Deficiency effects cadmium

Waalkes MP, Kovatch R, Rehm S (1991b) Effect of chronic dietary zinc deficiency on cadmium toxicity and carcinogenesis in the male Wistar [Hsd (WI)BR] rat. Toxicol Appl Pharmacol 108 448-456... 

Sublethal effects in birds are similar to those in other species and include growth retardation, anemia, renal effects, and testicular damage (Hammons et al. 1978 Di Giulio et al. 1984 Blus et al. 1993). However, harmful damage effects were observed at higher concentrations when compared to aquatic biota. For example, Japanese quail (Coturnix japonica) fed 75 mg Cd/kg diet developed bone marrow hypoplasia, anemia, and hypertrophy of both heart ventricles at 6 weeks (Richardson et al. 1974). In zinc-deficient diets, effects were especially pronounced and included all of the signs mentioned plus testicular hypoplasia. A similar pattern was evident in cadmium-stressed quail on an iron-deficient diet. In all tests, 1% ascorbic acid in the diet prevented cadmium-induced effects in Japanese quail (Richardson et al. 1974). In studies with Japanese quail at environmentally relevant concentrations of 10 pg Cd/kg B W daily (for 4 days, administered per os), absorbed cadmium was transported in blood in a form that enhanced deposition in the kidney less than 0.7% of the total administered dose was recovered from liver plus kidneys plus duodenum (Scheuhammer 1988). 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Devineau, J. and C. Amiard Triquet 1985. Patterns of bioaccumulation of an essential trace element (zinc) and a pollutant metal (cadmium) in larvae of the prawn Palaemon serratus. Mar. Biol. 86 139-143. Dib, A., J.P Clavel, and J.P. Carreau. 1989. Effects of gamma-linolenic acid supplementation on lipid composition of liver microsomal membranes. I. Pregnant rats fed a zinc-deficient diet and those fed a balanced one. Jour. Clin. Biochem. Nutr. 6 95-102. 

Sato, M. and Y. Nagai. 1989. Effect of zinc deficiency on the accumulation of metallothionein and cadmium in the rat liver and kidney. Arch. Environ. Contam. Toxicol. 18 587-593. 

Selenium is readily available in a variety of foods including shrimp, meat, dairy products, and grains, with a recommended daily intake of 55 to 70 jug. It occurs in several forms with Se+6 being biologically most important. Selenium is readily absorbed by the intestine and is widely distributed throughout the tissues of the body, with the highest levels in the liver and kidney. It is active in a variety of cellular functions and interacts with vitamin E. Selenium appears to reduce the toxic effects of metals such as cadmium and mercury and to have anticarcinogenic activity. Selenium produces notable adverse effects both in deficiency and excess thus recommended daily intake for adults is approximately 70 Jg/day but should not exceed 200 pg/day. 

Transferrin is mainly synthesized in the hepatocytes. There are about 20 known variants. Iron is transported by transferrin (approx. 30% of transferrin is saturated with iron). With the help of a membrane receptor, the iron-transferrin complex is taken up and released in the liver cell, where it is immediately bound (because of its toxicity) to ferritin. The liver cells take up iron predominantly from transferrin, to a lesser degree also from haptoglobin, haemopexin, lactoferrin and circulating ferrin. Transferrin, which is mainly formed in the hepatocytes, may also bind and transport, in decreasing order, chromium, copper, manganese, cobalt, cadmium, zinc and nickel. The half-life of transferrin is 1 - 2 hours, which is very short in view of its total blood concentration of 3-4 mg. Approximately 0.4 g ferritin iron is stored in the liver. In the case of transferrin deficiency, its bacteriostatic and fungistatic effects are also reduced. Transferrin without iron saturation is known as apo-transferrin. (31, 66, 67)... 

The association between metal exposure and renal failure can be approached from two points of view. On the one hand environmental/industrial exposure to heavy metals, more particularly, lead, cadmium and mercury and other inorganic substances such as silicon has been linked to a reduced renal function and/or the development of acute or chronic renal failure [1]. This issue has been dealt with in other chapters of this book. On the other hand patients with chronic renal failure, especially those treated by dialysis are at an increased risk for trace element disturbances (Figure 1). Indeed in these subjects the reduced renal function, the presence of proteinuria, metabolic alterations associated with renal insufficiency, the dialysis treatment, medication etc. all may contribute to either accumulation or deficiency of trace metals. With regard to aluminum intensive research on the element s toxic effects has been performed in the past. Recently, new metal-containing medications have been introduced of which the potential toxic effects should be considered and put in a justified context. 

Trace metal disturbances may be due to the uremia per se. Indeed, as the urinary excretion route is an important pathway of elimination of many trace elements, i.e. silicon, strontium, aluminum,... impairment of the kidney will be an important determinant of their accumulation, whilst in the presence of a reabsorptive defect a number of trace elements, especially those that are reabsorbed because of their essential role, be lost resulting in a deficient state. The presence of proteinuria may reasonably result in losses of protein bound elements. It has also been shown also that residual renal funchon may importantly alter the accumulation and hence toxic effects of aluminum [2]. In uremia translocation of a particular metal from one tissue to another may also occur. As an example, under normal circumstances the kidney is an important target organ for cadmium. In chronic renal failure however, possibly as a consequence of a reduction in binding proteins (e.g. metallothionein), the concentrahon of cadmium in this tissue decreases to extremely low levels which... 

