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Results for “cadmium toxicity”

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At least 19 recordsLinked to original sources
PubMed1979

Nutritional influences on metal toxicity: cadmium as a model toxic element.

The nutrient quality of the diet has been shown repeatedly to be a significant factor in modifying the response of man and animals to toxic element exposure. Deficiencies of several essential nutrients have been shown to exacerbate the effects of cadmium and supplements of such nutrients have been shown to ameliorate the toxicity. Thus the effects of exposure to a toxic element, such as cadmium, may vary, depending on interactions with other elements which are present in the diet in different concentrations.

Adolescent↗
PubMed1978

Long-term effectiveness of dietary iron and ascorbic acid in the prevention and cure of cadmium toxicity in rats.

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.

Animals↗
PubMed1978

[Lead and cadmium toxicity in established mammalian cell lines].

Lead and cadmium toxicity was evaluated in three mammalian cell lines (tumour : HeLa, transformed : XC and normal : NRK) by means of the modifications of the 3H-TdR incorporation rate in the nucleus of the treated cells. The three cell lines showed different degrees of sensitivity. Sensitivity depended on the line, metal, its concentration and duration of incubation. Cadmium was found to be at least five times more toxic than lead except at low concentration. The normal cell line was more sensitive to cadmium and less sensitive to lead than other lines.

Cadmium↗
PubMed1978

Cadmium toxicity and liver mitochondria. I. Different effects of cadmium administered in vivo to adult, young, and ethionine-fed rats.

The changes in liver mitochondrial respiratory activities and cytochrome concentrations were investigated when cadmium chloride was administered orally to adult, young, and ethionine-fed rats. Following a seven-day administration of 30 ppm cadmium in drinking water, adult rats showed no change, while young rats and ethionine-fed rats exhibited a marked increase in mitochondrial respiration with concomitant decrease of respiratory control index and P/O ratio. The concentrations of cytochromes aa3, b, and c + c1 in liver mitochondria were unchanged in adult rats, but increased significantly in ethionine-fed rats. In young rats receiving cadmium the liver mitochondrial protein increased with a slight change in the cytochrome concentration in mitochondria. It was further found that in adult rats a higher concentration (300 ppm) of cadmium in drinking water was toxic to the liver mitochondrial functions. Thus, the effect of oral administration of cadmium on the liver mitochondrial function depends on the condition of the animals.

Aging↗
PubMed1979

Influence of some factors on cadmium pharmacokinetics and toxicity.

Cadmium metabolism in the young and in conditions of dietary contamination with ash from coal gasification were investigated. The experiments were performed in adult rats which received ash in the diet (5%) and/or cadmium in drinking water (100 ppm) over a period of five weeks and in sucklings whose mothers were given the same treatment throughout pregnancy and lactation. In pharmacokinetic studies, (115m)Cd was administered orally or intraperitoneally to determine the intestinal absorption, retention, and distribution. Cadmium toxicity (LD(50)) was determined in different age groups of animals treated with ash for five weeks before a single oral or intraperitoneal administration of cadmium chloride. After intraperitoneal administration, (115m)Cd body retention decreased with age and was independent of the dietary treatment. Sucklings had a higher retention in the blood, carcass, and gut than adults. After oral administration, sucklings had a much higher body retention than adults regardless of the dietary treatment of their mothers. Cadmium toxicity was also independent of the dietary treatment. Most striking was a very high oral toxicity of cadmium in sucklings. It is concluded that the young might be at a special risk at the same level of environmental cadmium exposure because of the high oral cadmium toxicity at this age which is most probably due to a high cadmium retention in the gut. It is also concluded that the mixture of elements contained in ash is not likely to influence cadmium metabolism and toxicity in conditions of dietary exposure.

Age Factors↗
PubMed1978

Some observations on the interaction of zinc, copper, and iron metabolism in lead and cadmium toxicity.

A brief review of the literature indicates that nutritional deficiencies have been shown to increase the absorption and toxicity of orally ingested lead and cadmium. Results from recent studies indicates that low level oral ingestion of cadmium and lead perturbs the metabolism of zinc, copper, and iron and that these changes may be the earliest manifestation of the toxicity of lead and cadmium. The significance of these findings reveals itself in two ways: namely, that toxicologic investigations of lead and cadmium, whether experimental or clinical, must be based on a definitive consideration of the nutritional status of animals or people, and, secondly, that the preventive role of nutrition, especially that of trace metal intakes, must be taken seriously when establishing measures for reducing, eliminating, or combatting the toxic effects of widespread exposure to lead and cadmium in humans.

