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      Toxicodynamics of Lead, Cadmium, Mercury and Arsenic- induced kidney toxicity and treatment strategy: A mini review

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          Highlights

          • •

            Oxidative Stress is the key mechanism involved in Lead, Mercury, Cadmium and Arsenic-induced kidney toxicity.

          • •

            Proteinuria is common to all heavy metals as manifestation of kidney damage.

          • •

            Chelation therapy is recommended based on the dose size of heavy metals, though fatal drawbacks limit their success.

          • •

            Possible effectiveness of plants and plants derived compound against heavy metals is due to their antioxidant activity.

          • •

            Other possible effectiveness of plant includes protecting integrity of mitochondria, Ca 2+ homeostasis and apoptosis regulation.

          Abstract

          Environmental pollution has become a concerning matter to human beings. Flint water crisis in the USA pointed out that pollution by heavy metal is getting worse day by day, predominantly by Lead, Cadmium, Mercury and Arsenic. Despite of not having any biological role in flora and fauna, they exhibit detrimental effect following exposure (acute or chronic). Even at low dose, they affect brain, kidney and heart. Oxidative stress has been termed as cause and effect in heavy metal-induced kidney toxicity. In treatment strategy, different chelating agent, vitamins and minerals are included, though chelating agents has been showed different fatal drawbacks. Interestingly, plants and plants derived compounds had shown possible effectiveness against heavy metals induced kidney toxicity. This review will provide detail information on toxicodynamics of Pb, Cd, Hg and As, treatment strategy along with the possible beneficiary role of plant derived compound to protect kidney.

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          Protection of SH-SY5Y Neuronal Cells from Glutamate-Induced Apoptosis by 3,6′-Disinapoyl Sucrose, a Bioactive Compound Isolated from Radix Polygala

          Yuan-yuan Hu, Jie Li, Ping Liu … (2011)
          The neuroprotective effects of 3,6′-disinapoyl sucrose (DISS) from Radix Polygala against glutamate-induced SH-SY5Y neuronal cells injury were evaluated in the present study. SH-SY5Y neuronal cells were pretreated with glutamate (8 mM) for 30 min followed by cotreatment with DISS for 12 h. Cell viability was determined by (3,4,5-dimethylthiazol-2-yl)-2,5-diphenylte-trazolium bromide (MTT) assay, and apoptosis was confirmed by cell morphology and flow cytometry assay, evaluated with propidium iodide dye. Treatment with DISS (0.6, 6, and 60 μmol/L) increased cell viability dose dependently, inhibited LDH release, and attenuated apoptosis. The mechanisms by which DISS protected neuron cells from glutamate-induced excitotoxicity included the downregulation of proapoptotic gene Bax and the upregulation of antiapoptotic gene Bcl-2. The present findings indicated that DISS exerts neuroprotective effects against glutamate toxicity, which might be of importance and contribute to its clinical efficacy for the treatment of neurodegenerative diseases.
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            Historical perspectives on cadmium toxicology.

            Gunnar F. Nordberg (2009)
            The first health effects of cadmium (Cd) were reported already in 1858. Respiratory and gastrointestinal symptoms occurred among persons using Cd-containing polishing agent. The first experimental toxicological studies are from 1919. Bone effects and proteinuria in humans were reported in the 1940's. After World War II, a bone disease with fractures and severe pain, the itai-itai disease, a form of Cd-induced renal osteomalacia, was identified in Japan. Subsequently, the toxicokinetics and toxicodynamics of Cd were described including its binding to the protein metallothionein. International warnings of health risks from Cd-pollution were issued in the 1970's. Reproductive and carcinogenic effects were studied at an early stage, but a quantitative assessment of these effects in humans is still subject to considerable uncertainty. The World Health Organization in its International Program on Chemical Safety, WHO/IPCS (1992) (Cadmium. Environmental Health Criteria Document 134, IPCS. WHO, Geneva, 1-280.) identified renal dysfunction as the critical effect and a crude quantitative evaluation was presented. In the 1990's and 2000 several epidemiological studies have reported adverse health effects, sometimes at low environmental exposures to Cd, in population groups in Japan, China, Europe and USA (reviewed in other contributions to the present volume). The early identification of an important role of metallothionein in cadmium toxicology formed the basis for recent studies using biomarkers of susceptibility to development of Cd-related renal dysfunction such as gene expression of metallothionein in peripheral lymphocytes and autoantibodies against metallothionein in blood plasma. Findings in these studies indicate that very low exposure levels to cadmium may give rise to renal dysfunction among sensitive subgroups of human populations such as persons with diabetes.
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              Antioxidant nutrients and lead toxicity.

