniline for industrial use but diverted for human consumption. The precise aetiologic agent in the oil responsible for the outbreak has not been identified. To learn more about possible contaminants and how the contamination might have occurred, we visited two French companies that process rapeseed oil and that were identified in Spanish administrative and judicial records as the ones exporting aniline-denatured rapeseed oil to Spain in 1981. With the apparently full and voluntary co-operation of personnel at both companies, we reviewed the processes involved in manufacturing, treating and transporting rapeseed oil, and we have summarized the information provided to us. Of particular importance is the finding that oil exported to Spain was taken from stock, the rest of which was sold for human consumption in the French domestic market, apparently without any adverse health effects. The differences between the oil exported to Spain and the oil sold as food in France were that aniline equivalent to 2% of the weight of the oil was added to most of the Spanish oil but not to that sold in France, and that contamination of the Spanish oil may have occurred in the tank trucks used for transportation to Spain, which had previously carried industrial chemicals. There is no assurance that the trucks were cleaned appropriately for transporting a food product before the oil was loaded for the journey to Spain. Since the clinical manifestations of TOS are not those of aniline toxicity, we conclude that the aetiological agent of TOS is likely to be one of the following: (1) a contaminant in the aniline, (2) a contaminant introduced during transportation, (3) a reaction product of normal oil components or materials used in refining with either aniline or the potential contaminants mentioned under (1) or (2) above.

Aniline Compounds↗
PubMed1991

Factors influencing the accuracy of the national reference system total cholesterol reference method.

Previous comparisons between the Reference and Definitive Methods for measuring serum cholesterol have demonstrated a small but persistent positive bias in the Reference Method, averaging about +1.6%. Here we describe the results of further investigations designed to better characterize the nature of this bias. Analysis of a well-characterized model serum sample (SRM 909) suggests that more than half of the difference in cholesterol values determined by the two methods is the result of small contributions from cholesterol precursor sterols and phytosterols, which are also measured for the Reference Method. An additional significant contribution may be from cholesterol oxidation products, particularly 7-hydroxycholesterol isomers, which are active in the Liebermann-Burchard reaction. The 7-hydroxycholesterol in SRM 909, most of which appeared to be already present in the serum rather than formed during saponification, may account for as much as 20% of the observed difference between the methods. Contributions from other possible sources, including impurities in the cholesterol standard and incomplete saponification of cholesteryl esters, are very small. Because the observed bias is both quite small and consistent among samples, the cholesterol Reference Method continues to meet all of the requirements generally expected for a dependable and effective Reference Method.

Carbon Isotopes↗
PubMed1989

The estimation of total serum lipids by a completely enzymatic 'summation' method.

Expressing serum organic toxicant concentrations per weight of total lipid rather than by volume of serum is often advantageous, but it requires a reliable and convenient method for determining the total serum lipids. We compared a completely enzymatic 'summation' method for estimating serum total lipids with a traditional gravimetric analysis. Serum total cholesterol (TC), nonesterified cholesterol (FC), triglycerides (TG), and phospholipids (PL) were assayed by automated, enzymatic methods and total lipids (TL) were calculated from the expression TL = 1.677 * (TC-FC) + FC + TG + PL. Examining three reference serum pools by both summation and gravimetric methods yielded results that agreed within 1-3%. The evaluation of thirty serum samples resulted in similar mean total lipid values (697 mg/dl gravimetric; 675 mg/dl summation) with excellent correlation between the two methods (r2 = 0.978). We conclude that the enzymatic summation procedure is a useful method for routinely estimating serum total lipid content.

Adult↗
PubMed1989

Synthesis of N-(5-vinyl-1,3-thiazolidin-2-ylidene)phenylamine and analysis of oils implicated in the Spanish toxic oil syndrome for its presence.

