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S J Chirtel

Publications and source records attributed to S J Chirtel.

18 recordsLinked to original sources
PubMed1998

Influence of water temperature and salinity on Vibrio vulnificus in Northern Gulf and Atlantic Coast oysters (Crassostrea virginica).

This study investigated the temperature and salinity parameters associated with waters and oysters linked to food-borne Vibrio vulnificus infections. V. vulnificus was enumerated in oysters collected at three northern Gulf Coast sites and two Atlantic Coast sites from July 1994 through September 1995. Two of these sites, Black Bay, La., and Apalachicola Bay, Fla., are the source of the majority of the oysters implicated in V. vulnificus cases. Oysters in all Gulf Coast sites exhibited a similar seasonal distribution of V. vulnificus: a consistently large number (median concentration, 2,300 organisms [most probable number] per g of oyster meat) from May through October followed by a gradual reduction during November and December to < or = 10 per g, where it remained from January through mid-March, and a sharp increase in late March and April to summer levels. V. vulnificus was undetectable (< 3 per g) in oysters from the North and South Carolina sites for most of the year. An exception occurred when a late-summer flood caused a drop in salinity in the North Carolina estuary, apparently causing V. vulnificus numbers to increase briefly to Gulf Coast levels. At Gulf Coast sites, V. vulnificus numbers increased with water temperatures up to 26 degrees C and were constant at higher temperatures. High V. vulnificus levels (> 10(3) per g) were typically found in oysters from intermediate salinities (5 to 25 ppt). Smaller V. vulnificus numbers (< 10(2) per g) were found at salinities above 28 ppt, typical of Atlantic Coast sites. On 11 occasions oysters were sampled at times and locations near the source of oysters implicated in 13 V. vulnificus cases; the V. vulnificus levels and environmental parameters associated with these samples were consistent with those of other study samples collected from the Gulf Coast from April through November. These findings suggest that the hazard of V. vulnificus infection is not limited to brief periods of unusual abundance of V. vulnificus in Gulf Coast oysters or to environmental conditions that are unusual to Gulf Coast estuaries.

Animals↗
PubMed1997

Effect of substance P and receptor antagonists on secretion of lingual lipase and amylase from rat von Ebner's gland.

Substance P (SP, 1 microM) when incubated with minced von Ebner's glands for 15, 30, and 60 min, stimulated secretion of lingual lipase (12.14% +/- 0.90) and amylase (8.30% +/- 0.42). Only 10 microM of the SP receptor antagonist CP-96,345 significantly inhibited SP-evoked secretion. D-Pro2-D-Phe7-D-Trp9-SP (Ia), D-Pro2-D-Trp7,9-SP (Ib), D-Arg1-D-Trp7,9-D-Leu11-SP (Ic), or 1 microM CP-96,345 were not effective, suggesting that the SP receptor of von Ebner's gland might be an isoform. Propranolol and timolol, beta 1/beta 2-adrenergic receptor antagonists were not effective and the cholinergic receptor antagonist, atropine, was effective in only slightly reducing amylase secretion but not lingual lipase. Differential secretion of the two enzymes was observed for basal and stimulated secretion. Thus, exocytosis may not be the only pathway involved in SP-evoked protein secretion.

Amylases↗
PubMed1997

Assessment of the embryotoxic potential of the total hydrolysis product of fumonisin B1 using cultured organogenesis-staged rat embryos.

Aminopentol (AP1) is the total hydrolysis product of fumonisin B1 (FB1), the major and best characterized of the fumonisins, which are mycotoxins that are common contaminants of corn and corn meal. Some human populations expected to have significant exposure to AP1 have a high incidence of babies born with neural tube defects (NTD). The embryotoxicity of AP1 was evaluated in cultured rat embryos. Gestation day 9.5 embryos were exposed to 0, 3, 10, 30, 100 or 300 microM AP1 throughout the entire 45-hr culture period. At 100 microM AP1, growth and overall development were reduced significantly. There was also a significant increase in the incidence of abnormal embryos. 29% of the embryos had NTD, and 36% of the embryos had other abnormalities. At 300 microM AP1, the incidence of NTD was 15%, and 85% of the embryos had other abnormalities. These findings suggest that AP1, at concentrations of 100 microM and above, can induce NTD in organogenesis-stage cultured rat embryos. However, these NTD are in conjunction with significant overall retardation of growth and development as well as significant increases in the incidence of other defects. These studies also showed, when compared with previous findings, that AP1 is over 100-fold less toxic than FB1 to cultured rat embryos.

