Int. J. Environ. Res. Public Health 2009, 6 3133 Figure 3. Summary of pathohistological findings (PH) of renal tissues and incidence of toxic elements in kidney from slaughtered pigs (n = 90). Necrosis of proximal tubule cells (1), hypercellularity of vascular loop (2), vascular changes (3), exudat in Bowman’s space (4), focal interstitial nephritis (5), dystrophy of proximal tubule cells (6), swelling of proximal tubule cells (7), renal hemorrhages (8), fatty changes of proximal tubules cells (9). N-number of pathohistological findings of renal tissues and co-incidence of toxic elements in kidney. Lipidosis of proximal tubule cells, renal hemorrhages, and swelling of proximal tubule cells were seen in 41 (45.5%), 34 (37.7%) and 31 (34.4%) kidneys of slaughtered pigs, respectively. Twenty seven (30%) of the examined pigs kidneys had a dystrophy of proximal tubules cells, while exudate in Bowman`s space as well as focal interstitial fibrosis were seen in 20 (22.2%) kidneys of slaughtered pigs. Vascular changes expresed as a hyperaemia of blood vessels was seen in 12 (13.3%) kidneys, while hypercellularity of vascular loops, necrosis of proximal tubule cells and renal adenoma occurred in a lesser degree. From a total of 56 analyzed kidneys samples in which the presence of toxic elements was found in 11 samples were determinet co-occurrence of Cd and Hg, while in only one samples is determined co-occurrence of Cd and As (Figure 3). The kidney is clearly the major target organ of chronic Cd and Hg toxicity [35–38] Accumulated evidence also indicates that kidney is a target organ for As toxicity. Since kidney is the major organ for As elimination and most of the As is rapidly eliminated through the kidney [39,40], renal cells are, thus, exposed to a major portion of the absorbed As dose. After absorption, most of the toxic elements are accumulated in the liver where it induces the production of metallothioneins (MT) a family of low- molecular-weight metal-binding proteins that aid in the intracellular processing of metal ions [41,42]. Metallothioneins exist in most tissues, have a high cysteine content, and hence may be similar to metal chelators in providing heavy metal tolerance and regulating Hg distribution and retention [43–45]. Intracellular metallothionein has also been demonstrated to protect against metal-induced hematotoxicity and immunotoxicity [46]. Metallothionein has been utilized as a sublethal cellular indicator in fish for Hg exposure [47]. When the synthesis of MT becomes insufficient for binding all Cd ions in the liver, Cd not bound to MT produce hepatocyte injury and a Cd–MT complex is released into the bloodstream. The complex in the plasma is then filtered through the glomeruli in the kidney