Cadmium poisoning has been reported from many parts of the world. It is one of the global health problems that affect many organs and in some cases it can cause deaths annually. Long-term exposure to cadmium through air, water, soil, and food leads to cancer and organ system toxicity such as skeletal, urinary, reproductive, cardiovascular, central and peripheral nervous, and respiratory systems. Cadmium levels can be measured in the blood, urine, hair, nail and saliva samples. Patients with cadmium toxicity need gastrointestinal tract irrigation, supportive care, and chemical decontamination traditional-based chelation therapy with appropriate new chelating agents and nanoparticle-based antidotes. Furthermore it has been likewise recommended to determine the level of food contamination and suspicious areas, consider public education and awareness programs for the exposed people to prevent cadmium poisoning.

Cadmium toxicity and treatment: An update.

The last edition of Tietz's Fundamentals of Clinical Chemistry appeared more than ten years ago and survives as a dated but valuable reference. The successor to Fundamentals, Textbook of Clinical Chemistry , follows an outline similar to the original text but adds many new subjects and updates older topics. This has resulted in a text that is 50% larger than its predecessor. Much of the newer material centers on interpretation and understanding of data and its limitations. For example, more than 200 pages (compared with 50 pages) are dedicated to an introductory section entitled "Acquisition, Management, and Application of Laboratory Data," covering the use of reference ranges, statistics, quality assurance, method evaluation, and computers. The remaining introductory chapters discuss general procedures, instrumentation, and automation. Unfortunately, the chapter that discusses current automated instrumentation already has been outdated by equipment evolution and could have been incorporated into the chapter about general instrumentation principles.

Textbook of Clinical Chemistry

Chromium (Cr) has been studied since the end of the 19 th century, when carcinogenic effects of hexavalent Cr were discovered. Essentiality of trivalent Cr was demonstrated in 1959; Cr 3+ has been studied in humans and laboratory animals since the 1970s and it is only since the 1990s that Cr has been studied as an essen- tial element in livestock animals with the same intensity. Trivalent chromium is essential to normal carbohydrate, lipid and protein metabolism. Chromium is biologically active as part of an oligopeptide - chromodulin - poten- tiating the effect of insulin by facilitating insulin binding to receptors at the cell surface. With chromium acting as a cofactor of insulin, Cr activity in the organism is parallel to insulin functions. Cr absorption is low, ranging between 0.4 and 2.0% for inorganic compounds while the availability of organic Cr is more than 10 times higher. Absorbed Cr circulates in blood bound to the β-globulin plasma fraction and is transported to tissues bound to transferrin. Absorbed Cr is excreted primarily in urine, by glomerular filtration; a small amount is excreted through perspiration, bile and in milk. The demand for Cr has been growing as a result of factors commonly referred to as stressors, especially during different forms of nutritional, metabolic and physical strain. This review describes Cr metabolism, the different biological functions of Cr and symptoms of Cr deficiency.

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Chromium as an essential nutrient: a review

Chromium is a non-essential and well-known toxic metal for microorganisms and plants. The widespread industrial use of this heavy metal has caused it to be considered as a serious environmental pollutant. Chromium exists in nature as two main species, the trivalent form, Cr(III), which is relatively innocuous, and the hexavalent form, Cr(VI), considered a more toxic species. At the intracellular level, however, Cr(III) seems to be responsible for most toxic effects of chromium. Cr(VI) is usually present as the oxyanion chromate. Inhibition of sulfate membrane transport and oxidative damage to biomolecules are associated with the toxic effects of chromate in bacteria. Several bacterial mechanisms of resistance to chromate have been reported. The best characterized mechanisms comprise efflux of chromate ions from the cell cytoplasm and reduction of Cr(VI) to Cr(III). Chromate efflux by the ChrA transporter has been established in Pseudomonas aeruginosa and Cupriavidusmetallidurans (formerly Alcaligenes eutrophus) and consists of an energy-dependent process driven by the membrane potential. The CHR protein family, which includes putative ChrA orthologs, currently contains about 135 sequences from all three domains of life. Chromate reduction is carried out by chromate reductases from diverse bacterial species generating Cr(III) that may be detoxified by other mechanisms. Most characterized enzymes belong to the widespread NAD(P)H-dependent flavoprotein family of reductases. Several examples of bacterial systems protecting from the oxidative stress caused by chromate have been described. Other mechanisms of bacterial resistance to chromate involve the expression of components of the machinery for repair of DNA damage, and systems related to the homeostasis of iron and sulfur.

Mechanisms of bacterial resistance to chromium compounds.

The long-term effects of metal-on-metal arthroplasty are currently under scrutiny because of the potential biological effects of metal wear debris. This review summarises data describing the release, dissemination, uptake, biological activity, and potential toxicity of metal wear debris released from alloys currently used in modern orthopaedics. The introduction of risk assessment for the evaluation of metal alloys and their use in arthroplasty patients is discussed and this should include potential harmful effects on immunity, reproduction, the kidney, developmental toxicity, the nervous system and carcinogenesis.

Orthopaedic metals and their potential toxicity in the arthroplasty patient: A review of current knowledge and future strategies.

The effect of chromium on some parameters related to iron metabolism was investigated. Preliminary experiments showed that this metal ion was taken up by serum proteins and was dependent on the amount of chromium present in the medium. It was also shown that the uptake of iron was reduced significantly in the presence of chromium. In vivo study showed that the serum levels of iron and total iron binding capacity (TIBC) were reduced by 28 and 11%, respectively, following daily administration of chromium (1 mg/kg) for 45 d. Serum ferritin was reduced by 22% under this condition. Hematocrit and hemoglobin levels were also affected in chromium-treated animals and were both reduced by 17%. Spectrophotometric titration of each individual amino acid located in the iron binding site of transferrin revealed that tyrosin might be the most suitable ligand for the binding of chromium to transferrin. These results suggest that chromium may compete with iron in binding to apo-transferrin, and influence iron metabolism and its related biochemical parameters.