Abnormalities, Drug-Induced↗
PubMed1996

Interactions in indices of vitamin A, zinc and copper status when these nutrients are fed to rats at adequate and increased levels.

The purpose of the present study was to determine the effects of feeding nutritionally adequate and increased levels of vitamin A (retinyl acetate at 1.4, 34.4, and 206.4 mg/kg diet) in combination with adequate or increased Zn (12 and 240 mg/kg) and Cu (5 and 50 mg/kg) on serum and tissue concentrations of retinol and retinyl palmitate and on indices of Cu and Zn status in female Sprague-Dawley rats, and to measure interactive effects of such nutrient imbalances. Rats fed on diets containing 34.4 and 206.4 mg vitamin A/kg had higher feed intakes and relative liver weights than those fed on diets containing 1.4 mg vitamin A/kg. An interaction between dietary Cu and Zn and an independent effect of vitamin A affected serum ceruloplasmin oxidase (EC 1.16.3.1) activity. Rats fed on high Zn, adequate-Cu diets (240 and 5 mg Zn and Cu/kg respectively) had lower serum ceruloplasmin oxidase levels than rats fed on adequate-Zn, adequate-Cu diets (12 and 5 mg Zn and Cu/kg respectively). This effect was not observed in rats fed on high-Zn, high-Cu diets (240 and 50 mg Zn and Cu/kg respectively). Alterations in dietary levels of Cu and vitamin A independently affected haemoglobin levels. Serum cholesterol concentration was affected by interactions between Zn and vitamin A and Cu and vitamin A. Levels of retinol and retinyl palmitate in liver and kidney were significantly higher in rats fed on diets with increased dietary vitamin A than in those fed on diets with adequate vitamin A. Three-way interactions among Cu, Zn, and vitamin A affected levels of retinol in serum and liver. Two-way interactions between Cu and vitamin A affected liver retinyl palmitate and the sum of liver retinol+retinyl palmitate. An independent effect of dietary Zn on these variables was also observed. Interactions between Cu and vitamin A affected levels of Cu in liver and kidney, while Fe and Zn in kidney were affected by interactions between Cu and Zn. This study demonstrates that differing interactions among variables of vitamin A metabolism and mineral status occur with higher dietary levels of vitamin A, Zn and Cu in the rat.

Animals↗
PubMed1994

The protective but nonsynergistic effect of dietary beta-carotene and vitamin E on skin tumorigenesis in Skh mice.

Various epidemiological and experimental studies have indicated that beta-carotene and vitamin E protect against a variety of cancers. This investigation determined whether a synergistic protective effect could be observed against chemically induced skin tumorigenesis in Skh mice by combining these two antioxidants in the diet. Forty-five mice were used in each of four diet groups. Control animals were fed standard mouse chow. Three other groups received the chow supplemented with one of the following: 0.5% beta-carotene, 0.12% vitamin E (added as d-alpha-tocopheryl succinate), or 0.5% beta-carotene + 0.12% vitamin E. Mice were topically treated with a single application of the initiator 7,12-dimethylbenz[a]anthracene and promoted with multiple applications of phorbol 12-myristate 13-acetate. Mice were observed for tumors each week for 27 weeks after initiation. The protective effect of each diet was determined by the decrease in the number of skin tumors in supplemented diet groups compared with that of the control diet group. Decreases in the number of cumulative tumors at Week 27 were 32% for beta-carotene-, 25% for vitamin E-, and 21% for beta-carotene+vitamin E-supplemented diet groups. However, differences in the number of tumors among the three groups supplemented with beta-carotene and/or vitamin E were not statistically significant. Thus, although protection was provided by the individual supplements, there was no synergistic effect for a decrease in the number of chemically induced skin tumors by the simultaneous dietary administration of beta-carotene and vitamin E.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

The effects of histamine, pyrilamine, cimetidine, and ranitidine on secretion of lingual lipase and amylase from rat von Ebner's glands.

