Effect of delayed gastric emptying on fluoride absorption in the rat.

The rate and site of fluoride (F) absorption were compared in fasted 350 g male rats given 50 micrograms F (as NaF) in either water or a 7.5% pectin solution. Absorption was measured at intervals up to 2 h following gastric intubation. Gastric emptying was measured by inclusion of 14C-PEG in the F solution. The extent of gastric F absorption was derived from rates of gastric emptying (14C-PEG loss) and F loss. Pectin markedly slowed gastric emptying, but by 2 h, more than 90% of the solution had passed into the small intestine in both groups, and F absorption exceeded 90% in both groups. The rate of F absorption was initially much slower in the pectin group than in the group given F in water, and plasma F concentration increased more slowly and reached a lower maximum value. Absorption from the stomach was greater in the pectin group, but still accounted for only approx 25% of total gastrointestinal absorption. The reduced rate of F absorption and slower rise in plasma F concentration accompanying delayed gastric emptying indicate that passage of F into the small intestine is the major factor in rapid F absorption.

An investigation of calcium intake, 1-alpha(OH)D3, and etidronate on bone.

The synthetic metabolite of vitamin D3 [1 alpha(OH)D3] caused a significant plasma calcium elevation in rats only when dietary calcium was low. Animals given the low calcium diet (0.005%) had lower plasma parathyroid hormone (PTH) levels when the diet contained 1 alpha(OH)D3 and significantly higher levels than animals on a high calcium (0.95%) diet, with or without the vitamin. The nutritional stress of a low calcium diet without 1 alpha(OH)D3 resulted in a prolonged severe hypocalcemia and elevated serum PTH levels. A higher ash, phosphate, and calcium content was found in the bones of animals fed the high calcium diet, with no vitamin D3 that were given etidronate (EHDP). When animals received the same calcium diet with 1 alpha(OH)D3 supplementation, EHDP administration increased the percentage of bone ash but had no effect on ash weight. 1 alpha(OH)D3 or EHDP did not affect ash weight, dry fat free weight, and percentage of ash of bone of animals receiving a low calcium diet. The percentage of calcium and phosphorus in bone ash was similar among all groups, although the amounts per humerus were characteristically related to the calcium intake. There was approximately 20-25% less bone mineral and calcium and phosphorus in the humeri of low calcium intake animals than in animals provided an adequate dietary calcium.

The effect of vitamin A deficiency and fluoride on glycosaminoglycan metabolism in bone.

The effects of fluoride intake and vitamin A deficiency on glycosaminoglycan metabolism in vivo were investigated. Weanling female rats were fed either a vitamin A deficient diet ad libitum, a vitamin A supplemented diet pair-fed to the deficient animals, or the vitamin A supplemented diet ad libitum. Additionally, each vitamin A dietary group was divided into three subgroups with the animals receiving water containing 0, 10 or 50 ppm fluoride. The results showed that the groups receiving 10 and 50 ppm fluoride at all dietary levels of vitamin A had significantly higher in vivo 35SO4 incorporation in both the epiphyseal and diaphyseal regions of the bone than the animals receiving 0 ppm fluoride. The vitamin A deficient animals incorporated significantly less 35SO4 into glycosaminoglycans in the epiphyseal and diaphyseal regions of the bone compared to the pair-fed, vitamin A sufficient animals for all three fluoride receiving groups. There was no interaction between fluoride intake and dietary vitamin A levels on 35SO4 incorporation into glycosaminoglycans. Fluoride either increased sulfation or turnover of glycosaminoglycans.

Lack of cytogenetic effects in mice or mutations in Salmonella receiving sodium fluoride.

We have examined the possible effect of fluoride intake on chromosome damage. There was no evidence of increased frequency of chromosomal aberration in bone marrow or testis cells of mice with either 50 ppm fluoride intake over several generations or 100 ppm intake for 6 weeks compared to animals drinking distilled water. Fluoride was not found to be mutagenic in a widely used bacterial mutagenesis assay over a range of 0.1 to as high as 2000 microgram fluoride per plate.