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At least 163 records · Page 9Linked to original sources
PubMed1984

The effects of ascorbic acid deficiency and excess on the metabolism and toxicity of N-nitrosodimethylamine and N-nitrosodiethylamine in the guinea pig.

The influence of ascorbate deficiency and megadosage on the metabolism of N-nitrosodimethylamine (NDMA) and N-nitrosodiethylamine (NDEA) was investigated in the guinea pig. After 21 days on a scorbutogenic diet, microsomal cytochrome P-450 and cytochrome b5 levels fell by 51 and 32%, respectively, while cytochrome c reductase activity remained constant. The activities of NDMA and NDEA dealkylase I were also depressed significantly. The Vmax of NDMA demethylase I and NDEA deethylase I was significantly depressed. Also, ascorbate deficiency significantly decreased the plasma clearance of both nitrosamines though the LD50 of neither were altered by ascorbate nutrition. Covalent binding of 14C from [14C]NDMA and [14C]NDEA to DNA obtained from liver slices was significantly lower in the deficient than in the control samples; megadosage appeared to have the opposite effect.

Animals↗
PubMed1976

Effect of ascorbic acid deficiency on mouse second molar tooth germs cultivated in vitro.

Mandibular second molar tooth germs from two-day old mice were cultured in vitro, on millipore membranes, for periods of up to 20 days in liquid medium with or without added ascorbic acid. Tooth germs grown in ascorbate medium were characterized by relatively normal growth, differentiation, morphology and histology. Cuspation patterns were maintained. The epithelial root sheath continued to grow along the millipore membrane. Tooth germs cultured in ascorbate-deficient medium manifested a consistent and striking failure in maintenance of differentiated odontoblastic and ameloblastic tissue with arrest of predentin synthesis, severe structural collapse and reduction in size. Cuspation patterns were lost in scorbutic molars, with sinking of surface layers into pulpal tissue and flattening of the entire organ. This resulted in a lack of recognizable morphology and in severe disorganization of tissues. Only growing areas of the root sheath with associated proliferation of preameloblasts and pre-odontoblasts and adjacent pulpal tissue remained normal and refractory to ascorbate deficiency. Odontoblastic as well as ameloblastic layers were disrupted and cells were dedifferentiated. Newly differentiated odontoblasts became highly vacuolated when they became polarized and started to secrete extracellular matrix.

Ameloblasts↗
PubMed1975

[Effects of ascorbic acid deficiency on lactate dehydrogenase. Quantitative and isoenzymatic study].

Light, acute vitamin C deficiency or repletion had no uniform effect on lactiodeshydrogenase, each organ reaching specifically (skeletal muscle, heart, kidney, spleen, liver adrenals, testes). There was no correlation with the age of the animal except in the case of testicular lacticodeshydrogenase isoenzymes. Reduction of food intake caracteristic of the late state of scurvy had no effect on the distribution of isoenzymes which was also independent of quantitative variations of enzyme activity. Vitamin C repletion restored the normal distribution of isoenzymes in spleen and liver but not in skeletal muscle. In the last phase of acute vitamin C deficiency, lactiodeshydrogenase activity was generaly elevated (heart and skeletal muscle excepted). When ascorbic acid was given back lacticodeshydrogenase activity remained elevated in liver and spleen but was lowered in skeletal muscle.

Acute Disease↗
PubMed1977

Localization of the interference of ascorbic acid deficiency with bile acid biogenesis.

The catabolism of 26-14C-cholesterol and of 26-14C-7alpha-hydroxycholesterol, the first stage in the transformation of cholesterol to bile acids, was studied in guinea-pigs with chronic latent vitamin C deficiency. Vitamin C deficiency markedly inhibited the oxidation of 26-14C-cholesterol to 14CO2, but did not significantly affect the catabolism of 26-14C-7alpha-hydroxycholesterol. The distribution of 14C in the tissues and body fluids of control and vitamin-deficient guinea pigs injected with labelled 7alpha-hydroxycholesterol was likewise the same. Ascorbic acids is probably needed only for 7alpha-hydroxylation of cholesterol, while the other stages of bile acid biogenesis are independent of vitamin C.

Animals↗