Previous reports have implicated 1-phenyl-5-vinyl imidazolidine-2-thione (PVIZT), a cyclic reaction product of aniline and naturally occurring rapeseed oil isothiocyanates, as the potential causative agent of the Spanish toxic oil syndrome (TOS). This report describes the synthesis, preliminary characterization and analysis of that reaction product, which has been identified as N-(5-vinyl-1,3-thiazolidin-2-ylidene)phenylamine (5-VTPA) rather than PVIZT. Oil samples (n = 21) that contained fatty acid anilides and were epidemiologically linked to TOS were analysed for the presence of 5-VTPA by extraction of the oil with methanol and clean-up on an ion-exchange column, followed by capillary gas chromatography-mass spectrometry using selected ion detection. A limit of detection of less than 500 ppb was established for these analyses. No 5-VTPA could be detected, however, in any of the TOS oils. As 5-VTPA was shown to be unstable in both heated and unheated food oils, it is possible that the compound had been lost from the oils since the time of the epidemic in 1981. However, no direct evidence for the involvement of 5-VTPA in TOS could be obtained in this study.

Brassica↗
PubMed1989

Structural identification of a heterocyclic compound implicated in the Spanish toxic oil syndrome.

The compound 1-phenyl-5-vinylimidazolidine-2-thione was previously reported to be the causative agent in the outbreak referred to as Spanish toxic oil syndrome. X-ray crystallography, together with nuclear magnetic resonance and infra-red spectroscopy, now show the correct structure of this compound to be N-(5-vinyl-1,3-thiazolidin-2-ylidene)phenylamine (5-VTPA). Data for the structural characterization of 5-VTPA and the closely related isomer N-(4-vinyl-1,3-thiazolidin-2-ylidene)phenylamine are reported.

Brassica↗
PubMed1988

Chemical correlates of pathogenicity of oils related to the toxic oil syndrome epidemic in Spain.

The identity of the etiologic agent that caused the 1981 epidemic of toxic oil syndrome in Spain has not been established, and toxicologic study of oil specimens from the outbreak has been hampered by uncertainty about which oils were actually capable of causing illness. To identify chemical characteristics associated with pathogenicity, the authors compared specimens collected during the Spanish government's oil recall program in June and July 1981 from affected and unaffected households in the two contiguous towns of Alcorcón and Leganés (Madrid Province). Oils were blind-coded for laboratory analysis, and personnel with no knowledge of the laboratory results determined whether illness was present in a family. Contamination with free aniline and oleyl, linoleyl, and palmityl anilides was strikingly more frequent and extensive in oils collected from the case (affected) families. There was a clear-cut dose-response effect, with increasing concentrations of aniline and anilides associated with increasing risk of illness. Differences in fatty acid and sterol compositions among oils indicated more rapeseed oil admixture in the case group, but these indicators of rapeseed oil admixture did not contribute significantly to risk after the degree of aniline/anilide contamination had been taken into account. The authors conclude that the presence of relatively high levels of aniline and fatty acid anilides in oil specimens collected during the epidemic in the two towns studied indicates a high probability of the current or prior presence of the etiologic agent of toxic oil syndrome. Although these data do not necessarily indicate that any of the compounds measured actually caused the illness, further toxicologic work should concentrate on oils with substantial concentrations of the marker compounds.

Anilides↗
PubMed1988

Pseudouridine is unsuitable as an endogenous renal clearance marker.

We assessed the clearance of endogenous pseudouridine in humans to evaluate the potential use of this modified nucleoside as a marker of glomerular filtration rate. Pseudouridine concentrations in serum ultrafiltrates and in the corresponding 24-h urine specimens from 19 healthy men were determined by high-performance liquid chromatography. Mean (and SD) pseudouridine concentrations in serum and urine from this group averaged 2.77 (0.34) mumol/L and 203.2 (64.8) mumol/L, respectively. The calculated clearances of the nucleoside [87.3 (24.9) mL/min, n = 19], however, averaged approximately one-third lower than the corresponding creatinine clearances in the same individuals [131.8 (28.4) mL/min]. Measurement of simultaneous clearances of [3H]pseudouridine and [14C]inulin in rats also yielded a lower pseudouridine clearance, 0.78 relative to inulin. Our results are thus consistent with a partial net reabsorption of pseudouridine in both experimental animals and in humans, indicating that this compound would not be a suitable endogenous marker for routine estimation of the glomerular filtration rate.

