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Biomedical subjects

G E Rottinghaus

Publications and source records attributed to G E Rottinghaus.

At least 73 records · Page 4Linked to original sources
PubMed1994

Chronic effects of dietary fumonisin on the heart and pulmonary vasculature of swine.

Fumonisins, mycotoxins produced in Fusarium moniliforme-infected corn, are hepatotoxic in several species and induce hepatocarcinomas in laboratory rats, leukoencephalomalacia in equine species, and fulminant pulmonary edema in swine. To date, the effects of fumonisin on pigs has dealt solely with the high levels required to induce the dramatic development of acute fulminant, and usually lethal, pulmonary edema. Less sensational, but equally important, are the chronic effects of fumonisin on swine health. In the first trial, six gilts were fed, ad libitum, a formulated complete ration containing 100 mg fumonisin B1 (FB1)/kg for 10 days followed by a ration containing 190 mg FB1/kg for up to 83 days. In the second trial, five gilts were fed, ad libitum, rations containing 150-170 mg FB1/kg for up to 210 days. The concentration of fumonisin B2 (FB2) was 31 +/- 2% that of the FB1. Weight-matched controls were selected for cardiac parameter comparison. Pigs fed fumonisin for at least 93 days developed nodular hyperplasia of the liver. Evidence from the microscopic examination of heart and lungs and gravimetric measurements of cardiac tissues from four pigs exposed to dietary fumonisins for 6 months suggests that the pulmonary vasculature is a target of chronic exposure. This study provides additional evidence linking the pathogenesis of fumonisin-induced lesions in a variety of organ systems of various animal species to a vascular mechanism.

Animal Feed↗
PubMed1994

Developmental effects of fumonisin B1-containing Fusarium moniliforme culture extract in CD1 mice.

Pregnant Charles River CD1 mice were treated with a semipurified extract of Fusarium moniliforme culture containing 0, 12.5, 25, 50 or 100 mg FB1/kg each day orally (diluted in distilled water) between gestational days (GD) 7 and 15 to evaluate the developmental toxicity of FB1. Following sacrifice of dams on GD 18, litters were examined for gross abnormalities and divided equally for skeletal or visceral examination by routine techniques. Significant maternal mortality was observed at doses of 50 and 100 mg FB1/kg. Dose-dependent decreases in maternal body weight gains, number of live offsprings per litter, and mean body weight of the offspring were produced at FB1 doses of 25 mg/kg or higher. The percentage of implants resorbed increased at all doses in a dose-dependant manner. A dose-dependant increase, except at the lowest dose tested, in the incidence of ossification deficits involving digits and sternum, short and wavy ribs, and hydrocephalus of lateral and third ventricles was also evident. Cleft palate was seen only at the highest FB1 dose. Maternal intoxication manifested as a dose-dependant increase in the severity of ascites associated mainly with increased histopathologic scores reflecting hepatocellular damage at day 18. Concommittant increases in serum alanine amino transferase (ALT) on GD 12, reflecting parenchymal liver cell damage, was also observed at all doses above 12.5 mg of FB1/kg. These results suggest that FB1-containing F. moniliforme culture extract is developmentally toxic in mice, and that this toxicity may be mediated by maternal hepatotoxicity.

Abnormalities, Drug-Induced↗
PubMed1994

Development toxicity of fumonisin in Syrian hamsters.

The effects of fumonisin on development of Syrian hamster fetuses were studied using fumonisin B1 and B2 extracted from Fusarium moniliforme corn-culture and purified fumonisin B1. A significant increase in litters with fetal deaths occurred with the high doses of purified (18 mg FB1/kg) and culture-extracted (18 mg FB1 plus 4.5 mg FB2) fumonisin. It is concluded that prenatal exposure to fumonisin on days 8 and 9 of gestation is detrimental to fetal hamster survivability but does not induce clinical maternal intoxication at these doses. Equivalent doses of fumonisin B1, whether from culture-extract or pure solution produced similar results.

