Measurement of ischaemia-reperfusion in patients with intermittent claudication using NMR-based metabonomics.

Intermittent claudication has proved to be a good in vivo model for ischaemia-reperfusion. For assessment of ischaemia-reperfusion damage, the known biochemical markers all have disadvantages with respect to sensitivity and interference with other physiological events. In this work, we studied the metabolic effects of ischaemia-reperfusion in patients with intermittent claudication, and the effects of vitamin C and E intervention, using both traditional biochemical measurements and 1H-NMR-based metabonomics on urine and plasma.

Plasma concentrations of individual tea catechins after a single oral dose in humans.

1. Ten healthy volunteers ingested 1.5 mmole epicatechin gallate (ECg), epigallocatechin (EGC) or epigallocatechin gallate (EGCg) in a randomized crossover design.

Dietary non-tocopherol antioxidants present in extra virgin olive oil increase the resistance of low density lipoproteins to oxidation in rabbits.

Consumption of a range of dietary antioxidants may be beneficial in protecting low density lipoprotein (LDL) against oxidative modification, as studies have demonstrated that antioxidants other than vitamin E may also function against oxidation of LDL in vitro. In the present study, the effect of polyphenol antioxidants on the susceptibility of LDL to copper-mediated oxidation was investigated after feeding semi-purified diets to 3 groups of New Zealand white (NZW) rabbits. All diets comprised 40% energy as fat with 17% energy as oleic acid.

Increasing phosphorus intake reduces urinary concentrations of magnesium and calcium in adult ovariectomized cats fed purified diets.

We assessed the phosphorus requirement of adult cats and the relationship between phosphorus intake and the fecal and urinary excretion of calcium, magnesium and phosphorus. Female cats (ovariectomized at the onset of sexual maturity) were fed purified diets containing 4.6, 9.

Increasing calcium intakes lower urinary concentrations of phosphorus and magnesium in adult ovariectomized cats.

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.

Long-term phosphorus restriction prevents corticomedullary nephrocalcinosis and sustains reproductive performance but delays bone mineralization in rats.

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.

Inbred strains of rats have differential sensitivity to dietary phosphorus-induced 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.

Vitamin D, within its range of fluctuation in commercial rat diets, does not influence nephrocalcinogenesis in female rats.

Massive, toxic doses of vitamin D have been shown to cause nephrocalcinosis in rats, but the effect of this vitamin within its range of fluctuation in commercial rat diets was unknown. Therefore, in two experiments with young female rats, the effect on nephrocalcinosis of a moderately increased level of vitamin D in the diet was studied, that is 5000 IU/kg versus the recommended concentration of 1000 IU/kg. This was done using purified diets with 0.

Dietary fluoride prevents phosphorus-induced nephrocalcinosis in female rats.

The effect of dietary fluoride (F) on nephrocalcinosis was studied in young, female rats. Nephrocalcinosis was induced by a diet rich in phosphorus (P). F in the diet effectively counteracted P-induced nephrocalcinosis in a dose-dependent fashion.

Commercial rodent diets and nephrocalcinosis in weanling female rats.

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 influence of dietary lactose on phosphorus-induced nephrocalcinosis in female rats.

The effect of dietary lactose, when compared with glucose, on phosphorus-induced nephrocalcinosis was studied in young, female rats. Nephrocalcinogenic diets containing either 0.4 or 0.