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Cytotoxicity: Environmental Pollutants and Human Health
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Cytotoxicity: Environmental Pollutants and Human Health

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Environmental Health".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 6268

Special Issue Editors

Dr. Masaaki Kurasaki

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Guest Editor
Faculty of Environmental Earth Science, Hokkaido University, 060-0810 Sapporo, Japan
Interests: beneficial and toxic roles of nutrients and environmental pollutants on human health; environmental remediation technology; molecular mechanism of chemicals for cell death pathways; environmental pollutants in water environments
Prof. Dr. Md. Shariful Islam

E-Mail Website
Assistant Guest Editor
Department of Agricultural Chemistry, Patuakhali Science and Technology University, Dumki, Patuakhali, Bangladesh
Interests: arsenic toxicity; phytoremediation; salinity; metal binding substances in plants
Prof. Dr. Md. Tajuddin Sikder

E-Mail Website
Assistant Guest Editor
Department of Public Health and Informatics, Jahangirnagar University, Dhaka, Bangladesh
Interests: chemical remediation; nanotechnology; improvement of metal toxicity; water pollution
Dr. Md. Mostafizur Rahman

E-Mail Website
Assistant Guest Editor
Department of Environmental Sciences, Jahangirnagar University, Dhaka 1342, Bangladesh
Interests: environmental pollution; exposure risk assessment; environmental health; pollution remediation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is recognized worldwide that the importance of public health is essential to protecting human health. As living environments have changed at an accelerating pace, and the accompanying industrial technology and civilization have evolved, unintended environmental factors have begun to threaten our health. There are many chemicals, heavy metals, and newly generated organic compounds around us, which become environmental pollutants and cause serious health problems. Several studies have reported that environmental pollutants enhanced their oxidative status leading to in vivo toxicity. However, much remains to be clarified about the mechanisms of the effects of many chemicals on living organisms. Various suggestions have also been proposed on ways to reduce toxicity. It has been suggested to use plant-derived polyphenols; however, the exact mechanism of action has not been clarified. On the other hand, many methods have been studied to remove environmental pollutants. Although many studies have reported methods of purifying heavy metals in soil using plants, there are only a few reports on methods of removing seawater contained in groundwater and well water. In coastal areas from Southeast Asia to South Asia, salinity and arsenic pollution are major health problems. This is another issue we would like to address in this Special Issue.

This Special Issue of the International Journal of Environmental Research and Public Health (IJERPH) focuses on the current state of our knowledge about the effects of environmental pollutants on human health and its improvement. We welcome new research papers, reviews, and case reports on this issue. We also welcome papers dealing with the development of new methods to solve the issues discussed here. Reports and commentary on the current status of environmental pollution and health impacts will also be included. The following are some examples of topics covered in this Special Issue:

  • Environmental pollutants and health: heavy metals, organic chemicals (VOCs, POPs, etc), salinity
  • Mechanism of toxicity of contaminants (in vivo and in vitro)
  • Ameliorative effects of toxicity from environmental pollutants and its mechanism
  • Environmental pollutant removal (biological and chemical) restoration techniques
  • In vivo interaction of heavy metals
  • Combined contamination and biological effects
  • Effective removal method for salinity
  • Interaction between arsenic and salinity on human health

Dr. Masaaki Kurasaki
Prof. Md. Shariful Islam
Prof. Md. Tajuddin Sikder
Dr. Md. Mostafizur Rahman
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Human health
  • Heavy metals
  • Cadmium
  • Mercury
  • Arsenic
  • Organic chemicals
  • VOPs
  • POPs
  • Polyphenols
  • Apoptosis
  • Oxidants
  • Autophagy
  • Cells
  • Liver
  • Kidney
  • Brain

Published Papers (2 papers)

