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Results for “ASCORBIC ACID DEFICIENCY”

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At least 181 records · Page 10Linked to original sources
PubMed1971

Suppression of adrenocorticotrophic activity in the ascorbic acid deficient guinea-pig.

1. Adrenocortical hyperactivity caused by a marked increase in circulating corticotrophin occurred in guinea-pigs on a diet deficient in ascorbic acid.2. Betamethasone prevented the rise in the blood ACTH concentration in scorbutic animals and also the increased steroid production per gramme adrenal tissue in vitro. It diminished the adrenal hypertrophy and partially suppressed the rise in plasma cortisol.3. Ninety minutes after the injection of ascorbic acid corticotrophin could no longer be detected in the plasma of scorbutic animals.4. Neither the survival time nor the weight loss was affected by betamethasone treatment.

Adrenal Glands↗
PubMed1978

Suspected ascorbic acid deficiency in a colony of squirrel monkeys (Saimiri sciureus).

Subperiosteal cranial hematomas were observed in five female squirrel monkeys. The absence of trauma in the clinical history, the characteristic clinical changes, and the pathological lesions suggested that the animals were scorbutic. Analysis of feed which was soaked in water, or left on the ground for varying time periods at different temperatures, indicated that there was loss of ascorbic acid. During the manufacture of monkey feed, ascorbic acid is dusted on as a final process. The practice of soaking feed resulted in the "washing off" or the destruction of ascorbic acid. This disease outbreak emphasized the important of management practices in a primate colony.

Animals↗
PubMed1995

[Hepatocellular transplantation in rats with congenital ascorbic acid deficiency].

The purpose of this study was to investigate suitable sites for hepatocyte transplantation in rats with congenital liver enzyme deficiency. Hepatocytes were isolated from ODS-(+)/+ rats, which are congenic to ODS-od/od rats and have hepatic L-gulonolactone oxidase. A total of 1 x 10(7), 1 x 10(7), and 2.5 x 10(6) hepatocytes were respectively transplanted into the peritoneal cavity, spleen, or portal vein of ODS-od/od rats, which are unable to synthesize ascorbic acid (AsA) due to lack of hepatic L-gulonolactone oxidase. After 4 days of oral pretreatment with 0.05% 2-acetylaminofluorene, recipients underwent 70% partial hepatectomy just before transplantation. AsA administration was discontinued at 6 weeks after transplantation. The symptom-free survival rate and the serum AsA level of recipient rats were determined at 6 weeks after discontinuing AsA administration. The symptom-free survival rate of untransplanted rats and recipient rats with intraperitoneal, intrasplenic and intraportal hepatocyte transplantation were 0%, 0%, 60%, and 100%, respectively. The serum AsA levels were 0.20 +/- 0.20 microgram/ml, 0.14 +/- 0.05 microgram/ml, 1.06 +/- 0.26 microgram/ml, and 1.58 +/- 0.61 microgram/ml, respectively. Intrasplenic or intraportal transplantation was able to cure ODS-od/od rats. A subsequent splenectomy study showed that hepatocytes reaching the liver via the splenic vein following intrasplenic hepatocyte transplantation played a major role in this experimental success.

Animals↗
PubMed1974

Ascorbic acid deficiency in malignant diseases: a clinical and biochemical study.

In a study of the vitamin C status of 50 patients with malignant disease, 46 had leucocyte levels less than the lower limit of the normal range (18-50,μg/10(8) W.B.C.) and of these 30 had very low levels (< 12.5 μg/10(8) W.B.C.). Physical signs compatible with subclinical scurvy were frequently recorded and there was a significant decrease in capillary fragility in those with the lowest levels. Most patients had an inadequate dietary intake of ascorbic acid-containing foods and this was felt to be the major factor in producing the vitamin depletion.

Adult↗