The effect of chromium on parameters related to iron metabolism.

The characteristics of aluminum and chromium binding to apo-transferrin (apo-tf) have been investigated and compared. Both metal ions were taken up by human transferrin forming complexes with the maximum absorbances at 405 nm for chromium-transferrin (cr-tf) and 240 nm for aluminum-transferrin (Al-tf). In the presence of citric acid, chromium binding to transferrin is five times more than aluminum. The binding of aluminum or chromium to apo-transferrin was reduced by 18 and 22% in the presence of 200 ng/mL of iron. The binding of both metals to apo-tf appears to be pH dependent. In acidic pHs, less chromium and more aluminum binding occurred.

Comparative Binding Study of Aluminum and Chromium to Human Transferrin Effect of Iron

Thyroid cancer is the most common sort of endocrine-related cancer with more prevalent in women and elderly individuals which has quickly widespread expansion in worldwide over the recent decades. Common features of malignant thyroid cells are to have accelerated metabolism and increased glucose uptake to optimize their energy supply which provides a fundamental advantage for growth. In tumor cells the retaining of required energy charge for cell survival is imperative, indeed glucose transporters are enable of promoting of this task. According to this relation it has been reported the upregulation of glucose transporters in various types of cancers. Human studies indicated that poor survival can be occurred following the high levels of GLUT1 expression in tumors. GLUT-1 and GLUT3 are the glucose transporters which seems to be mainly engaged with the oncogenesis of thyroid cancer and their expression in malignant tissues is much more than in the normal one. They are promising targets for the advancement of anticancer strategies. The lack of oncosuppressors have dominant effect on the membrane expression of GLUT1 and glucose uptake. Overexpression of hypoxia inducible factors have been additionally connected with distant metastasis in thyroid cancers which mediates transcriptional regulation of glycolytic genes including GLUT1 and GLUT3. Though the physiological role of the thyroid gland is well illustrated, but the metabolic regulations in thyroid cancer remain evasive. In this study we discuss proliferation pathways of the key regulators and signaling molecules such as PI3K-Akt, HIF-1, MicroRNA, PTEN, AMPK, BRAF, c-Myc, TSH, Iodide and p53 which includes in the regulation of GLUTs in thyroid cancer cells. Incidence of deregulations in cellular energetics and metabolism are the most serious signs of cancers. In conclusion, understanding the mechanisms of glucose transportation in normal and pathologic thyroid tissues is critically important and could provide significant insights in science of diagnosis and treatment of thyroid disease.

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Regulators of Glucose Uptake in Thyroid Cancer Cell Lines

The short term effects of waterborne cadmium (Cd+2) on the levels of serum parameters related to bone metabolism including calcium (Ca), inorganic phosphorus (Pi) and alkaline phosphatase (ALP) in common carp fish (Cyprinus carpio L.) were studied. Fish were treated with varying concentrations of Cd+2 (0.22, 1.1 and 2.2 mg l−1) daily for 14 days. The results obtained show that serum Pi and ALP concentrations were elevated by increasing Cd+2 concentration in water containing fish whereas serum Ca level was decreased. At the same time, the protective role of waterborne zinc (Zn+2, 1 mg l−1) on the same parameters was also investigated. Results showing that daily treatment of fish with Zn+2, increased the concentrations of Ca and ALP in serum by 2.07 and 1.86 fold and decreased serum Pi level by 57.7% in comparison with Cd+2 treatment. The combination of Cd+2 and Zn+2 on the same parameters was studied next. There was a significant (P < 0.05) elevation in serum Ca and ALP levels in comparison with Cd+2 treatment. Decreasing in serum Pi level was not significant in comparison with Cd+2 treatments. The protective effect of Zn+2 on Cd+2 disturbances in serum parameters related to bone metabolism in this manuscript has been also discussed.

Protective effect of zinc on related parameters to bone metabolism in common carp fish (Cyprinus carpio L.) intoxified with cadmium.

Cadmium (Cd) is a highly toxic element, which may cause toxicity to most organs in the body. Zinc (Zn) and magnesium (Mg) are essential minerals with probable benefits on Cd harmful effects. Finding an efficient and non-pathological treatment against Cd toxicity seems promising. Fifty adult rats were divided into ten experimental groups of five rats each. The Cd group was treated with 1 mg Cd/kg and the control group received 0.5 cm3 normal saline. The other eight groups received Zn (0.5 and 1.5 mg/kg) and Mg (0.5 and 1.5 mg/kg) either alone or in combination with 1 mg Cd/kg through IP injection for 3 weeks. Testis malondialdehyde (MDA), sperm parameters, and testis histopathology were investigated. Cd reduced sperm parameters and increased testis MDA. Moreover, Cd exposure caused a significant histological damage in testis of male rats. However, Zn or Mg treatment prevented and reversed Cd toxic alterations in testis. These findings suggest that co-administration of Zn or Mg could improve cadmium testicular toxicity in male Wistar rats.

Ali Asghar Moshtaghie

Papers

The effect of chromium on parameters related to iron metabolism.

Comparative Binding Study of Aluminum and Chromium to Human Transferrin Effect of Iron

Regulators of Glucose Uptake in Thyroid Cancer Cell Lines

Protective effect of zinc on related parameters to bone metabolism in common carp fish (Cyprinus carpio L.) intoxified with cadmium.

Cadmium Testicular Toxicity in Male Wistar Rats: Protective Roles of Zinc and Magnesium