In Vitro Formation of αß-Unsaturated Ketones by Adrenal Tissues in Ascorbic Acid Deficiency

1957 ◽  
Vol 188 (2) ◽  
pp. 303-307 ◽  
Author(s):  
Habeeb Bacchus

In vitro studies on the formation of Δ4-3-ketones from the Δ5-3 ß-ol structure of dehydroepiandrosterone acetate by adrenal tissue were conducted. The adrenal tissue of normal and control guinea pigs is capable of this conversion to the extent of 0.46 µm/100 mg adrenal tissue, in the absence of any added cofactors. The conversion by adrenals of ascorbic acid-deficient animals is significantly less than this and is decreased progressively with the duration of the scorbutigenic fare. Addition of ascorbate to the incubation preparation corrects the disturbance in this process in the adrenal of the ascorbic acid-deficient animal.

1957 ◽  
Vol 188 (2) ◽  
pp. 297-302 ◽  
Author(s):  
Habeeb Bacchus

The influence of ascorbic acid nutrition on the ability of adrenal tissue to convert 11-desoxycortisol (compound S) to cortisol was studied. It was shown that this process of 11-beta-hydroxylation of desoxycortisol was decreased in ascorbic acid deficiency. Addition of ascorbate to preparations of normal adrenals with desoxycortisol enhanced the conversion. Ascorbate addition corrected the decreased 11-beta-hydroxylation ability of the adrenals of animals on the deficient fare for 13–25 days, but failed to affect the ability of the adrenals of animals on the fare for 35 days. Ascorbate decreased ( P < 0.01) the spontaneous formation of 17-OH,20,21-ketol corticosteroids by normal adrenals. The decreased spontaneous formation of these substances by the ascorbic acid deficient adrenal is corrected by ascorbate.


1959 ◽  
Vol 196 (3) ◽  
pp. 607-610 ◽  
Author(s):  
Habeeb Bacchus ◽  
Albert F. Debons ◽  
Sidney Levin ◽  
John W. Wallace

Blood and urinary levels of ketone bodies were studied in normal, ascorbic acid-deficient, and pair-fed control, guinea pigs. The resting levels of ketone bodies in the blood and urine throughout the course of ascorbic acid-deficiency do not differ significantly from those of control animals. The ketonemic response to fasting is greater in the control animals than in the ascorbic acid-deficient animals. The disappearance of injected ketone bodies (ß-hydroxybutyrate) is decreased in the ascorbic acid-deficient animal. The data suggest that in ascorbic acid-deficiency there is a decreased utilization of ketone bodies coupled with a decreased spontaneous ketogenesis.


2001 ◽  
Vol 71 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Yoshiji Ohta ◽  
Takafumi Niwa ◽  
Takashi Yamasaki

We examined the effect of prolonged marginal ascorbic acid deficiency of the levels of antioxidants and lipid peroxide in lenses of guinea pigs in order to clarify lenticular antioxidant status under ascorbic acid deficiency. Male guinea pigs aged 4 weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or sufficient ascorbic acid (1 g/animal per day) in drinking water for 3 and 6 months. The deficient group showed no lens opacity during the administration period. The deficient group had 62.3 and 53.9% of lenticular ascorbic acid content in the sufficient group at 3 and 6 months of ascorbic acid deficiency, respectively. There were no differences in lenticular contents of reduced glutathione and thiobarbituric acid reactive substances, an index of lipid peroxidation, between both groups at 3 and 6 months of ascorbic acid deficiency, while the deficient group tended to have higher lenticular vitamin E content than the sufficient group. The deficient group had higher serum vitamin E concentration than the sufficient group at 3 and 6 months of ascorbic acid deficiency. These results indicate that lenticular antioxidant status is maintained well in guinea pigs with prolonged marginal ascorbic acid deficiency, which may result in no cataract formation.


1971 ◽  
Vol 25 (3) ◽  
pp. 367-376 ◽  
Author(s):  
A. A. Wapnick ◽  
S. R. Lynch ◽  
H. C. Seftel ◽  
R. W. Charlton ◽  
T. H. Bothwell ◽  
...  

1. There is an association between iron overload, ascorbic acid deficiency and osteoporosis in middle-aged South African Bantu males. The iron overload contributes to the ascorbic acid deficiency by accelerating its oxidative catabolism. The object of the present investigation was to explore the possibility that the osteoporosis results from chronic ascorbic acid deficiency.2. On quantitative microradiography, percentage bone-formation surface was normal but percentage bone-resorption surface was significantly increased in ten osteoporotic subjects compared with seven control subjects.3. There was a significant inverse correlation between bone mineral density and liver storage iron concentration in thirty-five Bantu subjects. In thirteen individuals aged 39 years or less, liver storage iron concentration was significantly correlated with percentage bone-resorption surface.4. Guinea-pigs deprived of ascorbic acid for 21 d exhibited both significantly diminished percentage bone-formation surface and increased percentage bone-resorption surface.5. Guinea-pigs overloaded with iron by injections of iron dextran developed significantly reduced hepatic ascorbic acid concentrations and bone mineral densities; percentage bone-formation surface was significantly diminished and percentage bone-resorption surface significantly increased. Ascorbic acid injection largely prevented the bone changes.


1990 ◽  
Vol 267 (2) ◽  
pp. 535-537 ◽  
Author(s):  
B E Cham ◽  
H P Roeser ◽  
A C Nikles

Two physicochemically and metabolically separate pools of ferritin, namely cytosolic ferritin and lipid-associated ferritin, are present in the livers of guinea pigs. In this paper we establish that the iron content of cytosolic ferritin is dependent on and linearly related to ascorbic acid concentration, whereas changes in concentration of this vitamin do not affect the iron content of lipid-associated ferritin. In livers of ascorbic acid-deficient guinea pigs both synthesis and degradation of cytosolic ferritin are diminished equally. Consequently cytosolic ferritin is metabolized more slowly without changes in its pool size. In contrast with cytosolic ferritin, the metabolism of lipid-associated ferritin is unaffected by ascorbic acid deficiency. The differential effects of ascorbic acid deficiency on the physicochemical characteristics as well as on the metabolism of cytosolic ferritin and lipid-associated ferritin suggest that the two forms of ferritin have different functional roles.


1978 ◽  
Vol 56 (5) ◽  
pp. 352-356 ◽  
Author(s):  
Susan K. Hoehn ◽  
Julian N. Kanfer

The effects of L-ascorbic acid deficiency on guinea pig hepatic and brain lysosomal hydrolases were examined. In general, hepatic β-N-acetylhexosaminidase, β-D-glucoronidase, α-D-galactosidase, α-D-mannosidase, and acid phosphatase were elevated in scorbutic animals. This appears to be independent of the starved state. Brain β-D-glucoronidase and acid phosphatase followed a similar pattern to that observed with the liver enzymes, but brain β-N-acetylhexosaminidase was not affected by L-ascorbic acid deficiency. Supplementing the in vitro assay system with L-ascorbic acid decreased the activity of hepatic β-N-acetylhexosaminidase somewhat but had no effect on the brain enzyme. Serum total β-N-acetylhexosaminidase was unaffected by dietary treatments although the activity of β-N- acetylhexosaminidase A tended to increase in the scorbutic animals. Subcellular fractions were obtained from the three groups of animals and the recoveries of protein, β-N-acetylhexosaminidase, and glucose-6-phosphatase estimated.


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