Mechanisms of Cd toxicity

Cadmium has been found to be a micronutrient for an ecotype of Thalassiosira weissflogii, a marine alga [1] and many other heavy metals such as copper, nickel and zinc are well-known for a long time already as essential trace elements for plants. While general aspects of the entry of Cd into the environment are dealt with in detail in Chapter 2 of this book [2], we will summarize here in Sections 1.1 and 1.2 a few plant-specific aspects before discussing mechanisms of Cd toxicity in plants. 

Hence, we found it timely and necessary to summarize and integrate past and current knowledge by reviewing pioneering studies on the mechanisms of Cd toxicity in organisms, tissues, cells, and molecules in addition to recent state-of-the art pubhcations that take novel developments on causes and consequences of CLCE into consideration. 

The biochemical mechanisms of Cd toxicity in phytoplankton are in some respects similar to those in higher plants (see Chapter 13). One of the well-known effects is that Cd can compete with essential metals for uptake sites on the cell surface. High concentration of Cd inhibits the uptake of Mn and thus causes Mn deficiency in cells at low Mn concentrations [47 9]. Similarly, Cd also inhibits Fe uptake and assimilation and thus causes Fe deficiency, as evidenced by decreases in cytochrome / to chlorophyll a ratio and nitrate reductase activity... 

Interestingly, even at a concentration where it is beneficial to growth, Cd can become toxic if the Zn concentration becomes severely limiting [37,38]. This presumably reflects a loss of activity caused by Cd substitution for Zn in some essential Zn enzymes ([36,37] and references therein). Other mechanisms of Cd toxicity include oxidative stress, as reviewed in [52] and inhibition of photosynthesis via interference with the xanthophyll cycle in the diatom Phaeodactylum tricornutum [53]. 

Zn(II) is one of the most important inorganic elements in the biological systems, as discussed somewhere else (Chap. 6). Cd(ll), being similar to Zn(II), can replace Zn(ll) of the active site of zinc-dependent enzymes and proteins. Some of the enzymes with Cd(ll) bound instead of Zn(II) may retain some enzymatic activities, but the majority of such enzymes and proteins lose their biological activities. This would be very likely due to the fact that Cd(Il) is similar to Zn(II) but not sufficiently so. Cd(II) is much larger and less acidic than Zn(ll). Hence, replacement of the essential Zn(Il) in enzymes and proteins constitutes the basic mechanism of the toxic effects of cadmium. 

Cements have been suggested as materials that could be used to immobilize heavy metals produced by various industries. Cadmium and its compounds are highly toxic and can effectively be retained in concrete provided the pH does not fall below 7. The main mechanism of Cd stabilization is related to its precipitation as cadmium hydroxide and physical entrapment. The possibility of Cd substituting Ca " by solid diffusion or dissolution mechanism, forming a precipitate of Ca Cd(OH)4 has been proposed by Goni, et al.,t l based on TG/DTG studies. 

Cadmium toxicity in plants has been a focus of intense research for several decades. Many mechanisms of Cd-induced damage to plants have been described, and those which seem most important according to our present state of knowledge have been reviewed in this chapter. As discussed in detail in the previous sectirais of this review, however, the environmental relevance of many of these proposed mechanisms of Cd-induced damage remains unclear, because they were investigated under conditions (especially high Cd concentrations) that never or only very rarely occur in the environment. Therefore, future studies should establish time and Cd concentration thresholds of these mechanisms under environmentally relevant growth conditions. 

Gregus Z, Klaassen CD. Mechanisms of toxicity. In Klaassen CD, ed. Cassarett and DouII s Toxicology, The Basic Science of Toxicology. 6th ed. New York McGraw Hill, 2001. 

An intriguing problem about which we know very little is the mechanism of metal identification by the body that triggers Its response, as in the case of the huild-up of metallothioneins upon exposure to toxic metals. Perhaps the best understood of the metalloregulatory proteins is MerR that protects bacteria from mercurial toxicity. It is extremely sensitive to Hg, and distinguishes it from its congeners Zn and Cd. There is good evidence that the mercury receptor forms three-coordinate mercury(II) complexes (see Fig. 12.1c), making possible this specificity. ... 

Plants could maintain the necessary concentrations of essential metal ions in cells by homeostatic mechanisms. They are also involved in the reduction of damage induced by heavy metal toxicity. One of the major tolerance mechanisms is chelation of heavy metals by a family of peptide ligands, the phytochelatins (similar to other xenobiotics) [108], The molecular basis for the chelators and chaperone synthesis is well known and could be applied in the modification of tolerant plants. Tolerance to Cd and As is largely dependent on the phytochelatin pathway, but molecular biology of Cd hypertolerance in certain plant species, such as the... 

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