Animals↗
PubMed1984

Acute response of rat liver microsomal lipids, lipid peroxidation, and membrane anisotropy to a single oral dose of polybrominated biphenyls.

Liver microsomal lipids and lipid peroxidation activities were examined in adult male rats at intervals over a 2-mo period after the administration of a single oral dose of 0 or 500 mg/kg of FireMaster BP-6 in corn oil. Microsomal lipids were markedly altered in the polybrominated biphenyl- (PBB-) dosed animals at the earliest time examined (1 wk), and these changes persisted throughout the remainder of the study. An early decrease in the cholesterol-phospholipid ratio was noted, which probably contributed to the significant decrease in the steady-state fluorescence anisotropy demonstrable in both intact microsomes and in liposomes prepared from microsomal lipid extracts. Significant concentrations of PBBs were present in dosed rat microsomes, but the changes in anisotropy appeared to result from membrane lipid alterations rather than from a direct perturbation by PBBs. Iron ascorbate-induced peroxidation was also greatly enhanced in dosed rat microsomes, even when rats were maintained on a low-iron (25 ppm) diet. These early alterations in membrane fluidity and peroxidative capacity of microsomes may ultimately contribute to the hepatotoxicity of PBBs.

Administration, Oral↗
PubMed1984

Influence of incomplete cholesteryl ester hydrolysis on enzymic measurements of cholesterol.

Esterolytic activity of three enzymic cholesterol reagents was evaluated with use of human serum-based reference materials. Primary cholesterol standards were used to calibrate the enzymic methods, and incomplete cholesteryl ester hydrolysis was measured as the bias between the enzymic cholesterol values and corresponding reference values. The average biases observed with eight reference specimens were 0.15, -1.16, and -7.24%, respectively, for a commercial enzymic reagent with microbial cholesterol esterase, a commercial reagent with an animal source of esterase, and a Centers for Disease Control (CDC) reagent preparation with a microbial cholesterol esterase. By liquid chromatography, we examined the respective specificities of the three esterase reagent preparations and found that the preparations differ in the rate and specificity of catalysis of cholesteryl ester hydrolysis. The CDC reagent was only partly active towards cholesteryl arachidonate, which probably accounts for most of the negative bias of this reagent. Esterolytic activity of the various enzymic reagents is related to the source and matrix of the cholesterol esterase and must be considered with respect to proper selection of calibration materials for serum cholesterol measurement.

Animals↗
PubMed1983

Long-term effects of a single oral dose of polybrominated biphenyls on serum and liver lipids in rats.

Adult (5 months) male Sherman strain rats received a single dose of either 0 or 500 mg polybrominated biphenyls (PBB) in corn oil/kg body weight by stomach tube. After an 18-month recovery period, serum and liver samples were examined. The primary serum lipid response was an increase in cholesterol (both free and esterified) and in total phospholipids. The percentage of esterified cholesterol was not significantly different from that of the controls, and no significant differences in the cholesterol ester fatty acid composition were observed. Serum triglycerides were also unaffected. In the PBB-dosed animals, the total hepatic fatty acids contained significantly less palmitic acid and more stearic acid, consistent with an increase in palmitic acid chain elongation activity. No significant differences could be detected in the n-3 or n-6 acids except for a slight decline in the content of 22:6 (n-3). Hepatic microsomal phospholipids were slightly higher (per milligram protein) in the PBB-dosed animals, and the cholesterol content was lower. Consequently, the cholesterol-phospholipid ratio was reduced, and microsomes from the latter group appeared to have an altered lipid domain on the basis of steady-state fluorescence anisotrophy measurements. In addition, total hepatic thiobarbituric acid-reactive substances (assayed as malondialdehyde) were significantly increased in the PBB-dosed animals. This observation appeared to reflect an increased susceptibility to peroxidative stress in the latter group, probably resulting from reduced membrane antioxidant concentrations. The PBB-dosed rats had significantly lower serum retinol levels and a reduced content of this vitamin in liver microsomes. Microsomes were also deficient in alpha-tocopherol in the PBB-dosed animals, although serum levels were normal.

