Mechanisms of Cadmium Toxicity to Various Trophic Saltwater Organisms


Metal pollution of the marine environment is a major problem of increasing magnitude that has become an issue of concern, because most of the metals are transported into the marine environment and accumulated without decomposition. GESAMP (the joint Group of Experts on the Scientific Aspects of Marine Pollution) defined marine pollution as "introduction by man directly or indirectly, of substances or energy into the marine environment (including estuaries) resulting in such deleterious effects as harm to living resources, hazards to human health, hindrance to marine activities including fishing, impairment of quality for use of sea-water, and reduction of amenities."

Cadmium is one of the metals whose concentration is increasing in aquatic environments, and characteristic of Group IIB elements (of the Periodic Table (Zn, Cd, Hg)) is scarce, fairly expensive and of low mechanical strength. It has atomic number 48 and an atomic weight of 112.40. Cadmium was first isolated and identified from the zinc ore smithsonite (ZnCO3), and over centuries has been released slowly into the environment from widespread sources such as the smelting of a variety of ores and the burning of wood and coal.

Cadmium can enter the environment from various anthropogenic sources such as by-products from zinc refining, coal combustion, mine wastes, electroplating processes, iron and steel production, pigments, fertilizers and pesticides. Through quantifying the relative importance of anthropogenic and natural contributions to cadmium cycling in the environment for both pre- and post-industrial times, it has Zaosheng Wang, Changzhou Yan, Hainan Kong et al. been consistently shown that the contribution from anthropogenic sources (e.g. non-ferrous metal industry) has increased greatly over the past century and currently dominates the cadmium biogeochemical cycle (Campbell, 2006).

Cadmium has been ranked as one of the major metal hazards, because there is now mounting evidence that it is present in aquatic and terrestrial environments at levels that are sufficient to produce biological effects to various organisms. Cadmium exerts harmful effects on aquatic organisms in many ways, although all the major mechanisms of toxicity are a consequence of the strong coordinating properties of cadmium cations [Cd2+] that affect the properties of many biological molecules (enzymes, etc.), often by blocking and reducing the thiol sites on proteins (Kneer and Zenk, 1992). Moreover, cadmium can be accumulated via the food chain, posing a serious threat to human health (Vijver et al., 2005).

Prediction of metal bioaccumulation and toxicity in aquatic organisms has been based on the free ion activity (e.g., free ion activity model; Campbell, 1995) or more recently on the binding with the biological/toxicological sites of action (e.g., biotic ligand model; Paquin et al., 2002). However, metals are bound to various intracellular ligands that may control metal toxicity. Among the five operationally defined subcellular fractions, namely metal-rich granules, cellular debris, organelles, heat-denatured protein (HDP), and heat-stable protein (HSP), cadmium was mostly bound to HSP, whereas it was least bound to HDP. Cadmium was redistributed with increasing [Cd] concentration from the biologically detoxified pool to the presumed metal-sensitive fractions (MSF, a combination of organelles and HDP), which led to higher cellular cadmium accumulation, toxicity, and sensitivity. The MSF can provide the better predictor of cadmium toxicity than [Cd2+] concentration or cellular accumulation, indicating that models predicting cadmium toxicity need to address the subcellular fate of cadmium and how this responds to external and internal conditions (Wang and Wang, 2008; Miao and Wang, 2006).

In this topic, the bioaccumulation, sub-cellular distribution, and toxicity of cadmium in aquatic organisms is described.

Overall, this topic underlines the need to better understand the uptake sites for dietary and/or waterborne exposure, and at how cadmium is taken up, eliminated and detoxified. This will improve our ability to predict the potential for toxic effects from aquatic organism exposure to environmentally realistic cadmium concentrations.

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