Abnormalities, Drug-Induced↗
PubMed1994

Influence of ochratoxin A and diacetoxyscirpenol singly and in combination on broiler chickens.

The effects of feeding 2 mg ochratoxin A (OA) and 6 mg 4,15-diacetoxyscirpenol (DAS)/kg of diet singly and in combination were characterized in male broiler chicks from 1 to 19 d of age. Body weights were depressed by OA, DAS, and the OA-DAS combination. There was a significant antagonistic interaction between OA and DAS for uric acid and cholesterol. The efficiency of feed utilization was reduced by DAS alone and by the OA-DAS combination. When compared with controls, additive toxicity was exhibited for reduced efficiency of feed utilization, increased relative weights of the liver and gizzard, and decreased concentration of serum total protein, mean corpuscular volume, and mean corpuscular hemoglobin. All chicks were scored for oral lesions using a scale of 1 to 4 (0 = no visible lesions; 3 = severe lesions). Oral lesions (average score = 2.6) were present in over 90% of the chicks receiving the DAS diet with or without OA. These data demonstrate that both OA and DAS alone and the OA-DAS combination can adversely affect broiler performance and health.

Animal Feed↗
PubMed1994

Individual and combined toxicity of T-2 toxin and cyclopiazonic acid in broiler chicks.

The effects of feeding 6 mg T-2 toxin (T-2) and 34 mg cyclopiazonic acid (CPA)/kg of diet singly and in combination were characterized in male broiler chicks from 1 d to 3 wk of age. Body weights were depressed by T-2, CPA, and the combination of T-2 and CPA. There was a significant synergistic interaction between T-2 and CPA for relative liver and kidney weights and serum cholesterol and triglyceride concentrations and a significant interaction between T-2 and CPA for 3-wk body weights and relative bursa of Fabricius weights, which were less than additive. Neither the efficiency of feed utilization nor mortality was affected by dietary treatments. Oral lesions were present in a majority of the chicks fed diets containing T-2 with or without CPA. When compared with controls, other variables measured exhibited additive or less than additive toxicity. These data demonstrate that T-2 and CPA alone and in combination can cause reduced performance and adversely affect broiler health. The effects of these mycotoxins may be exacerbated by other factors when under field conditions; hence, the potential detrimental effects of these two mycotoxins when present alone or in combination cannot be dismissed.

Animals↗
PubMed1994

Individual and combined effects of feeding Fusarium moniliforme culture material, containing known levels of fumonisin B1, and aflatoxin B1 in the young turkey poult.

The individual and combined effects of fumonisin B1 (FB1) and aflatoxin B1 (AF) were evaluated using a 2 x 2 factorial with treatments of 0 and 75 mg FB1/kg feed and 0 and 200 micrograms AF/kg feed. Each of the four diets was fed to eight pen replicates of six poults from Day 1 to 21. Body weight gain was reduced (P < .05) by AF and the FB1-AF combination. Poults fed AF or the FB1-AF combination were less efficient (P < .05) in converting feed to gain. Fumonisin B1 increased (P < .05) liver weights whereas AF and the FB1-AF combination increased (P < .05) spleen weights. The AF and the FB1-AF combination decreased (P < .05) serum concentrations of albumin, total protein, and cholesterol. Fumonisin B1 and the FB1-AF combination increased (P < .05) serum sphinganine:sphingosine (SA:SO) ratios. Treatment-associated lesions were observed only in the liver. Hepatocellular hyperplasia and biliary hyperplasia were seen in poults fed 75 mg FB1/kg and 200 micrograms AF/kg, respectively. The combination of FB1 and AF caused an increased primary immune response to sheep red blood cells. However, the phytohemagglutinin delayed hypersensitivity response was not affected by dietary treatment. These data indicate that FB1 and AF, alone and in combination, can adversely affect poult performance and health at these dietary concentrations.

Aflatoxin B1↗
PubMed1994

Administration of ochratoxin A and T-2 toxin to growing swine.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed; for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum creatinine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.

