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Adrenal necrosis

The lesion in the duodenum developed even more rapidly (e.g., perforation in 24 h after a single dose) and more predictably than with propionitrile. Acetanilide was the first aryl chemical noted to cause duodenal ulcer ( 18). Subsequently, 3,4-toluenediamine ( ) and 3,4-toluenedithiol (20) were also shown to induce duodenal ulcers and occasionally adrenal necrosis in rats. [Pg.177]

Fitoussi, G., Negre-Salvayre, A., Pieraggi, M.-T., Salvayre, R. New pathogenetic hypothesis for Wohnan s disease possible role of oxidized low-density lipoproteins in adrenal necrosis and calcification. Bio-chem. J. 1994 301 267 - 273... [Pg.630]

Ciccantelli MJ, Gallagher WB, Skemp FC, Dietz PC. Fatal nephropathy and adrenal necrosis after translumbar aortography. N Engl J Med I958 258(9) 433-5. [Pg.1894]

Dao TL, Tanaka Y. 1963. Inhibitory effect of polynuclear hydrocarbons and amphenone analogs on induction of acute adrenal necrosis by 7,12-dimethyl-benz(a)anthracene. Cancer Res. 23 1148— 52... [Pg.23]

Adrenal necrosis caused by 2-dimethylbenzanthracene (IMBA) is blocked by M or impaired liver function 3 while that brought on by its metabolite, 7-hydroxymethyl methylbenzanthracene is blocked only by This metab-... [Pg.267]

The metabolism of DMBA is stimulated by pretreatment of rats with various PAH and aromatic azo derivatives (50, 105, 148, 231-234, 294, 425, 502). Pretreatment also protects against adrenal necrosis caused by DMBA 210, 489). Pretreatment with 3-methylcholanthrene causes higher rates of ring oxidation of... [Pg.197]

Pantothenic acid deficiency induced either by a deficient diet or by the administration of pantothenic acid antimetabolites causes adrenal deficiency in rats. The ACTH content of the adrenal venous blood is reduced, and the concentration of coenzyme A is decreased in the gland. Pantothenic acid administration normalizes the coenzyme A concentration. The administration of growth hormone to pantothenic acid-deficient rats that have also been hypophysecto-mized increases the death rate and the incidence of adrenal necrosis. How the vitamin deficiency affects the humoral interrelationship remains to be investi-... [Pg.277]

Z8. Zuckerman, S. H., Shellhaas, J., and Butler, L. D., Differential regulation of lipopolysaccharide-induced interleukin I and tumor necrosis factor synthesis Effects of endogenous and exogenous glucocorticoids and the role of the pituitary-adrenal axis. Eur. J. Immunol. 19,301-305 (1989). [Pg.131]

The 1-hour LCso in rats was 262 ppm, and the oral LDso was lOOmg/kg. In animal experiments lung edema and hydrothorax have occurred after inhalation exposure. Repeated oral administration causes necrosis of the liver, spleen, adrenal gland, and testis, as well as ulceration and perforation in the gastric area in rats. The dermal LDso in rabbits was 141 mg/ kg, indicating significant skin absorption. ... [Pg.143]

Szabo, S. Selye, H. (1971) Adrenal apoplexy and necrosis produced by acrylonitrile. Endo-krinologie, 51, 405-408... [Pg.104]

Szabo, S., Hiittner, I., Kovacs, K., Horvath, E., Szabo, D. Horner, H.C. (1980) Pathogenesis of experimental adrenal hemorrhagic necrosis ( apoplexy ). Ultrastructural, biochemical, neuro-pharmacologic, and blood coagulation studies with acrylonitrile in the rat. Lab. Im est.. 42, 533-546... [Pg.104]

Following short-term inhalation exposure to 160 ppm [620 mg/m ] methyl bromide (6 h per day on five days per week for up to six weeks), B6C3F, mice were found to be more sensitive than Fischer 344/N rats 50% of male mice died after eight exposures and 50% of female mice after six exposures, while similar mortality was observed in male rats only after 14 exposures. Neuronal necrosis and testicular degeneration were observed in both species nephrosis was observed in nearly all mice, while necrosis of the olfactory epithelium was more marked in rats. Myocardial degeneration occurred in rats and to a lesser degree in male mice. In the adrenal cortex, there was cytoplasmic vacuolation in rats and inner zone atrophy in female mice (Eustis et al., 1988). [Pg.726]

Rats and dogs given intravenous doses of triethylene glycol diglycidyl ether showed necrosis of the renal tubule epithelium, of the adrenal cortex and of the intestinal epithelium. In dogs, blood neutrophils disappeared and lymphocyte counts fell to 50% of normal. Though the erythrocyte and platelet counts remained constant, the brief appearance of polychromatic and nucleated red cells indicated that erythropoiesis was also affected. [Pg.1540]

In chronic benzene intoxication, mild poisoning produces headache, dizziness, nausea, stomach pain, anorexia, and hypothermia. In severe cases, pale skin, weakness, blurred vision, and dyspnea occur on exertion. Hemorrhagic tendencies include petechia, easy bruising, and bleeding gums. Bone marrow depression produces a decrease in circulating peripheral erythrocytes and leucocytes (101). Fatalities from chronic exposure show at autopsy severe bone marrow aplasia, and necrosis or fatty degeneration of the heart, fiver, and adrenals (125). [Pg.47]

Other systemic effects have been observed in a small number of individuals intentionally or accidentally ingesting white phosphorus containing poison or firework. Some of these effects, such as fatty infiltration of the pancreas (Humphreys and Halpert 1931), splenomegaly (Greenberger et al. 1964), and necrosis of the adrenal medulla and cortex (Wechsler and Wechsler 1951), are consistent with effects that have been widely reported in... [Pg.136]

It was noted that she had gram-negative rods on her blood smear her blood culture grew penicillin-sensitive Streptococcus pneumoniae, in 6 hours. At autopsy, she was noted to have Streptococcus pneumoniae endocarditis of the right ventricle, focal ischemia of the left ventricle, bilateral pleural effusions, hepatic congestion with thrombosis, renal congestion, bilateral adrenal hemorrhage, and necrosis. Death was due to septic shock from Streptococcus pneumoniae. [Pg.18]

Rats on a pantothenic acid-free diet show rapid depletion of adrenal corticosteroids, and reduced production of the steroids in isolated adrenal glands in response to stimulation with adrenocorticotrophic hormone (ACTH). This presumably reflects the role of acetyl CoA in the synthesis of steroids deficiency also results in atrophy of the seminiferous mbules of male rats and delayed sexual maturation in females. As deficiency progresses, there is enlargement, then congestion, and finally hemorrhage, of the adrenal cortex. In young animals, but not in adults, pantothenic acid deprivation eventually leads to necrosis of the adrenal cortex. [Pg.353]


See other pages where Adrenal necrosis is mentioned: [Pg.1385]    [Pg.1385]    [Pg.320]    [Pg.179]    [Pg.1881]    [Pg.306]    [Pg.667]    [Pg.197]    [Pg.284]    [Pg.57]    [Pg.1385]    [Pg.1385]    [Pg.320]    [Pg.179]    [Pg.1881]    [Pg.306]    [Pg.667]    [Pg.197]    [Pg.284]    [Pg.57]    [Pg.47]    [Pg.220]    [Pg.856]    [Pg.517]    [Pg.196]    [Pg.158]    [Pg.145]    [Pg.205]    [Pg.260]    [Pg.458]    [Pg.336]    [Pg.78]    [Pg.78]    [Pg.741]    [Pg.741]    [Pg.137]    [Pg.77]   
See also in sourсe #XX -- [ Pg.55 ]




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