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Research

15 pages, 26460 KiB  
Article
Amelioration of Metal-Induced Cellular Stress by α-Lipoic Acid and Dihydrolipoic Acid through Antioxidative Effects in PC12 Cells and Caco-2 Cells
by Kaniz Fatima Binte Hossain, Mahmuda Akter, Md. Mostafizur Rahman, Md. Tajuddin Sikder, Md. Shiblur Rahaman, Shojiro Yamasaki, Goh Kimura, Tomomi Tomihara, Masaaki Kurasaki and Takeshi Saito
Int. J. Environ. Res. Public Health 2021, 18(4), 2126; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph18042126 - 22 Feb 2021
Cited by 11 | Viewed by 2726
Abstract
α-Lipoic acid (ALA) and its reduced form dihydrolipoic acid (DHLA) are endogenous dithiol compounds with significant antioxidant properties, both of which have the potential to detoxify cells. In this study, ALA (250 μM) and DHLA (50 μM) were applied to reduce metal (As, [...] Read more.
α-Lipoic acid (ALA) and its reduced form dihydrolipoic acid (DHLA) are endogenous dithiol compounds with significant antioxidant properties, both of which have the potential to detoxify cells. In this study, ALA (250 μM) and DHLA (50 μM) were applied to reduce metal (As, Cd, and Pb)-induced toxicity in PC12 and Caco-2 cells as simultaneous exposure. Both significantly decreased Cd (5 μM)-, As (5 μM)-, and Pb (5 μM)-induced cell death. Subsequently, both ALA and DHLA restored cell membrane integrity and intracellular glutathione (GSH) levels, which were affected by metal-induced toxicity. In addition, DHLA protected PC12 cells from metal-induced DNA damage upon co-exposure to metals. Furthermore, ALA and DHLA upregulated the expression of survival-related proteins mTOR (mammalian target of rapamycin), Akt (protein kinase B), and Nrf2 (nuclear factor erythroid 2-related factor 2) in PC12 cells, which were previously downregulated by metal exposure. In contrast, in Caco-2 cells, upon co-exposure to metals and ALA, Nrf2 was upregulated and cleaved PARP-1 (poly (ADP-ribose) polymerase-1) was downregulated. These findings suggest that ALA and DHLA can counterbalance the toxic effects of metals. The protection of ALA or DHLA against metal toxicity may be largely due to an enhancement of antioxidant defense along with reduced glutathione level, which ultimately reduces the cellular oxidative stress. Full article
(This article belongs to the Special Issue Cytotoxicity: Environmental Pollutants and Human Health)
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13 pages, 3552 KiB  
Article
Long-Term Exposure to Low-Dose Di-(2-ethylhexyl) Phthalate Impairs Cholesterol Metabolism in Hepatic Stellate Cells and Exacerbates Liver Fibrosis
by Chun-Ya Lee, Fat-Moon Suk, Yuh-Ching Twu and Yi-Jen Liao
Int. J. Environ. Res. Public Health 2020, 17(11), 3802; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17113802 - 27 May 2020
Cited by 27 | Viewed by 2537
Abstract
Phthalates are often added to plastic products to increase their flexibility. Di-(2-ethylhexyl) phthalate (DEHP) is one of the most common plasticizers. Previously, a major incident involving phthalate-contaminated foodstuffs occurred, where phthalates were deliberately added to foodstuffs as a substitute for emulsifiers, resulting in [...] Read more.
Phthalates are often added to plastic products to increase their flexibility. Di-(2-ethylhexyl) phthalate (DEHP) is one of the most common plasticizers. Previously, a major incident involving phthalate-contaminated foodstuffs occurred, where phthalates were deliberately added to foodstuffs as a substitute for emulsifiers, resulting in a threat to public health. DEHP exposure can cause liver damage and further lead to cancer; however, the effects of long-term exposure to low-dose DEHP on hepatic stellate cells (HSCs) and on liver fibrosis are still unclear. In this study, we showed that chronic exposure to low-dose DEHP results in an accumulation of cholesterol in HSCs by disturbing the cholesterol metabolism and enhancing endogenous cholesterol synthesis. In addition, long-term exposure to low-dose DEHP reduces the sensitivity of HSCs to platelet-derived growth factor BB (PDGF-BB)-induced proliferation by blocking the MAPK pathway. Dysfunction of mitochondrial respiration and induction of caspase 3/PARP-dependent apoptosis were observed in HSCs following chronic, low-dose exposure. The carbon tetrachloride (CCl4)-induced liver fibrosis mouse model showed that long-term administration of DEHP significantly promoted liver damage, inflammatory infiltration, cholesterol accumulation, and deposition of hepatic collagen. In conclusion, long-term exposure to low-dose DEHP may perturb the cholesterol metabolism in HSCs and accelerate liver damage and fibrosis. Full article
(This article belongs to the Special Issue Cytotoxicity: Environmental Pollutants and Human Health)
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