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Publications (3)7.03 Total impact

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    ABSTRACT: The effects of long-term (9 y) po administration of daily low doses of cadmium on blood pressure, heart rate, electrocardiogram and plasma cholesterol and triglyceride concentrations were examined in rhesus monkeys. Thirty-five male rhesus monkeys were divided into 5 groups and fed pelleted food containing cadmium chloride at dosages of 0, 3, 10, 30 or 100 micrograms cadmium/g food (= ppm). The 100 ppm group had increased blood pressure during the initial 1 1/2 y. Thereafter, the expected increase in blood pressure that occurred due to aging in the control and 3 ppm groups was not evident in the 100 ppm group. No changes attributable to cadmium were detected in pulse rates or in electrocardiograms. Plasma cholesterol in the 2 highest dosage groups and triglyceride in the 100 ppm group were slightly lower than in controls after 2 1/2 y. Long-term exposure to cadmium contributed to the development of elevated blood pressure during the first and second years and then inhibited the hypertension expected due to aging.
    Veterinary and human toxicology 09/1994; 36(4):290-4.
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    ABSTRACT: Thirty-five male rhesus monkeys (Macaca mulatta) 2-5 y-of-age were separated into 5 groups and fed 200 g solid food daily which contained 0, 3, 10, 30 or 100 micrograms cadmium/g (ppm) as cadmium chloride for 462 w (9 y). The control feed (0 ppm) contained 0.27 micrograms cadmium/g. Dietary zinc intake was limited to the minimum requirement of 6 mg zinc/day (control food concentration was 3 mg zinc/100 g) to avoid impacting cadmium toxicity due to excessive zinc intake. Urine was collected at 3-w intervals. Decreased development (reduced body weight and body length) was observed in groups that received 10 ppm cadmium or more. The 100 ppm group had glucose in the urine after 48 w, elevated urine protein at 98 w, and markedly increased urine volume after the 102nd week. No abnormalities in renal functions were noted in the 3 or 10 ppm groups. Despite the development of these clinical signs of renal dysfunction, none of the 100 ppm group had aggravated renal dysfunction or renal failure during the 9 y of study.
    Veterinary and human toxicology 07/1994; 36(3):189-94.
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    ABSTRACT: Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.
    Environmental Health Perspectives 03/1979; 28:223-43. DOI:10.2307/3428925 · 7.03 Impact Factor