Relationship of the wasting syndrome to lethality in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin |
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| Authors: | B J Christian S L Inhorn R E Peterson |
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| Affiliation: | 1. School of Pharmacy, University of Wisconsin, Madison, Wisconsin 53706 USA;2. Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, Wisconsin 53706 USA;3. Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin 53706 USA;1. Department of Civil and Environmental Engineering, Jackson State University, Jackson, MS 39217, United States;2. Department of Civil and Environmental Engineering, Jackson State University, 1400 J. R. Lynch Street, Jackson, MS, 39217, United States;3. Department of Civil and Architectural Engineering, Tennessee State University, Nashville, TN 37209, United States;1. Superfund Research Center, University of Kentucky, Lexington, KY, USA;2. Department of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, USA;3. Division of Cardiovascular Medicine, College of Medicine, University of Kentucky, Lexington, KY, USA;4. Lexington Veterans Affairs Medical Center, Lexington, KY, USA;5. Department of Animal and Food Sciences, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY, USA;1. Department of Preventive Medicine and Public Health, School of Medicine, Universidad Autónoma de Madrid, CEI UAM+CSIC, Madrid, Spain;2. Unit of Nutritional and Cardiovascular Epidemiology, Environmental Medicine Institute (IMM), Karolinska Institutet, Stockholm, Sweden;3. IIS Aragón, Hospital Universitario Miguel Servet, Universidad de Zaragoza, Spain;4. CIBERCV Instituto de Salud Carlos III, Madrid, Spain;5. Agencia Aragonesa para la Investigación y el Desarrollo (ARAID), Zaragoza, Spain;6. CIBERESP (CIBER of Epidemiology and Public Health) Instituto de Salud Carlos III, Madrid, Spain;7. Instituto de Investigación IdiPaz, Madrid, Spain;8. IMDEA-Food Institute, Madrid, Spain;1. Department of Small Animal Clinical Sciences, University of Tennessee, Knoxville, TN, USA;2. Department of Large Animal Clinical Sciences, University of Tennessee, Knoxville, TN, USA;3. Department of Biological and Diagnostic Sciences, University of Tennessee, Knoxville, TN, USA;4. Office of Information and Technology, University of Tennessee, Knoxville, TN, USA;5. KL Maddy Equine Analytical Chemistry Laboratory, University of California Davis, Davis, CA, USA |
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| Abstract: | ![]()
Young adult male Sprague-Dawley rats treated with a LD95 dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibited a progressive reduction in feed intake and body weight until death occurred 15 to 32 days post-treatment. The time course and magnitude of weight loss and lethality of pair-fed control rats were essentially identical to that of TCDD-treated rats with each pair-fed control animal dying within 3 days of its TCDD-treated partner. Body composition analysis of the dead animals revealed that the total amounts of protein, fat, water, and ash in the carcasses of TCDD-treated and pair-fed control rats were each reduced to a similar extent. The temporal pattern of daily feed intake in TCDD-treated and pair-fed control rats (3 meals/day) or (1 meal/day) did not influence the results. Studies conducted at LD25-62 doses of TCDD in male Sprague-Dawley rats of different ages--weanling (90 g), young adult (275 g), and mature (450 g)--showed that the severity of the wasting syndrome in all age groups was greatest for animals that died. Also, young adult rats treated with a LD25 dose of TCDD that died displayed the same degree of hypophagia and weight loss prior to death as rats administered a LD95 dose. Histopathology of the liver and gastrointestinal tract was compared in TCDD-treated (LD95 dose) and pair-fed control rats killed 1 day before they otherwise would have died. Hepatocytes of TCDD-treated rats were enlarged relative to those of pair-fed control rats and contained nuclei that varied in size and number. Pair-fed control rats exhibited atrophy of the liver cords due to a decrease in the cytoplasmic volume of their hepatocytes. The stomach and small intestine of TCDD-treated rats were histologically similar to those of ad libitum-fed controls. In contrast, the glandular mucosa of the stomach of pair-fed control rats was ulcerated and the intestinal mucosa was atrophied. Stomach ulcers were the source of clotted blood found throughout the gastrointestinal tract of pair-fed control rats but not that of TCDD-treated animals. These findings demonstrate that hypophagia-induced weight loss is one of perhaps several responses that contribute to the death of TCDD-treated rats. That other responses are also involved is suggested by differences between pair-fed control and TCDD-treated rats in the weight and histopathology of certain organs. In addition, gastrointestinal blood loss contributes to the death of pair-fed control rats but not TCDD-treated animals. |
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