Fluoride and silicon intake in normal and endemic fluorotic areas.

Precise quantitative information on (a) the contribution of diet to the daily intake of fluoride; and (b) the intake of silicon, which the current work suggests can aggravate fluorosis, is not available for fluorotic and non-fluorotic areas of India. Therefore, an attempt has been made in the present study to collect the above information in normal and fluorotic villages. The daily intake of fluoride (mean +/- SD) over water and diet in normal villages was 1.2 +/- 0.67 mg and 1.0 +/- 0.60 mg, while the corresponding values in a normal urban area were 0.5 +/- 0.03 mg and 1.2 +/- 0.73 mg, respectively. With respect to the intake over water the mean values in normal areas (urban vs. rural) were significantly different (P < 0.001), while there was no significant difference in dietary contribution in the normal areas. In fluorotic villages the daily intake of fluoride was 12.1 +/- 4.11 mg over water and 3.4 +/- 2.43 mg over the diet. These values from fluorotic villages were significantly higher (P < 0.001) than those observed in the normal rural areas. The total intake of silicon (mean +/- SD) in rural and urban normal areas was 204 +/- 58.6 mg and 143 +/- 29.4 mg per day, respectively. The corresponding value from fluorotic villages was 277 +/- 65.5 mg, which was significantly higher (P < 0.01) than those observed in both the normal areas. The situation was similar in fluorotic villages with respect to silicon intake over diet and water. However, the intake of this element over water in the normal rural area (74.0 +/- 18.51 mg per day) was significantly higher (P < 0.001) than the value obtained in the normal urban area (7.5 +/- 1.82 mg per day). This study clearly shows that in the fluorosis-affected areas studied, (a) the total intake of both fluoride and silicon is significantly higher than the intake in non-fluorotic areas; and (b) diets contribute significantly to the intake of both these elements. Our observations on silicon intake and its probable relation to fluorosis are the first of their kind in the literature.

Biochemical assessment of vitamin B6 nutritional status in pregnant women with orolingual manifestations.

Two groups of pregnant women belonging to a low socioeconomic group, one with oral lesions and the other without lesions, were studied in the 3rd trimester of pregnancy for vitamin B6 nutritional status. Both the groups showed evidence of abnormal tryptophan metabolism, and in pregnant women with clinical signs the postload xanthurenic acid excretion in urine was higher than in the other group, suggesting a severe deficiency of vitamin B6. Treatment with vitamin B6 cured the oral lesions and also corrected the abnormalities in tryptophan metabolism. Excretion of 4-pyridoxic acid was low in both the groups and more so in women with oral lesions. Administration of tryptophan load significantly elevated the excretion of 4-pyridoxic acid in urine. These results indicated that pregnant women belonging to a low socioeconomic group were, in general, deficient in vitamin B6. In pregnant women with oral lesions the deficiency of vitamin B6 was more severe than in those pregnant women without oral lesions. Whether the severity of vitamin B6 deficiency would precipitate clinical signs like oral lesions is not yet known.

Vitamin B6 nutritional status of pellagrins and their leucine tolerance.

Disturbances in tryptophan-nicotinamide adenine dinucleotide pathway, seen in pellagrins whose staple is sorghum have been ascribed to an amino acid imbalance caused by excess intake of leucine. Studies in normal human volunteers and in experimental animals have shown that administration of vitamin B6 will counteract some of the metabolic effects of leucine. In view of these observations, two clinical studies were conducted--one to investigate the vitamin B6 nutritional status of pellagrins and the other to determine whether plasma leucine clearance in pellagrins is different from that of normals. Vitamin B6 nutritional status of pellagrins was found to be far from satisfactory, as indicated by elevated levels of xanthurenic acid and kynurenic acid in urine after a tryptophan load and low plasma pyridoxal phosphate levels. Plasma leucine concentrations at 1, 2, and 4 hr after a leucine load were significantly higher in pellagrins than those in normals. Administration of 25 mg of vitamin B6, intramuscularly 30 min before leucine load significantly decreased plasma leucine concentration in pellagrins. However, the leucine concentration at 4th hr did not return to basal level. Administration of vitamin B6 10 TO 20 mg/day orally for 10 to 15 days normalized leucine tolerance in pellagrins. Data presented here suggest that when the diets contain excess leucine, additional amounts of vitamin B6 are required.

Effect of leucine at different levels of pyridoxine on hepatic quinolinate phosphoribosyl transferase (EC 2.4.2.19) and leucine aminotransferase (EC 2.6.1.6) in rats.

1. Effects of incorporating 30 g leucine/kg into diets on quinolinate phosphoribosyl transferase (QPRT; EC 2.4.2.19) activity and leucine aminotransferase (EC 2.6.1.6) activity were studied in groups of rats receiving 5, 30 and 60 micrograms of pyridoxine/10 g diet. 2. The results indicated that 30 g leucine/kg diet significantly reduced the QPRT activity when the diets provided 5 micrograms pyridoxine/10 g and that the effect was only marginal when the diet included 30 micrograms pyridoxine/10 g. The inhibitory effect was completely absent when the diet provided higher amounts of pyridoxine (60 microgram/10 g). 3. These results suggest that additional amounts of pyridoxine are necessary to counteract the effects of excess of leucine in the diet. 4. Leucine aminotransferase activity was increased in rats given diets containing higher amounts of pyridoxine; supplementary leucine also increased the enzyme activity.