Animals↗
PubMed1994

Developmental toxicity in hamsters of an aqueous extract of Fusarium moniliforme culture material containing known quantities of fumonisin B1.

The purpose of this study was to investigate potential detrimental effects of fumonisin B1 on the developing hamster. In experiments 1 and 2, timed-bred hamsters were dosed with 0.0 to 12.0 mg fumonisin B1/kg from day 8 to day 10 or day 12 of gestation. Clinical signs of material toxicity were not observed. Pregnant animals had reduced weight gains and lower total bilirubin levels than nonpregnant females. Hamsters were euthanized on day 15 of gestation. Histologic evaluation revealed autolytic placental changes expected in terminal gestation, as well as more advanced placental necrosis in association with fetal resorptions. Mean fetal weights and crown-rump lengths of living term fetuses on a per-litter basis did not differ between untreated controls and treated animals given 6.0 mg fumonisin B1/kg or less. However, at higher doses of fumonisin B1, there was an increased incidence of prenatal losses (deaths and resorptions). A greater percentage of litters had 1 or more fetuses affected, and a greater percentage of total fetuses were lost/litter as the fumonisin dosage increased. At 12.0 mg/kg, all litters were affected and 100% of the fetuses were dead and resorbing. Fumonisin B1 appears a developmental toxicant in hamsters. Toxicity is manifest by increased numbers of prenatal deaths and resorptions at doses that do not induce clinicopathologic evidence of maternal toxicity.

Animal Feed↗
PubMed1993

Aldrin intoxication and clearance of associated dieldrin residues in a group of feedlot cattle.

A sudden onset of bizarre neurologic dysfunction was found in 8 of 90 mixed-breed feeder calves. Seven other calves were dead, and 3 more died during the next week. A diagnosis of organochlorine toxicosis was made when rumen and abomasal contents from 1 of the calves revealed 22.4 and 20.6 micrograms of aldrin/g of ingesta, respectively. Complete feeds retrieved from self-feeders contained 54 and 528 micrograms of aldrin/g of feed. The initial concentration range in fat from 40 live calves was 6.01 to 42.44 micrograms of dieldrin/g of fat. Additional fat samples were analyzed to verify residue compliance until the entire herd was clear of residue 18 months after removal of the contaminated ration. The range of apparent half-lives for dieldrin in body fat of heifers and steers was 69 to 231 and 53 to 116 days, respectively. These findings demonstrate the considerable variability in apparent half-life of dieldrin in field cases. In cases of dieldrin-contaminated livestock, veterinarians and regulatory personnel must accurately determine the necessary slaughter withholding times so that informed economic decisions are made in the best interest of the producer while enhancing the probability of a safe food supply. Excretion rates of dieldrin from field-contaminated cattle may not be consistent with results obtained under experimental conditions.

Adipose Tissue↗
PubMed1993

Two new modified trichothecenes from Fusarium sporotrichioides.

Two new modified trichothecenes, 2-deoxy-11-epi-3 alpha-hydroxysambucoin [1] and 2-deoxy-11-epi-12-acetyl-3 alpha-hydroxysambucoin [2], were isolated from Fusarium sporotrichioides culture. This is the first report of modified trichothecenes where the two six-membered rings are cis-fused. Structures were elucidated using gc-ms, nmr, X-ray crystallography, and other spectroscopic techniques. Compounds 1 and 2 were screened for relative cytotoxicity in cultured baby hamster kidney (BHK-21) cells and found to be non-toxic.

Animals↗
PubMed1993

Fumonisin toxicity in turkey poults.