Aminolevulinic Acid↗
PubMed1978

alpha 1-antitrypsin in cadmium toxicity: an evaluation of its suggested role.

Chowdhury and Louria [1] reported that cadmium could reduce in vitro the concentration and the trypsin inhibitory capacity of plasma alpha 1-antitrypsin. They suggested that this could explain the emphysema observed in some workers exposed to cadmium. Using the same experimental approach as these authors, we could not reproduce their observations. Furthermore, in vivo results obtained on workers excessively exposed to cadmium during more than 20 years and exhibiting obvious signs of chronic cadmium intoxication did not reveal a decrease in the concentration and the activity of plasma alpha 1-antitrypsin.

Cadmium Poisoning↗
PubMed1979

Cadmium toxicity.

Explore the source record for details and available documents.

Animal Feed↗
PubMed1979

Metallothionein in the extracellular fluids as an index of cadmium toxicity.

In rats injected with 5 micron mole CdCl2/kg, 5 days/week, metallothionein was detected in plasma by gel filtration chromatography as early as four weeks. The mean renal concentration of cadmium was 80 microgram/g. The excretion of cadmium in urine at this time was rather low and amounted to 0.01% of the total dose. The amount of metallothionein in plasma, as determined by 109Cd-binding to the 10,000 molecular weight fraction, increased markedly during week 14. Its excretion in urine, however, did not start until about 10 weeks, when the cadmium concentration in kidney approached a mean value of 212 microgram/g. Signs of renal toxicity were evident from glucosuria and proteinuria which became severe during the next four weeks. The excretion of cadmium in urine increased markedly and the majority of it was in the form of metallothionein. It is suggested that the appearance of metallothionein in plasma and urine can be used as specific indices of cadmium poisoning and that the assay of the protein in these fluids may be useful in screening for excessive cadmium exposure.

Animals↗
PubMed1979

Evidence of cadmium toxicity in a population living in a zinc-mining area. Pilot survey of Shipham residents.

22 of 31 residents of a Somerset village where soil levels of cadmium were high had raised blood-cadmium levels, and some had clinical and biochemical findings (including hypertension and biochemical evidence of renal tubular damage) indicating toxic effects which could be attributed to the metal. It is suggested that more detailed studies should be carried out as a matter of urgency and that advice on avoiding local garden produce and not smoking should be emphasised. Probably more serious, however, is the summation effect with industrial exposure.

Acetylglucosaminidase↗
PubMed1977

Role of dietary calcium and calcium binding protein in cadmium toxicity in rats.

Growing male rats were fed a purified diet containing 0.6% Ca (two groups) or 0.1% Ca (two groups) for 8 weeks. One 0.6% Ca group and one 0.1% Ca group received 25 ppm Cd (as CdC12) in the drinking water. Diets were fed on an equalized basis with the 0.1% Ca + Cd group determining the amount of diet fed to the other groups. Water was provided ad libitum. Terminal body weights were not different among the four groups. Packed cell volumes were depressed in the Cd-exposed groups, especially the 0.1% Ca + Cd group. The highest concentrations of Cd were found in the lungs, liver, and kidneys of the 0.1% Ca + Cd group. More Cd was bound to low molecular weight proteins of the intestinal mucosa from the 0.1% Ca + Cd group than the 0.6% Ca + Cd group. Rats fed the 0.1% Ca diet appeared to have a greater capacity to absorb either Ca or Cd than rats fed the 0.6% Ca diet, as shown by an enhanced binding of 45Ca and 115mCd to intestinal calcium-binding protein (CaBP) in the rats fed the low calcium diet. A portion of the mucosal Cd was accounted for as Cd bound to metallothionein. It was concluded, based upon these experiments, that cadmium retention and signs of toxicity are enhanced by feeding low Ca diet and that the increased CaBP activity due to Ca restrictions is responsible for the increased Cd uptake observed.

Animals↗