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Results for “ASCORBIC ACID DEFICIENCY”

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PubMed1979

The role of ascorbic acid on the structural integrity of developing tooth germs.

Tooth germs grown in ascorbate deficient medium for up to 20 days underwent progressive and widespread changes. Proliferation and differentiation of preameloblasts and preodontoblasts progressed normally. Newly differentiated odontoblasts, however, became vacuolated when they began secreting: this suggested a metabolic disturbance. Failure to maintain differentiated odontoblasts, ameloblasts and pulpal cells resulted in aberrant dentin matrix, cessation of dentin production, and finally overall structural collapse with loss of normal morphology. Biochemical studies then were undertaken to define the lesion involved. The relative rate of collagen synthesis in ascorbate deficient cultures was comparable to that of ascorbate supplemented cultures, but the collagen was found to be underhydroxylated. In this state it would be unstable at 37 degrees and subject to preferential degradation. This correlates with the observation that a major fraction of the hydroxyproline in the scorbutic cultures was found in the medium as small molecular weight peptides. The overall effect of ascorbate deficiency was to deprive the tooth germ of the normal quality and quantity of collagen resulting in the characteristic histological and structural abnormalities observed. Flattening and deterioration due to structural failure most likely resulted from abnormal extracellular matrix synthesis in the supportive pulp and dentin due to the aberrant collagen.

Animals↗
PubMed2000

Ascorbate deficiency impairs the muscarinic-cholinergic and ss-adrenergic receptor signaling systems in the guinea pig submandibular salivary gland.

Ascorbic acid is preferentially concentrated in the hypothalamus, pituitary and adrenal glands. Its level in the acini of salivary glands is relatively high. We therefore hypothesized that ascorbate may have a role in salivary gland function. Ascorbate-deficient guinea pigs had lower stimulated whole salivary flow rates than well-fed, age-matched controls (P: < 0.005). Total salivary protein concentration was also markedly (P: < 0.005) reduced in the deficient guinea pigs. SDS-PAGE and densitometric quantification of protein bands confirmed significant reduction in specific salivary proteins (e.g., amylase, proline-rich proteins) in the saliva samples of malnourished guinea pigs. Some protein bands not seen in control saliva were detected in the saliva of malnourished guinea pigs. Ascorbate deficiency also produced a significant (P: < 0.005) reduction in the ss-adrenergic receptor density (subtype 1; 95 +/- 19 fmol/mg protein compared with 179 +/- 27 fmol/mg protein for the controls). No significant difference was observed between the two groups with respect to the ss-adrenergic receptor subtype 2. Additionally, ascorbate-deficient guinea pigs had significantly lower muscarinic-cholinergic receptor densities (50 +/- 5 vs. 74 +/- 8 fmol/mg protein for controls). Our data support the conclusion that diminished membrane receptors might impair the capacity of the transmembrane signaling system, resulting in salivary gland hypofunction in ascorbate-deficient guinea pigs. Without implying extrapolation of our findings in experimental animals to humans, it is perhaps relevant that many conditions often associated with salivary gland hypofunction in humans (e.g., smoking or drug ingestion) deplete cellular ascorbate.

Amylases↗
PubMed2005

Is sudden death with vitamin C deficiency caused by lack of carnitine?

We investigated the effect of carnitine supplementation during vitamin C (ASC) deficiency by measuring the levels of ASC and carnitine in plasma and cardiac muscle cells (CMC), and histological analysis with electron microscopy. The levels of carnitine were significantly decreased in ASC-deficient rats in plasma and the heart than those in the control. In carnitine supplemented ASC-deficient rats, a significant increase of carnitine levels were observed in both plasma and heart. The number of lipid droplets significantly increased in the ASC-deficient rats compared to the control rats, but did not increase in carnitine supplemented rats. These results indicate that ASC deficiency causes a generalized mitochondrial abnormality and accumulation of lipid droplets in CMC as observed in carnitine deficiency, and supplementation of carnitine prevented these changes even in the presence of ASC deficiency.

Animals↗