Minced von Ebner's glands of rat tongue were incubated in vitro with histamine and histamine receptor antagonists. At various time intervals, media and homogenates of the tissue were assayed for lingual lipase and amylase activity and percentage secretion calculated. Histamine elicited moderate secretion (approximately 10%) of lingual lipase and amylase. In contrast, pyrilamine, an H1 receptor antagonist, elicited > 60% secretion. There were statistically significant differences between the percentage secretion of lingual lipase and amylase for basal secretion, as well as for histamine- and pyrilamine-evoked secretion above basal. The H2 receptor inhibitors, cimetidine and ranitidine, stimulated secretion of only amylase, but not lingual lipase. When combined with histamine, these antagonists partially inhibited only the secretion of histamine-evoked lingual lipase, but not amylase. The differences in percentage secretion between the two enzymes indicate that exocytosis may not be the only process involved in protein secretion. The anomalous effects of the H1 and H2 receptor antagonists necessitate a more detailed characterization of the receptors of von Ebner's glands.

Amylases↗
PubMed1991

Mechanism of action of 2,3,7,8-tetrachlorodibenzo-p-dioxin on intermediary metabolism in the rat.

A single 20-microgram/kg dose of TCDD caused, within 3 days, a significant mobilization of depot fat into the plasma compartment resulting in 1.44- to 2.8-fold increase in plasma free-fatty acid concentrations. With respect to the fate of mobilized fatty acids, the same treatment of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) caused a 32% inhibition (P less than .008) of the rate of hepatic oleate oxidation without significantly affecting the rate of fatty acid esterification. In contrast, hepatic ketogenic rate from oleate and octanoate was stimulated markedly by 85% (P less than .001) and 69% (P less than .001), respectively. These results support the concept that although the beta-oxidation pathway of the fatty acids must be operating normally, their complete oxidation to CO2 via the Tricarboxylic acid (TCA) cycle is impaired. At the same time, TCDD seems to preferentially divert the acetyl CoA generated from the beta-oxidation of fatty acids to the ketogenic pathway. Surprisingly, TCDD treatment inhibited the hepatic ketogenic rate from glycerol by 21% (P less than .001) and its oxidation to CO2 by 31% (P less than .025) without affecting its esterification to triglycerides. These results imply that the other possible major site which is sensitive to TCDD inhibition may be the generation of acetyl CoA from glycerol via the pyruvate dehydrogenase complex.

Animals↗
PubMed1991

Effect of chronic ethanol on apolipoprotein (Apo) E synthesis and glycosylation in rats.

We have previously shown in rats that chronic ethanol feeding significantly inhibits the incorporation of labeled leucine into Apo E secreted into the liver perfusate (p less than 0.01). Fish oil has been shown to counteract many of the adverse effects of ethanol. In order to explore whether this inhibitory effect of ethanol was due to the decreased synthesis and/or defective glycosylation of this glycoprotein, we have determined the effects of chronic ethanol and fish oil on the synthesis and glycosylation of Apo E in vivo. Four groups of male Wistar rats were pair-fed the following liquid diets for 8 weeks; (1) Ethanol Regular Fat, (2) Control Regular Fat, (3) Ethanol Fish Oil, and (4) Control Fish Oil. At the end, the rats were intraportally injected with a single dose of [U-14C]leucine (0.2 microCi/g body weight) and/or [2-3H]mannose (1 microCi/g body weight) and killed after 30 min. The incorporation of the labeled precursors into the immunoprecipitable Apo E was measured in the liver and its microsomal and Golgi fractions. The results showed marked decreases in mannose incorporation into total glycoproteins and specifically of Apo E in whole liver, microsomal, and Golgi fractions under ethanol treatment. In contrast, the leucine incorporation into liver Apo E increased 11% (p less than 0.048) by ethanol treatment. As a result, the [3H]mannose/[14C] leucine incorporation ratio also decreased 41% to 47% at the whole liver, microsomal, and Golgi fractions indicating a marked inhibition in glycosylation of Apo E in the ethanol group.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1989

Hepatic synthesis of apoproteins of very low density and high density lipoproteins in perfused rat liver: influence of chronic heavy and moderate doses of ethanol.