The effects of dietary fumonisin B1 were evaluated in young turkey poults. The experimental design consisted of 3 treatments, with 24 female turkey poults allotted randomly per treatment. Day-old poults were fed diets containing 0 mg (feed control), 100 mg, and 200 mg fumonisin B1/kg feed for 21 days. Body weight gains and efficiency of feed conversion decreased linearly with increasing dietary fumonisin. Liver, kidney, and pancreas weights increased linearly with increasing dietary fumonisin, and spleen and heart weights decreased. Serum aspartate aminotransferase levels increased with increasing dietary fumonisin, and serum cholesterol; alkaline phosphatase, mean cell volume, and mean cell hemoglobin all decreased. Biliary hyperplasia, hypertrophy of Kupffer's cells, thymic cortical atrophy, and moderate widening of the proliferating and degenerating hypertrophied zones of tibial physes were present in poults fed diets containing fumonisin B1. Results indicate that fumonisin B1, from Fusarium moniliforme culture material, is toxic in young poults, and the poult appears to be more sensitive to fumonisin than the broiler chick.

Alkaline Phosphatase↗
PubMed1993

An HPLC method for the detection of ergot in ground and pelleted feeds.

A high performance liquid chromatography (HPLC) method is described for detecting ergot in ground or pelleted forages and grains. Samples were extracted with alkaline chloroform, filtered, and applied to silica gel/organic binder cleanup columns. Following elution of pigments with acetone: chloroform, ergopeptine alkaloids were eluted with methanol and analyzed by HPLC with fluorescence detection. Average recovery of ergotamine, the major ergopeptine alkaloid produced by Claviceps, was 93%, with a relative standard deviation of 4.9%. The detection limit of ergotamine was approximately 50 ppb in all feedstuffs. Confirmation of ergopeptine alkaloids was accomplished by treating the parent ergopeptine alkaloids with 0.2% acetic acid to produce their -inine isomers and reexamining by HPLC with fluorescence detection or silica gel/organic binder column cleanup in combination with tandem mass spectroscopy. The method described is a valid alternative to microscopic inspection for detecting ergot contamination in ground or pelleted feedstuffs.

Animal Feed↗
PubMed1993

Chronic toxicity of fumonisin in weanling pigs.

Three gilts fed a diet containing 100 mg fumonisin B1/kg for 7 days followed by a diet containing 190 mg/kg for 83 days developed nodular hyperplasia of the liver. These nodules of various diameters were composed of solid sheets or nests of hepatocytes. There were no discernible central veins or portal triads, and the perilobular connective tissue and adjacent parenchyma were compressed. Three other gilts maintained on the same diet for 27-80 days developed severe hepatopathies, but not nodular hyperplasia, necessitating euthanasia prior to conclusion of the feeding trial. At necropsy, 1 of the 6 gilts had grossly apparent hyperplastic plaques within the distal esophageal mucosa. On histopathologic examination, 6 of 6 gilts had mild to severe hyperkeratosis, parakeratosis, and formation of papillary downgrowths of the stratum basale of the distal esophageal mucosa. The hyperplastic nodules in the liver and the changes in the distal esophageal mucosa illustrate the unique chronic toxicity of this mycotoxin in pigs.

Animal Feed↗
PubMed1993

Efficacy of a hydrated sodium calcium aluminosilicate to reduce the toxicity of aflatoxin and diacetoxyscirpenol.

A hydrated sodium calcium aluminosilicate (HSCAS) was incorporated into diets (.5%) containing 3.5 mg/kg aflatoxin (AF) and 5.0 mg/kg diacetoxyscirpenol (DAS) singly and in combination. Male broiler chicks received ad libitum access to their respective diets and water from 1 to 21 days of age. Body weight gains were significantly (P < .05) depressed by AF and DAS singly and a synergistic interaction occurred between AF and DAS for a further depression of body weight gains. Alterations in hematological and serum biochemical values, as well as serum enzyme activities, were observed for the AF and the AF and DAS combination. Additionally, a significant interaction occurred between AF and DAS for some biochemical values and enzyme activities. Adding HSCAS resulted in almost total protection against the effects caused by AF alone, limited protection against the combination, but no protection against the DAS alone. These findings indicate that HSCAS can diminish the adverse effects of AF but not of DAS.

Aflatoxins↗
PubMed1993

Effects of feeding Fusarium moniliforme culture material, containing known levels of fumonisin B1, on the young broiler chick.