              P. Hsu, Yue Leon GUO (2002)
              Lead-induced oxidative stress contributes to the pathogenesis of lead poisoning for disrupting the delicate prooxidant/antioxidant balance that exists within mammalian cells. Production of reactive oxygen species (ROS) is increased after lead treatment in in vitro studies. In vivo studies suggest that lead exposure causes generation of ROS and alteration of antioxidant defense systems in animals and occupationally exposed workers. The mechanisms for lead-induced oxidative stress include the effect of lead on membrane, DNA, and antioxidant defense systems of cells. From low to high doses of lead exposure, there are different responses of lead-induced oxidative stress in various target sites including lung, blood vessels, testes, sperm, liver, and brain in epidemiological as well as animal studies. Therefore, reducing the possibility of lead interacting with critical biomolecules and inducing oxidative damage, or bolstering the cell's antioxidant defenses might be associated with the beneficial role of antioxidant nutrients through exogenous supplementation of antioxidant molecules. Although many researchers have investigated the benefit of antioxidants in preventing lead toxicity, the mechanisms of antioxidant nutrients being effective via rebalancing the impaired prooxidant/antioxidant ratio are not completely clear. Antioxidant nutrients including, vitamin E, vitamin C, vitamin B(6), beta-carotene, zinc, and selenium, are addressed in this review to discuss their beneficial role in lead-induced oxidative stress.
              Article 0 comments Cited 95 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Mohammad Nasiruddin Rana
                Jitbanjong Tangpong
                Md. Masudur Rahman
                Journal
                Journal ID (nlm-ta): Toxicol Rep
                Journal ID (iso-abbrev): Toxicol Rep
                Title: Toxicology Reports
                Publisher: Elsevier
                ISSN (Electronic): 2214-7500
                Publication date PMC-release: 26 May 2018
                Publication date Collection: 2018
                Publication date (Electronic): 26 May 2018
                Volume: 5
                Pages: 704-713
                Affiliations
                [a ]Biomedical Sciences, School of Allied Health Sciences, Walailak University, Thasala, Nakhon Si Thammarat, Thailand
                [b ]Department of Pharmacy, Faculty of Science and Engineering, International Islamic University Chittagong, Kumira, Chittagong-4318, Bangladesh
                Author notes
                [* ]Corresponding author at: Biomedical Sciences, School of Allied Health Sciences, Walailak University, Thasala, Nakhon Si Thammarat, Thailand. nasiriiuc09@ 123456yahoo.com
                Article
                Publisher ID: S2214-7500(18)30388-3
                DOI: 10.1016/j.toxrep.2018.05.012
                PMC ID: 6035907
                PubMed ID: 29992094
                SO-VID: 87758933-b4b6-4389-bda8-b523929c75ea
                Copyright © © 2018 The Authors. Published by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 9 May 2017
                Date revision received : 13 April 2018
                Date accepted : 21 May 2018
                Categories
                Subject: Article

                Keywords: heavy metals,oxidative stress,proteinuria,kidney toxicity,antioxidant
                Data availability:
                Keywords: heavy metals, oxidative stress, proteinuria, kidney toxicity, antioxidant

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