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Results for “ASCORBIC ACID DEFICIENCY”

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At least 451 records · Page 25Linked to original sources
PubMed1992

A delayed response to acute stimulation with human chorionic gonadotropin in scorbutic rats.

Since our previous study revealed low basal testosterone (T) levels and a failure in response to an acute stimulation with human chorionic gonadotropin (HCG) despite of a good response to chronic stimulation in scorbutic mutant rats, time course of the response to HCG was studied and plasma LH level was measured in young adult rats deficient in ascorbic acid for 3 weeks. A single subcutaneous injection of HCG (200 IU) elevated T levels only slightly in plasma and not in testicular tissues of scorbutic rats 1 h after the injection when the levels in ascorbutic rats reached a maximum, while it yielded the same response pattern as in ascorbutic rats after 3 h. A pretreatment with HCG to scorbutic rats for 1 or 4 days resulted in the same response of plasma T as in ascorbutic rats. Plasma LH levels in unstimulated scorbutic rats were about 40% of those in ascorbutic rats. These findings indicate that a prolonged deficiency of ascorbic acid decreases plasma LH, and may reduce the sensitivity of testes to LH.

Animals↗
PubMed1985

Requirement for ascorbic acid in a rat mutant unable to synthesize ascorbic acid.

The activities of several enzymes involved in hepatic ascorbic acid synthesis and the requirement of dietary ascorbic acid were investigated in the OD (osteogenic disorder) rat, which has a hereditary defect in ascorbic acid-synthesizing ability. No activity of hepatic L-gulonolactone oxidase was detected in OD rats. However, OD rats maintained the normal activities of hepatic UDPglucose dehydrogenase, UDPglucuronyl transferase and beta-glucuronidase. Hemorrhage in muscle and leg joints, lower hepatic content of cytochrome P-450 and lower activities of hepatic drug-metabolizing enzymes, higher serum and adrenal levels of corticosterone and lower urinary excretion of hydroxyproline were observed in ascorbic acid-deficient OD rats than in OD rats fed 300 mg ascorbic acid/kilogram diet. Consequently, we conclude that OD rats cannot synthesize ascorbic acid because of the lack of activity of hepatic L-gulonolactone oxidase and that the dietary addition of about 300 mg ascorbic acid (per kilogram diet) is enough to prevent signs of vitamin C deficiency and to achieve maximum growth, and that more than 300 mg ascorbic acid per kilogram diet may be required for the maximum activity of hepatic drug-metabolizing enzymes.

Adrenal Glands↗
PubMed1977

Effects of ascorbic acid on glucose-6-phosphate dehydrogenase-deficient erythrocytes: studies in an animal model.

There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) -deficient erythrocytes. We therefore studied the survival of G-6-PD-deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD-deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.

Animals↗
PubMed1993

Ascorbate-dependent elevation of mRNA levels for cytochrome P450s induced by polychlorinated biphenyls.

Trichlorobiphenyl induced only CYP1A2 mRNA, while pentachlorobiphenyl induced both CYP1A2 and CYP2B1 mRNAs in rat liver. The mRNA levels for these P450s were elevated when ascorbic acid-deficient ODS rats (mutant rats with a hereditary osteogenic disorder) were fed a diet supplemented with ascorbic acid. The amount of CYP2B1 mRNA increased rapidly and reached a maximum level of approximately double within 24 hr of injection of pentachlorobiphenyl. Thereafter, the amount of its mRNA decreased to a steady level. This pattern was roughly paralleled by changes in the amount of CYP1A2 mRNA.

Animals↗