A Review on Carcinogenic Heavy Metals

Akruti Amol Ingole, A. Mukherjee, Piyush Jagdish Balgote, Sampada Prakash Pendse, Surbhi Balwant Dhoke, Uddesh Ramesh Wanjari
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Keywords— Cancer, tumor, heavy metal, toxic, mortality INTRODUCTION Nowadays, over half of world populations face newly diagnosed cancers, and 70% of all cancer death occur in developing and undeveloped countries [1,2]. The prevalence of cancer varieties is multifactorial polygenic diseases that may vary depending upon the environmental factors and genetic susceptibility because they have identifiable heredity factors. Rapidly changing lifestyle and diet adaptation may influence the heritability of variant phenotypes dependent on the nutraceutical's supplementation for their expression [3,4]. To date, relevant information about carcinogens is available, and many of these agents have already been identified [5]. However, many potential carcinogenic heavy metals are present in food and beverage items and are assumed to be safe when consumed by humans that cause serious health problems. In this regard, Regular consumption of daily requirements may expose them to heavy metals in drinking water which pose the greatest threat to public health. Daily life's basic necessity is water, which is the primary source of heavy metals that contaminate the surface and ground waters by industrial sewage and agricultural runoff [6]. Some people may not afford the purified mineral water, and they consume tap water which is the direct source of contaminated heavy metal mixed water [7]. According to several research studies, the concentration of these carcinogenic groundwater elements is high in some countries, including India, Bangladesh, and Argentina [8,9]. These elements are known to induce cancer of different types leading to genetic and epigenetic effects [10]. Epigenetic mechanisms play a prominent role in the process of carcinogenesis. Such events include reversible modification of CpG islands of gene promoters and histone proteins that affect somatic cells and germ cells' gene expression level and cause indirect changes genetically [11,12]. Mammalia genes account for nearly 40% of CpG islands (5-CG-3 sequence). The C5 position of cytosine residue results in hypermethylation and hypomethylation, which involved the inhibition of the expression of tumor suppression of genes or an increase in oncogenic gene expression, jointly contributing to cancer development and progression [13]. Deamination of methylated cytosine base may produce a thymine base, resulting in a specific transition mutation in CpG island, for example, in p53 (tumor suppressor gene or as guardian of the genome), the chromatin configuration changes due to histone proteins' hypermethylation [14]. Corresponding alterations in growth control genes such as DNA-repair genes, oncogenes, protooncogenes, apoptotic genes combine to dictate the cellular phenotype and differentiation [12,15]. Comparing these epigenetic effects caused by the following elements in cancer concerned genes shows the impact in biological systems. I. TOXICITY AND CARCINOGENICITY The degree of toxicity can be acute and chronic. Toxic metals obstruct several physiological processes, including the central nervous system (CNS) and renal functions, having specific interactions with system cells, tissues, and organs. Like Mercury, Gold, Platinum, Beryllium, chromium, and Nickel, a few metals may induce type I, II, III, or IV hypersensitivity [16]. The half-life of metals within tissues is very important to learn about its toxicity. For Hg, the half-life is 60 -70 days [17], Cd is 10-20yrs [18], and Pb is 10yrs [19] depending upon the type of tissue, for example, lead has a half-life in soft tissues for few weeks however it is of 20yrs in bone tissue. Another factor is chemical complexity that may alter the metals' pharmacokinetic properties, including the ability for absorption and distribution to reach the cellular and intracellular targets [20]; chemical forms (elemental, organic, inorganic) strongly affect the route of exposure, bioavailability, and toxic profile. Organic forms are highly lipophilic and quickly cross the biological membrane (BloodBrain barrier and Gastrointestinal wall, Placental membrane). Organic forms of mercury metal (ethyl mercury, phenylmercury, and methylmercury) can accumulate in International Journal of Engineering Research & Technology (IJERT) ISSN: 2278-0181 http://www.ijert.org IJERTV10IS030216 (This work is licensed under a Creative Commons Attribution 4.0 International License.) 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Abstract

