1. Ten healthy volunteers ingested 1.5 mmole epicatechin gallate (ECg), epigallocatechin (EGC) or epigallocatechin gallate (EGCg) in a randomized crossover design. After deconjugation, catechins in plasma and 24-h urine samples were determined by high-performance liquid chromatography (HPLC). Antioxidant activity was measured in plasma by determining ferric reducing activity (FRAP). 2. The catechin levels in plasma after ingestion were significantly different: EGC rose quickly with a short elimination half-life (t1/2 elim = 1.7 h), ECg was intermediate in rise but slowest in decline (t1/2 elim = 6.9h), EGCg was slowest in rise but intermediate in decline (t1/2 elim = 3.9h). At 24h, EGC and EGCg had returned to base levels, but ECg was still elevated. Peak maximum varied between 1.3 (EGCg) and 5.0 micromol l(-1) (EGC). 3. Very limited interconversion (ECg-->epicatechin, EGCg-->EGC) occurred indicating that degallation is not required for uptake. 4. Up to 13.6% of the ingested EGC (partly methylated) was excreted in the urine, but ECg or EGCg were not detected. 5. EGC and ECg produced an increase in antioxidant activity in plasma, but with EGCg, no statistically significant effect was found. 6. The pattern of uric acid in plasma showed a clear resemblance with that of FRAP and linear regression analysis indicated a very significant relationship (R2 = 0.88, p < 0.0001). 7. It is concluded that tea catechins differ significantly in their pharmacokinetic behaviour.

The effect of dietary calcium level on the fecal and urinary excretion of calcium, phosphorus and magnesium was studied in adult cats. Ovariectomized cats were fed purified diets containing 3.2, 4.8, 9.5 or 19.3 mmol calcium/MJ in a 4 x 4 wk crossover study. During the experiment, balance studies were performed and blood samples were taken. The adult ovariectomized cats maintained calcium balance at all four levels of calcium tested. Extra dietary calcium, in the form of CaCO3, caused a slight increase in urinary pH. Urinary concentrations of phosphorus and magnesium dropped, but that of calcium remained unchanged, when the cats were fed diets with increasing calcium levels. The percentages of apparent absorption of phosphorus and magnesium fell when calcium intake was raised. The dietary calcium level did not affect plasma concentrations of calcium, magnesium and phosphorus or plasma activity of alkaline phosphatase.

In a long-term experiment with three successive generations of rats, the influence of dietary phosphorus restriction (2 instead of 4 g phosphorus/kg diet) on nephrocalcinosis, reproduction and bone mineralization was studied. Nephrocalcinosis in female rats, as based on kidney calcium concentration and histological examination, was prevented by phosphorus restriction. The low phosphorus diet caused reduced femur concentrations of magnesium, calcium and phosphorus in rats of the first and second generation aged 4 to 12 wk. The low phosphorus diet resulted in lower plasma phosphorus concentrations. In the kidneys of female rats, immediately after lactation, a higher degree of tubular hyperplasia was seen after the low phosphorus diet was fed. Reproductive performance was not affected by phosphorus restriction. We conclude that 0.2% phosphorus in the diet prevents nephrocalcinosis in female rats while it sustains reproduction but delays bone mineralization.

This study addresses the questions to what extent commercial rodent diets would induce nephrocalcinosis, and which dietary components would be responsible for inducing this condition. For this purpose, 10 commercial diets were analysed for selected components and fed to weanling female rats. On the basis of histological inspection of kidney sections, two diets were found to produce significant nephrocalcinosis. The condition could be considered relatively mild because concentrations of Ca in kidney tissue were not increased. There was considerable variation between the commercial diets in the (analysed) concentrations of Ca, P, Mg and protein as well as in the diet-induced urinary pH, urinary volume and caecal weight. Of these parameters, only the dietary Ca:P ratio and group mean urinary pH correlated significantly with the observed variation in group mean calcification scores, the relationships being negative. It is suggested that the Ca:P ratio of commercial rodent diets is an important determinant of nephrocalcinosis.

The degree of nephrocalcinosis after increasing the dietary phosphorus concentration from 0.2 to 0.5 g/100 g was measured in weanling female rats of 10 inbred strains. Based on kidney calcium concentrations and histological kidney calcification scores, there were considerable strain differences in nephrocalcinogenesis; 86% of the strain variability in nephrocalcinosis was attributable to genetic factors. Two strains with the most extreme nephrocalcinogenic responses were retested and the strain difference was found to be reproducible. Mean plasma phosphorus concentrations after phosphorus feeding were lower in the sensitive strain than in the insensitive strain. The high phosphorus diet produced greater urinary phosphorus concentrations, with the increase being greater in the sensitive strain. The strain difference in the response of urinary phosphorus concentrations after raising dietary phosphorus level may determine the strain difference in phosphorus-induced nephrocalcinosis. After consuming the high phosphorus diet, RP rats housed in groups in solid-floored cages had significantly higher degrees of nephrocalcinosis than their counterparts housed individually in metabolism cages with wire-mesh bases.