The effects of feeding Fusarium moniliforme culture material, containing known concentrations of fumonisin B1 (FB1), were studied in broiler chicks. Day-old chicks were allotted randomly to dietary treatments containing 0, 1.02, 2.04, 3.06, 4.08, 5.10, 6.12, and 7.14% fumonisin culture material (FCM). These levels of FCM supplied 0, 75, 150, 225, 300, 375, 450, and 525 mg of FB1/kg of feed. Each dietary treatment was fed to four pen replicates of six birds each for 21 days. Chicks fed FCM that supplied 450 and 525 mg FB1/kg diet had lower (P < .05) feed intakes and BW gains; increased (P < .05) liver and kidney weights; and increased (P < .05) mean cell hemoglobin, and mean cell hemoglobin concentrations. Compared with controls, chicks fed FCM had increased (P < .05) free sphinganine levels and sphinganine:sphingosine ratios. Treatment-associated histological lesions were only observed in the liver of chicks fed diets containing FCM that supplied 225 mg FB1/kg or higher. Diets containing FCM that supplied levels as low as 75 mg FB1/kg affected the physiology of chicks by increasing free sphinganine levels and sphinganine:sphingosine ratios. Because inhibition of sphingolipid biosynthesis has been hypothesized as the mechanism of action of FB1, this suggests that diets containing 75 mg FB1/kg FCM may be toxic to young broiler chicks.

Animal Feed↗
PubMed1992

A rapid, sensitive thin layer chromatography procedure for the detection of fumonisin B1 and B2.

A thin layer chromatography (TLC) method was developed for the detection of fumonisin B1 and B2 in corn and corn-based feedstuffs. Finely ground samples were extracted with acetonitrile:water (1:1), filtered, and applied to C18 cleanup columns. The columns were washed with 1% aqueous KCl followed by acetonitrile: 1% aqueous KCl (1:9), and the fumonisins were eluted with acetonitrile:water (7:3). The eluants were concentrated and spotted on reverse-phase C18 TLC plates along with fumonisin B1 and B2 standards, and the plates were developed in methanol: 4% aqueous KCl (3:2). The fumonisins were visualized by spraying the TLC plates successively with 0.1 M sodium borate buffer, fluorescamine, and 0.01 M boric acid. The plates were then dried and examined under longwave ultraviolet light. Fumonisin B1 and B2 appeared as bright yellowish-green fluorescent bands at Rfs of 0.5 and 0.1, respectively. The detection limit for the fumonisins on the TLC plate was 0.1 ppm in corn. Recoveries from spiked samples averaged greater than 80%. The identification of the fumonisins was confirmed by hydrolyzing the parent compounds of B1 and B2 to their respective C22 amino-alcohols and reexamining by TLC with the same visualizing reagents. This procedure was used to survey 193 corn samples collected from University of Missouri test plots in 1990 for fumonisin B1. Fumonisin B1 was detected in 15% of the corn samples.

Animal Feed↗
PubMed1992

Fumonisin toxicity in broiler chicks.

The effects of dietary fumonisin B1 were evaluated in young broiler chicks. The experimental design consisted of 5 treatments each with 9 randomly allotted male broiler chicks. Day-old chicks were fed diets containing 0 (feed control), 100, 200, 300, or 400 mg fumonisin B1/kg feed for 21 days. Response variables measured were chick performance, organ weights, serum biochemistry, and histologic parameters. Body weights and average daily gain dramatically decreased with increasing dietary fumonisin B1, and liver, proventriculus, and gizzard weights increased. Diarrhea, thymic cortical atrophy, multifocal hepatic necrosis, biliary hyperplasia, and rickets were present in chicks fed diets containing fumonisin B1. Serum calcium, cholesterol, and aspartate aminotransferase levels all increased at higher fumonisin dietary levels. Results indicate that fumonisin, from Fusarium moniliforme culture material, is toxic in young chicks.

Animal Feed↗