Cancer is the leading cause of various incidences of mortality, morbidity, and premature death worldwide. Toxic metals like arsenic, chromium, nickel, aluminium obstruct several physiological processes, including the central nervous system (CNS) and renal functions, having specific interactions with system cells, tissues, and organs. Most importantly, these metals result in the induction of tumors leading to cancer. This review focuses on various heavy metals in the induction of complex disorders and cancer. This work also aims to provide a brief understanding to ordinary people about the most simple day-to-day activities that can get us exposed to heavy metals. Keywords— Cancer, tumor, heavy metal, toxic, mortality INTRODUCTION Nowadays, over half of world populations face newly diagnosed cancers, and 70% of all cancer death occur in developing and undeveloped countries [1,2]. The prevalence of cancer varieties is multifactorial polygenic diseases that may vary depending upon the environmental factors and genetic susceptibility because they have identifiable heredity factors. Rapidly changing lifestyle and diet adaptation may influence the heritability of variant phenotypes dependent on the nutraceutical's supplementation for their expression [3,4]. To date, relevant information about carcinogens is available, and many of these agents have already been identified [5]. However, many potential carcinogenic heavy metals are present in food and beverage items and are assumed to be safe when consumed by humans that cause serious health problems. In this regard, Regular consumption of daily requirements may expose them to heavy metals in drinking water which pose the greatest threat to public health. Daily life's basic necessity is water, which is the primary source of heavy metals that contaminate the surface and ground waters by industrial sewage and agricultural runoff [6]. Some people may not afford the purified mineral water, and they consume tap water which is the direct source of contaminated heavy metal mixed water [7]. According to several research studies, the concentration of these carcinogenic groundwater elements is high in some countries, including India, Bangladesh, and Argentina [8,9]. These elements are known to induce cancer of different types leading to genetic and epigenetic effects [10]. Epigenetic mechanisms play a prominent role in the process of carcinogenesis. Such events include reversible modification of CpG islands of gene promoters and histone proteins that affect somatic cells and germ cells' gene expression level and cause indirect changes genetically [11,12]. Mammalia genes account for nearly 40% of CpG islands (5-CG-3 sequence). The C5 position of cytosine residue results in hypermethylation and hypomethylation, which involved the inhibition of the expression of tumor suppression of genes or an increase in oncogenic gene expression, jointly contributing to cancer development and progression [13]. Deamination of methylated cytosine base may produce a thymine base, resulting in a specific transition mutation in CpG island, for example, in p53 (tumor suppressor gene or as guardian of the genome), the chromatin configuration changes due to histone proteins' hypermethylation [14]. Corresponding alterations in growth control genes such as DNA-repair genes, oncogenes, protooncogenes, apoptotic genes combine to dictate the cellular phenotype and differentiation [12,15]. Comparing these epigenetic effects caused by the following elements in cancer concerned genes shows the impact in biological systems. I. TOXICITY AND CARCINOGENICITY The degree of toxicity can be acute and chronic. Toxic metals obstruct several physiological processes, including the central nervous system (CNS) and renal functions, having specific interactions with system cells, tissues, and organs. Like Mercury, Gold, Platinum, Beryllium, chromium, and Nickel, a few metals may induce type I, II, III, or IV hypersensitivity [16]. The half-life of metals within tissues is very important to learn about its toxicity. For Hg, the half-life is 60 -70 days [17], Cd is 10-20yrs [18], and Pb is 10yrs [19] depending upon the type of tissue, for example, lead has a half-life in soft tissues for few weeks however it is of 20yrs in bone tissue. Another factor is chemical complexity that may alter the metals' pharmacokinetic properties, including the ability for absorption and distribution to reach the cellular and intracellular targets [20]; chemical forms (elemental, organic, inorganic) strongly affect the route of exposure, bioavailability, and toxic profile. Organic forms are highly lipophilic and quickly cross the biological membrane (BloodBrain barrier and Gastrointestinal wall, Placental membrane). Organic forms of mercury metal (ethyl mercury, phenylmercury, and methylmercury) can accumulate in International Journal of Engineering Research & Technology (IJERT) ISSN: 2278-0181 http://www.ijert.org IJERTV10IS030216 (This work is licensed under a Creative Commons Attribution 4.0 International License.) Published by : www.ijert.org Vol. 10 Issue 03, March-2021
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本作品采用知识共享署名4.0国际许可协议。出版单位:www.ijert.org第10卷第03期,2021年3月
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