Data concerning the toxicity of the four discussed toxic minerals are presented in Tables 4.5 and 4.6. The uptake of elements is not entirely independent of one another. Elements of similar chemical properties tend to be taken up together. Sometimes one element has an inhibiting effect on another, or there can be a synergistic effect, e.g., enhancement of absorption of calcium in the presence of adequate amounts of phosphorus, or cadmium and lead hindering calcium and iron absorption, or zinc and copper antagonism and their influence on the ratio of Zn/Cu on copper deficiency. 

Soil plays an integral part in our lives and is inherently linked to public health. For example, many of the essential trace elements which we require in our diet to remain healthy are derived from soils and parent rock material, and low concentrations or the unavailability of these elements in soil can cause dietary deficiencies. Soils can also be contaminated with a range of potentially hazardous substances (both chemical and biological) which, if present at sufficiently elevated levels, can present a potential public health problem. For example, soils may contain elevated levels of heavy metals such as cadmium and lead which can have measurable and often severe effects on local populations. The soils of Cappadocia in central Turkey are naturally rich in fibrous asbestos-like minerals that are thought to be the cause of a rare cancer in local communities1 while exposure to the bacterium Clostridium tetani in soils can cause tetanus. Despite such examples, the effects of contaminated land have, until recently, been relatively ignored and, even today, our understanding of the mechanisms and level of risk associated with contaminated land is poor in relation to air and water. 

According to the investigations of Fattinger (1950), the fungicidal action of copper is enhanced by cadmium, cobalt, nickel and zinc compounds in Alternaria tenuis and Trichothecium roseum cultures. Zinc sulfate (ZnSO 7HjO) was tried in place of copper sulfate its effect however was inferior to that of the copper compound. Nevertheless, it is still used against rosette disease a physiological disease caused by zinc deficiency. 

The essentiality of cadmium was investigated systematically in control goats with 300 pg Cd kg ration DM, and in corresponding Cd-deficient animals with < 15 pg kg ration DM. The cadmium-poor nutrition did not have any effect on feed intake (629 and 644 g/day, respectively). Live weight gain (18.2 and 16.8 kg by day 91 of life, respectively) was not affected by Cd-poor nutrition, whereas Cd deficiency had a significant effect on first insemination, rate of abortion and number of services. The Cd-poor nutrition of mothers affected the activity of the kids. The intrauterine Cd-depleted kids were often very... 

Anke M, MasaokaT, Schmidt A and Arnhold W (1988) Antagonistic effects of a hi sulphur, molybdenum and cadmium content of diets on copper metabolism and deficiency symptoms in cattle andpi. In Hurley LS, et al., eds. Trace Element in Man and Animals - 6, pp. 317-318. 

The toxic effects of cadmiun are further manifested by a negative action on the metabolism of iron, copper and zinc which results in a deficiency of these metals with relevant disturbances. Cadmium also exerts teratogenic, mutagenic and carcinogenic effects [10]. 

Some trace metals are classified as toxic. There is, perhaps, justification for this classification for such metals as arsenic, lead, and mercury. In addition, extended exposure of mammals to small amounts of cadmium, lead, selenium, antimony, and nickel carbonyl can shorten life or cause cancer, and lead, nickel, antimony, cadmium, and mercury in small amounts cause human health problems. However, all metals are toxic if ingested at sufficiently high levels. Frequently, the effects of a toxic metal are increased by nutritional deficiencies. ... 

Metabolism involving silica has been studied in diatoms by measuring the effects of silica-deficient growth conditions. Lewin found that silica is not taken up by washed cells until supplied, with a sulfur compound. Cadmium inhibited uptake. 

A) Periodicaiiy reassess The employee s work practices and personal hygiene the employee s respirator use, if any the employee s smoking history and status the respiratory protection program the hygiene facilities the maintenance and effectiveness of the relevant engineering controls and take all reasonable steps to correct the deficiencies found in the reassessment that may be responsible for the employee s excess exposure to cadmium. 

Fox MRS, Jacobs RM, Jones AOL, Fry BE Jr, Stone CL (1980) Effects of vitamin C and iron on cadmium metabolism. Ann. New York Acad. Sci. 335 249-261 Fox MRS, Tao S-H, Stone CL (1981) Increased cadmium in tissues with zinc, iron and copper deficiencies. Fed. Proc. 40 886... 

Ragan HA (1977) Effects of iron deficiency on the absorption and distribution of lead and cadmium in rats. J. Lab. Clin. Med. 90 700-706 Rosen JF, Chesney RW, Hanstra A, DeLuca HF, Mahaffey KR (1980) Reduction in 1,25-dihydroxyvitamin D in children with increased lead absorption. N. Engl. J. Med. 302 1128-1132... 

---