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At least 19 recordsLinked to original sources
PubMed1954

The effect of alcohol on the choline requirement. II. Incidence of renal necrosis in weanling rats following short term ingestion of alcohol.

The effect of alcohol on the choline requirement was assayed in weanling rats maintained on a basal diet of relatively low lipotropic activity containing the equivalent of 0.089 per cent choline. Alcohol was administered as a 15 per cent solution in lieu of drinking water. The incidence of renal cortical necrosis, the increase in kidney weight, and the mortality rate at the end of 14 days served as indices of choline deficiency. Under these conditions alcohol-fed animals developed more severe signs of choline deficiency than either pair-fed controls or pair-fed isocaloric controls receiving a sucrose supplement instead of alcohol. The addition of as little as 0.08 per cent of choline to the basal diet abolished these differences. It was concluded that (a) alcohol increases the choline requirement, and may, thus, induce a state of relative deficiency when the diet is marginal in lipotropic activity, and (b) this effect is independent of the caloric intake. The possible significance of these observations in relation to chronic alcoholism in the pathogenesis of Laennec's cirrhosis has been discussed.

Animals↗
PubMed1956

Effects of hormones on the adrenal necrosis produced by Besnoitia jellisoni in golden hamsters.

Adrenal necrosis has been described in golden hamsters where it occurs during the course of infection with Besnoilia jellisoni. This necrosis results directly from the active intracellular proliferation by this obligate intracellular protozoan organism. After infection, adrenal necrosis is rarely observed in hypophysectomized hamsters. In unoperated animals adrenal necrosis is suppressed to varying degrees by cortisone (E), hydrocortisone (F), corticosterone (B), 11-dehydrocorticosterone (A), and possibly by 11-desoxycorticosterone (DOCA). Besnoitia organisms proliferate in otherwise "immune" hamsters around the subcutaneous deposits of the acetates of cortisone (E), hydrocortisone (F), and 11-dehydrocorticosterone (A); a marked depression of general immunity follows the administration of pharmacologic doses of the former two hormones. Organisms do not proliferate around the sites of corticosterone acetate (B) and 11desoxycorticosterone acetate (DOCA) injection, nor next to deposits of testosterone propionate, 11-desoxy-17-hydroxycorticosterone acetate (Reichstein's compound S) and epinephrine in oil. It is postulated that certain glucocorticoids can so modify immunity mechanisms locally, that general immunity becomes ineffective; this occurs in the adrenal glands owing to endogenous corticoid production, at the sites of exogenous corticoid injection, and proximal to that in the lungs. A comparison is made with the pathogenesis of tuberculosis and histoplasmosis of the adrenal gland which results in Addison's disease in man, and it is concluded that a similar pathogenetic mechanism is operative. The use of glucocorticoids for replacement therapy is discussed in reference to their relative resistance-depressing activities in pharmacologic doses. These undesirable side effects would appear to be less pronounced, if not absent, if corticosterone (B) rather than cortisone (E) and hydrocortisone (F) therapy were used. Porcine adrenocorticotrophic hormone (ACTH) appearsto depress the incidence of adrenal necrosis in unoperated hamsters, and supports proliferation of organisms in the adrenal cortex with subsequent necrosis in only a small proportion of hypophysectomized hamsters. The possibility is discussed that ACTH from a different species (hog) might lead to a change in the secretory activity of the hamster adrenal gland.

Adrenal Gland Diseases↗
PubMed1961

Selective adrenal necrosis and apoplexy induced by 7, 12-dimethylbenz(a)anthracene.

Invariably in every normal rat a single dose of 7, 12-dimethylbenz(a)anthracene, by mouth or injected in a vein, was found to cause apoplexy and massive necrosis in the inner zones of the adrenal cortex; the zona glomerulosa, the adrenal medulla, and a small region of cortex adjacent to the great adrenal vessels were spared from damage. DMBA caused these selective lesions in females and in males of 2 strains of rats. Hemorrhage and necrosis were observed in no organ other than the adrenal gland. Whereas adrenal glands were heavily damaged by DMBA, pituitary and ovary escaped injury by the compound. A single huge but sublethal feeding of o, p'-DDD caused degenerative changes of minor magnitude in the adrenals and only in a small percentage of rats; the property of inducing adrenal damage was not shared by other polynuclear aromatic hydrocarbons which were investigated, including strong carcinogens. Presence of adrenal medulla is not a prerequisite to damage of the adrenal cortex by DMBA. The adrenal damage occurred in rats, given DMBA, from which the pituitary had been removed but the lesions were smaller in extent and less in incidence as post-hypophysectomy atrophy of the adrenal cortex progressed. The entire DMBA molecule was necessary to induce adrenal damage; fragments of this molecule did not induce adrenal lesions. Two components which are of cardinal importance in this specific damaging effect are: (a) electronic factor; (b) steric factor. The level of isocitric dehydrogenase in adrenal is modified considerably by presence or absence of estradiol-17beta.

Adrenal Cortex↗
PubMed1961

Studies of acute phase protein. I. An immunohistochemical method for the localization of Cx-reactive protein in rabbits. Association with necrosis in local inflammatory lesions.

A method is presented for the immunohistochemical localization of Cx-reactive protein in rabbits, based on the use of a defined antiserum and rigorous fixation techniques requisite for this antigen. In animals in which inflammatory lesions and CxRP response were induced by intramuscular injection of typhoid vaccine, Cx-reactive protein was localized only in the area of local inflammation within muscle fibers showing morphologic evidence of necrotic change. Within such altered fibers, CxRP was observed in peripheral segments of myofiber or in subsarcolemmal sarcoplasm, in scattered deposits in sarcoplasm, and in vacuolar inclusions. No CxRP was found at any time in polymorphonuclear or mononuclear cells in the inflammatory lesion, nor in contralateral muscle, regional or distal lymph nodes, liver, spleen, thymus, heart, or kidney, except as traces in lumens of vessels or interstitium. CxRP was first detected in necrotic myofibers at the inflammatory site after a latent period of 8 to 10 hours following injection of the inflammatory stimulus and could be demonstrated in these sites for the 48 hours of the experiment. It could not be observed at the inflammatory site before appearance in the blood. Identical histologic localization in necrotic myofibers at the site of the local lesions was found following induction of granulocytopenia with nitrogen mustard. These findings are consistent with the hypothesis that CxRP is formed locally at the site of inflammation from tissue elements undergoing necrotic change. Alternatively, secondary deposition from the blood at the inflammatory site cannot be excluded, but is considered less likely in view of the failure to obtain evidence of a cellular localization of CxRP in other organs.

Acute-Phase Proteins↗