Early signs of cadmium intoxication in rabbits

Nomiyama, Kazuo; Sato, Chizuko; Yamamoto, Akiko

doi:10.1016/0041-008x(73)90224-x

Cited by 64 publications

(21 citation statements)

References 20 publications

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“…This result agrees well with reports on cadmium health effects in rabbits (18,20); it also brings to mind a report on itai-itai disease patients with renal failure, who showed intermittent proteinuria and/or glycosuria in the early stage of itai-itai disease and persistent proteinuria, glycosuria, and aminoaciduria in the later stage (21). Therefore, in order to detect health effects of cadmium in residents of cadmium-polluted areas at an early stage, proteinuria, glycosuria, and aminoaciduria should be looked for repeatedly at suitable intervals.…”

Section: Discussion Biological Responses To Cadmiumsupporting

confidence: 81%

Effects of dietary cadmium on rhesus monkeys

Nomiyama¹,

Nomiyama²,

Nomura³

et al. 1979

Environ Health Perspect

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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 /.g/g wet weight and 18 ,g/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 ,ug/g wet weight and those in the liver were 110 and 160 ,ug/g wet weight, respectively.In the highest exposure group (300 ppm), urine cadmium increased to 250,ug/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, 1g/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 ,lg/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine 832-microglobulin, increased plasma urea nitrogen, and increased plasma a2-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 ,ug/g wet weight and 410 and 630 ,g/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 ,uLg/g wet weight for low molecular weight proteinuria and 470 ,ug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 ,tg/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.

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Section: Discussion Biological Responses To Cadmiumsupporting

confidence: 81%

Effects of dietary cadmium on rhesus monkeys

Nomiyama¹,

Nomiyama²,

Nomura³

et al. 1979

Environ Health Perspect

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“…There have been very few other reports, however, on clinical picture of animals given cadmium for more than 1 year (18, 19). This result agrees well with reports on cadmium health effects in rabbits (18,20); it also brings to mind a report on itai-itai disease patients with renal failure, who showed intermittent proteinuria and/or glycosuria in the early stage of itai-itai disease and persistent proteinuria, glycosuria, and aminoaciduria in the later stage (21). another group of rabbits given 300 ppm of cadmium over a period of 54 weeks.…”

Section: Biological Responses To Cadmiumsupporting

confidence: 91%

Effects of Dietary Cadmium on Rhesus Monkeys

Nomiyama¹,

Nomiyama²,

Nomura³

et al. 1979

Environmental Health Perspectives

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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 /.g/g wet weight and 18 ,g/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 ,ug/g wet weight and those in the liver were 110 and 160 ,ug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250,ug/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, 1g/l. Hypohemoglobinopathy and proteinuria (qualita-tive determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 ,lg/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine 832-microglobulin, increased plasma urea nitrogen, and increased plasma a2-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 ,ug/g wet weight and 410 and 630 ,g/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 ,uLg/g wet weight for low molecular weight proteinuria and 470 ,ug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 ,tg/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.

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“…As mentioned before (27), since ALP is located in the renal proximal tubules and GOT and GPT are found in the renal distal tubules of rabbits, enzymuria is a good indicator for detecting the localization of renal injury in an early stage of intoxication. As urinary ALP increased more markedly than GPT and GOT after cadmium administration, cadmium was thought to injure proximal tubular cells more severely than distal tubular cells.…”

Section: Localization Of Cadmium-induced Nephropathymentioning

confidence: 77%

Reversibility of Cadmium-Induced Health Effects in Rabbits

Nomiyama¹,

Nomiyama²

1984

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Twenty-one male rabbits were divided into three groups: rabbits of two groups were given pelleted food containing cadmium chloride at a dose level of 300 gg Cd/g over periods of 44 or 19 weeks. Rabbits of the last group were given ordinary commercial pelleted food and served as controls. Cadmium increased urinary protein and amino acid by week 19 and increased it to a remarkably high level by week 44. After cessation of cadmium exposure, rabbits of the first group (44 weeks exposure group) showed only little recovery from cadmium health effects: proteinuria and aminoaciduria were slightly improved. Depressed hepatic functions were also slightly improved, but did not return to the control level in 24 weeks. Fat and bone metabolism also remained depressed below the control level. Anemia did not also readily recover. On the other hand, rabbits of the second group (19 weeks exposure) recovered from the effects of cadmium: proteinuria and aminoaciduria in most animals disappeared soon after the end of cadmium exposure, plasma GPT fell after 1 week, and hemoglobin and hematocrit returned to normal in 6-11 weeks. The above results show that after cessation of cadmium exposure, mild cadmiuminduced health effects were reversible in a short period, while more severe effects were not readily reversible.High performance liquid chromatographic (HPLC) profiles of renal and hepatic cadmium-thionein (Cd-MT) during and after exposure to cadmium showed no correlation to the degree of cadmium health effects, and therefore, did not help to elucidate mechanisms of the recovery from cadmium-induced health effects, probably because cadmium not bound with metallothionein (non-MT-Cd) is responsible for inducing renal effects.

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Early signs of cadmium intoxication in rabbits

Cited by 64 publications

References 20 publications

Effects of dietary cadmium on rhesus monkeys

Effects of dietary cadmium on rhesus monkeys

Effects of Dietary Cadmium on Rhesus Monkeys

Reversibility of Cadmium-Induced Health Effects in Rabbits

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