The effects of 6 weeks of heavy and moderate ethanol feeding to rats upon lipids and lipoprotein metabolism were determined. As compared to the control group, the heavy ethanol feeding resulted in the following changes: liver weight/kilogram body weight increased by 48% (p less than 0.001) with a concomitant 52% increase (p less than 0.001) in liver protein/kilogram body weight and a 2.75-fold (p less than 0.001) increase in liver total lipids/kilogram body weight. In contrast, liver DNA/kilogram body weight or per liver was not affected significantly. Plasma cholesterol and triglycerides were higher by 53% (p less than 0.01) and 77% (p less than 0.01), respectively. Liver cholesterol and triglycerides were 4.4-fold and 3.8-fold higher (p less than 0.001), respectively. Plasma total A1 was 1.72-fold higher (p less than 0.001), whereas there was no significant difference in plasma apo E levels between the two groups. However, plasma high density lipoproteins (HDl) apo E was 48% lower (p less than 0.02) while the very low density lipoproteins (VLDL) E was 2.15-fold higher (p less than 0.02). Hepatic total protein synthetic rate in the ethanol group was not significantly different from the control group. In contrast, labeled leucine incorporation into the total secretory proteins was inhibited by 36% (p less than 0.01) in ethanol-fed group.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1989

A novel use of endpoint nephelometry to standardize the rate nephelometric assay of human and rat plasma apoprotein A.

A sensitive, accurate, and reliable method is described for calibrating the rate immunonephelometric assay of rat and human plasma apolipoprotein A (Apo A). Pure Apo A and high-density lipoprotein (HDL) of known Apo A concentration were used in endpoint nephelometry to determine Apo A concentrations of rat and human plasma pools. The endpoint method had coefficients of variation of 7.96% and 4.35% for rat and human plasma pools, respectively. These plasma pools were then used as secondary standards for the rate nephelometric assay. Excellent agreement (+/- 6%) existed between the plasma Apo A values determined by endpoint nephelometry and rate nephelometry. The Apo A concentration of a frozen human plasma pool determined by endpoint nephelometry was 125.2 +/- 9.6 mg/dl. The value of the same pool determined by rate nephelometry over a 1-year period with the Centers for Disease Control WHO lyophilized plasma standard was 125.4 +/- 21.2 mg/dl. Furthermore, it was found that the rat HDL was also a suitable standard in the rate nephelometric assay of Apo A. In contrast, Apo A, purified to homogeneity, showed different reaction kinetics from that of Apo A in the whole plasma and therefore was not a suitable standard in the rate nephelometric assay. We therefore conclude that primary standard Apo A, purified to homogeneity, can be used by endpoint nephelometry to calibrate plasma pools that can then be used as secondary standards in the rate nephelometric determination of rat and human plasma Apo A. The ready applicability of this method in the accurate determination of plasma Apo A under well-defined experimental conditions such as in chronic ethanol-fed rats and in human subjects with normal lipid levels and those with hyperlipidemia is demonstrated.

Animals↗
PubMed1989

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on lipid synthesis and lipogenic enzymes in the rat.

A single i.p. administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) caused within 1 wk of exposure a dose-dependent progressive inhibition of liver fatty acid synthetic rate with concomitant decreases in hepatic fatty acid synthetase and acetylcoenzyme A carboxylase activities. Similarly, hepatic cholesterol synthetic rate was markedly inhibited with increasing dosage of TCDD, although the corresponding decrease in 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity was of lesser magnitude. Linear regression analyses of the reciprocals of the responses versus the dose revealed that the TCDD concentration which caused 50% inhibition of the activities of various lipogenic enzymes and of lipid synthetic rates ranged from 11 to 20 micrograms/kg (34-67 nM) with an average of 15 micrograms/kg (47 nM). Hepatic cholesterol synthesis seemed to be more sensitive to inhibition than fatty acid synthesis whether it was based on TCDD dosage or duration of exposure. The degree of inhibition of all the above parameters except fatty acid synthesis in liver and adipose tissues increased from 1 to 2 wk of exposure but was less pronounced after 4 wk exposure. Significantly, the adipose tissue was found to be more sensitive than the liver with respect to inhibition of fatty acid synthesis by increasing dosage of TCDD. Thus, the biochemical mechanism of loss of adipose mass caused by TCDD exposure may well be mediated by strong inhibition of lipid synthesis in the adipose tissue coupled with increased mobilization of depot fat.