Animals↗
PubMed1982

Direct determination of the linoleate/oleate ratio in serum cholesterol esters by liquid chromatography.

We describe a convenient method for the direct determination of the serum cholesterol linoleate/cholesterol oleate (L/O) ratio by reversed-phase "high-performance" liquid chromatography. After removal of phospholipids by silicic acid chromatography, a serum extract is analyzed on a 5-micrometers particle size Ultrasphere-ODS column, eluted isocratically with acetonitrile/isopropanol (30/70, by vol). Detection is at 200 nm. Cholesterol palmitoleate interferes with the measurement when the analysis is based on peak area, but not when peak height is used. The overall precision of L/O measurements by this method was very similar to that observed with a gas-liquid chromatographic procedure, in which the cholesterol esters are first isolated and transesterified to the methyl esters. In both cases, the within-run CV for six replicate analyses was less than 2%. Analysis of 53 human serum samples by both methods yielded very similar L/O ratios. A plot of the data (our method = y) vs the usual gas-liquid chromatographic procedure gave a correlation coefficient of 0.988 and a regression equation of y = 1.03x + 0.013. Furthermore, direct analysis of serum cholesterol ester L/O ratios by our liquid-chromatographic method is simpler, quicker, and more readily adaptable to automation.

Cholesterol Esters↗
PubMed1981

Biosynthesis of sphingomyelin from erythro-ceramides and phosphatidylcholine by a microsomal cholinephosphotransferase.

Mouse liver microsomes were shown to be active in the synthesis of sphingomyelin from ceramide and phosphatidylcholine in a reaction independent of CDPcholine. The conversion was not inhibited by calcium chelating reagents, and no evidence for the involvement of phospholipase C activity in the transformation could be adduced. Activity was also demonstrated in monkey liver and heart microsomes. Mouse brain microsomes produced a sphingomyelin analogue, tentatively identified as ceramide phosphorylethanolamine, but not sphingomyelin. Both [14C]ceramide and [G-14]phosphatidylethanolamine were precursors of the brain product, while phosphatidylcholine was inactive. Progress in the partial characterization of the liver enzyme is also described.

Animals↗
PubMed1979

Solubilization and partial purification of an enzyme involved in rat liver microsomal fatty acid chain elongation: beta-hydroxyacyl-CoA dehydrase.

The solubilization and partial purification of beta-hydroxyacyl-CoA dehydrase from rat liver microsomes has been accomplished through deoxycholate solubilization, ammonium sulfate fractionation, and ion exchange chromatography. A purification of about 90-fold based on total soluble activity was achieved, with an overall yield of 40%. However, the initial solubilization is accompanied by the loss of the secondary portion of the v/s curve observed with intact microsomes. The enzyme requires detergent during the purification procedure to remain "soluble," and is strongly activated by the inclusion of Triton-X-100 at concentrations above its critical micelle concentration in the assay mixture. In addition a preference for micelles has been inferred based on discontinuities in the v/s curves relative to the measured critical micelle concentration of the substrates in the absence of Triton X-100. Kinetic parameters calculated on the basis of micelle-specific activity indicated that beta-hydroxyacyl-CoA substrates possessing even-numbered alkyl chains from 14 to 20 carbon atoms differed little in Vm', but had progressively larger Km' as the chain length increased. The partially purified preparation was also active with beta-hydroxy-8,11-eicosadienoyl-CoA; and with 2-trans-enoyl-CoA substrates in a reverse (hydration) reaction.

Animals↗