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      Cadmium toxicity and treatment: An update

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          Abstract

          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.

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          The toxicity of cadmium and resulting hazards for human health

          Johannes Godt, Franziska Scheidig, Christian Grosse-Siestrup … (2006)
          Cadmium (Cd) has been in industrial use for a long period of time. Its serious toxicity moved into scientific focus during the middle of the last century. In this review, we discuss historic and recent developments of toxicological and epidemiological questions, including exposition sources, resorption pathways and organ damage processes.
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            Cadmium carcinogenesis.

            Michael Waalkes (2003)
            Cadmium is a heavy metal of considerable environmental and occupational concern. Cadmium compounds are classified as human carcinogens by several regulatory agencies. The most convincing data that cadmium is carcinogenic in humans comes from studies indicating occupational cadmium exposure is associated with lung cancer. Cadmium exposure has also been linked to human prostate and renal cancer, although this linkage is weaker than for lung cancer. Other target sites of cadmium carcinogenesis in humans, such as liver, pancreas and stomach, are considered equivocal. In animals, cadmium effectively induces cancers at multiple sites and by various routes. Cadmium inhalation in rats induces pulmonary adenocarcinomas, in accord with its role in human lung cancer. Cadmium can induce tumors and/or preneoplastic lesions within the rat prostate after ingestion or injection. At relatively high doses, cadmium induces benign testicular tumors in rats, but these appear to be due to early toxic lesions and loss of testicular function, rather than from a specific carcinogenic effect of cadmium. Like many other metals, cadmium salts will induce mesenchymal tumors at the site of subcutaneous (s.c.) or intramuscular (i.m.) injections, but the human relevance of these is dubious. Other targets of cadmium in rodents include the liver, adrenal, pancreas, pituitary, and hematopoietic system. With the exception of testicular tumors in rodents, the mechanisms of cadmium carcinogenesis are poorly defined. Cadmium can cause any number of molecular lesions that would be relevant to oncogenesis in various cellular model systems. Most studies indicate cadmium is poorly mutagenic and probably acts through indirect or epigenetic mechanisms, potentially including aberrant activation of oncogenes and suppression of apoptosis.
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              Role of oxidative stress in cadmium toxicity and carcinogenesis.

              Jie Liu, Maria Kadiiska, Wei Qu (2009)
              Cadmium (Cd) is a toxic metal, targeting the lung, liver, kidney, and testes following acute intoxication, and causing nephrotoxicity, immunotoxicity, osteotoxicity and tumors after prolonged exposures. Reactive oxygen species (ROS) are often implicated in Cd toxicology. This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis. Cd-generated superoxide anion, hydrogen peroxide, and hydroxyl radicals in vivo have been detected by the electron spin resonance spectra, which are often accompanied by activation of redox sensitive transcription factors (e.g., NF-kappaB, AP-1 and Nrf2) and alteration of ROS-related gene expression. It is generally agreed upon that oxidative stress plays important roles in acute Cd poisoning. However, following long-term Cd exposure at environmentally-relevant low levels, direct evidence for oxidative stress is often obscure. Alterations in ROS-related gene expression during chronic exposures are also less significant compared to acute Cd poisoning. This is probably due to induced adaptation mechanisms (e.g., metallothionein and glutathione) following chronic Cd exposures, which in turn diminish Cd-induced oxidative stress. In chronic Cd-transformed cells, less ROS signals are detected with fluorescence probes. Acquired apoptotic tolerance renders damaged cells to proliferate with inherent oxidative DNA lesions, potentially leading to tumorigenesis. Thus, ROS are generated following acute Cd overload and play important roles in tissue damage. Adaptation to chronic Cd exposure reduces ROS production, but acquired Cd tolerance with aberrant gene expression plays important roles in chronic Cd toxicity and carcinogenesis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Caspian J Intern Med
                Journal ID (iso-abbrev): Caspian J Intern Med
                Journal ID (publisher-id): CJIM
                Title: Caspian Journal of Internal Medicine
                Publisher: Babol University of Medical Sciences (Babol, Iran )
                ISSN (Print): 2008-6164
                ISSN (Electronic): 2008-6172
                Publication date (Print): Summer 2017
                Volume: 8
                Issue: 3
                Pages: 135-145
                Affiliations
                [1 ]Department of Nursing, Babol University of Medical Sciences, Babol, Iran.
                [2 ]Department of Medical Physics, Kashan University of Medical Sciences, Kashan, Iran.
                [3 ]Cellular and Molecular Biology Research Center, Health Research Institute, Babol, Iran.
                [4 ]Neuroscience Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
                Author notes
                [* ]Correspondence: Ali-akbar Moghadamnia, Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. E-mail: moghadamnia@yahoo.com Tel: 0098 1132197667, Fax: 0098 1132197667
                Article
                DOI: 10.22088/cjim.8.3.135
                PMC ID: 5596182
                PubMed ID: 28932363
                SO-VID: 83376773-43d0-4351-9e30-88967d8645e6
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 June 2016
                Date revision received : 6 April 2017
                Date accepted : 8 April 2017
                Categories
                Subject: Review Article

                Keywords: cadmium,poisoning,decontamination,nanoparticles,chelating agents
                Data availability:
                Keywords: cadmium, poisoning, decontamination, nanoparticles, chelating agents

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