Adipose Tissue↗
PubMed1988

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on de novo fatty acid and cholesterol synthesis in the rat.

The effects of 1, 5, 10 and 20 micrograms/kg dosages of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) upon de novo fatty acid and cholesterol synthesis in liver and adipose tissue were determined in pair-fed rats. The incorporation of tritium from 3H2O into tissue lipids was measured. Hepatic and adipose fatty acid synthetic rates (mumoles acetyl units g-1 hr-1) in the control groups were 19.6 +/- 4 and 75.7 +/- 18.5, respectively, and the liver cholesterol synthetic rate was 2.9 +/- 0.5. TCDD (1 microgram/kg) inhibited fatty acid synthesis in the liver and adipose tissue, by 44% and 41%, respectively, and the liver cholesterol synthesis was inhibited by 37%. The extent of these inhibitions increased with increasing dosages of TCDD. The effect of TCDD on sterol synthesis in adipose tissue could not be determined, because the tritium incorporation into the sterol fraction in this tissue was not detectable.

Adipose Tissue↗
PubMed1988

Roles of omega 3 fatty acids and chronic ethanol in the regulation of plasma and liver lipids and plasma apoproteins A1 and E in rats.

Relative effects of feeding ethanol and/or omega 3 fatty acid-rich fish oil for 6 wk on body lipids and lipoproteins were investigated. Ethanol increased plasma cholesterol (P less than 0.06) and triglycerides (P less than 0.0005), whereas fish oil decreased plasma cholesterol (P less than 0.005) and triglycerides (P less than 0.02). Liver cholesterol and triglycerides were increased by ethanol (P less than 0.0001) while fish oil decreased liver cholesterol (P less than 0.01) but not triglycerides. Based on Scheffé contrasts (P less than 0.05), fish oil blocked the increases in liver cholesterol and triglycerides caused by ethanol. Substitution of normal dietary fat with omega 3 fatty acid-rich fat in ethanol-fed animals lowered plasma cholesterol by 29% (P less than 0.001) and triglycerides by 30% (P less than 0.05) within 2 wk. Plasma apo A1 was increased by ethanol (P less than 0.001) and decreased by fish oil (P less than 0.002). Plasma total apo E was unaffected by either ethanol or fish oil. However, HDL apo E was decreased by ethanol (P less than 0.04) and increased by fish oil (P less than 0.02). Scheffé contrasts (P less than 0.05) also showed that plasma apo A was increased by ethanol regardless of whether the animals were consuming regular fat (1.72-fold) or fish oil fat (1.49-fold). Thus, omega 3 fatty acids can not only prevent but also reverse many of the lipid and lipoprotein abnormalities caused by alcohol abuse in the rat.

Animals↗
PubMed1988

Roles of hormonal and nutritional factors in the regulation of rat liver alcohol dehydrogenase activity and ethanol elimination rate in vivo.

Fasting reduced the liver alcohol dehydrogenase (ADH) activity by 51% (p less than 0.001). Insulin, within 2 hr, increased the ADH activity found in fasted animals by 28% (p less than 0.02). Insulin administration failed to stimulate the reduced ADH activity in diabetic rats. However, ADH activity in the diabetic-fed rats decreased by 52-54% (p less than 0.001) compared to normal-fed rats regardless of whether they were meal-fed or refed the normal chow. Glucagon blocked by 15% (p less than 0.02) the increase in ADH activity associated with refeeding. Furthermore, insulin caused a marginal stimulation of ethanol elimination rate (EER) when administered to fasted rats. All these results imply that insulin and glucagon may not be the only determining factors in the control of liver ADH activity associated with fasting and refeeding. Meal-feeding or refeeding a high carbohydrate fat-free diet compared to the normal chow-diet caused 29% (p less than 0.001) and 36% (p less than 0.05) decreases in ADH activity, respectively. Concomitant decreases in EER caused by high carbohydrate fat-free diet feeding were also observed under identical conditions. These results raise the possibility that the amount and the type of carbohydrate may be crucial in the regulation of ADH and EER. Alternatively, the presence of fat may be important in maintaining the normal level of ADH and EER.

Alcohol Dehydrogenase↗
PubMed1986

Studies on the mechanism of absorption and distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the rat.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the toxic contaminant of Agent Orange, is absorbed essentially by the lymphatic route and is transported predominantly by chylomicrons after intestinal absorption. Plasma disappearance of [3H]TCDD-labeled chylomicrons followed first-order decay kinetics, with two exponential components having half-lives of 0.8 and 30 min, respectively. Liver and adipose tissues together accounted for 74 to 81% of the total radioactivity distributed among various tissues. The i.p. route of administration was as effective as the oral route for uptake in 24 h by the adipose and liver tissues, whereas the s.c. route was less efficient. Adipose tissue exhibited a progressive accumulation of labeled TCDD during the first 24 h, whereas the liver showed an exponential disappearance of the newly absorbed TCDD with a half-life of 21.3 h. In contrast, long-term pharmacokinetics of TCDD in the adipose and liver tissues revealed exponential decay patterns with half-lives of 7.6 and 5.3 weeks, respectively. These results show that the adipose tissue and the liver are the major sites of TCDD storage.

Adipose Tissue↗
PubMed1984

Net O2, CO2, lactate, and acid exchange by muscle during progressive working contractions.

The net O2 uptake (VO2), CO2 output (VCO2), lactate output (L), and non-CO2 acid output (HA) by the gastrocnemius-plantaris muscle group of the dog were measured during progressively loaded isotonic tetanic contractions. Shortening during the 1/s contractions was maintained constant as load was increased by raising the stimulus voltage applied to the motor nerve. Contractions at each load continued for 5 min with two arterial and four venous blood samples obtained during the last minute at each load. Work rate (W) during the contractions was calculated from the load and the shortening. The VO2 increased linearly with time and W. The VCO2 generally followed VO2 with a modest lag during the first two work periods. L increased with time, W, and VO2. Maximal L was lower than that seen during repetitive maximal twitch contractions. HA also increased with time, W, and VO2 and was much larger than L at the higher work rates. It is concluded that L and HA are independent variables during progressive working contractions, as they were during repetitive twitch contractions. Both L and HA patterns may be explained as summations of the respective exchanges of L and HA with time by sequentially recruited groups of muscle fibers.

Acid-Base Equilibrium↗
PubMedDate not supplied

A simple method for evaluating data from an interlaboratory study.

Large-scale laboratory- and method-performance studies involving more than about 30 laboratories may be evaluated by calculating the HORRAT ratio for each test sample (HORRAT = [experimentally found among-laboratories relative standard deviation] divided by [relative standard deviation calculated from the Horwitz formula]). The chemical analytical method is deemed acceptable per se if HORRAT approximately 1.0 (+/- 0.5). If HORRAT is > or approximately 2.0, the most extreme values are removed successively until an "acceptable" ratio is obtained. The laboratories responsible for the extreme values that are removed should examine their technique and procedures. If > or approximately 15% of the values have to be removed, the instructions and the methods should be examined. This suggested computation procedure is simple and does not require statistical outlier tables. Proposed action limits may be adjusted according to experience. Data supporting U.S. Environmental Protection Agency method 245.1 for mercury in waters (manual cold-vapor atomic absorption spectrometry), supplemented by subsequent laboratory-performance data, were reexamined in this manner. Method-performance parameters (means and among-laboratories relative standard deviations) were comparable with results from the original statistical analysis that used a robust biweight procedure for outlier removal. The precision of the current controlled performance is better by a factor of 4 than that of estimates resulting from the original method-performance study, at the expense of rejecting more experimental values as outliers.

Chemistry Techniques, Analytical↗