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Toxics
Special Issues
Nephrotoxicity Induced by Drugs and Chemicals in the Environment
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Nephrotoxicity Induced by Drugs and Chemicals in the Environment

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 24 January 2025 | Viewed by 6716

Special Issue Editors

Prof. Dr. Gary O. Rankin

E-Mail Website
Guest Editor
Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, One John Marshall Drive, Huntington, WV 25755, USA
Interests: nephrotoxicity mechanisms; renal bioactivation of toxicants; structure-toxicity relationships
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Monica Valentovic

E-Mail Website
Guest Editor
Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA
Interests: nephrotoxicity; hepatotoxicity; cancer chemotherapy drugs; acetaminophen; fungicides; solvents; oxidative stress; 4-hydroxynonenal; proximal tubule; protein carbonylation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The kidney is an organ with multiple functions. Kidneys are important for maintaining water and electrolyte balance and the excretion of endogenous and exogenous compounds. In addition, kidneys perform multiple essential endocrine functions. Unfortunately, the kidney is the target for toxicity induced by a wide range of chemicals or their metabolites, including drugs, pesticides, industrial chemicals, natural products, and environmental pollutants. Being a rapidly perfused organ, the kidney is exposed to significant amounts of blood-borne toxicants, which can induce toxicity to the kidney through many different mechanisms. Identifying potential nephrotoxic chemicals and understanding safe and nephrotoxic levels of those chemicals, their mechanisms of toxicity, and potential measures to reduce their toxic effects is critical to reducing the harmful effects of these agents on renal function in humans and other organisms.

This Special Issue will provide recent advances in understanding the nephrotoxic properties and mechanisms of toxicity induced by drugs and non-therapeutic chemicals, including environmental pollutants and natural products. Knowledge continues to be generated about known nephrotoxicants as well as newly identified chemical threats to the kidney from made-made and natural sources. This issue will contribute recent findings to advance the field of renal toxicology.

Prof. Dr. Gary O. Rankin
Prof. Dr. Monica Valentovic
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. Toxics 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 2600 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

  • kidney
  • nephrotoxicity
  • drugs
  • environmental pollutants
  • metals
  • halogenated hydrocarbons
  • pesticides

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Published Papers (3 papers)

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Research

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18 pages, 1302 KiB  
Article
Benchmark Dose of Melamine Exposure for a Renal Injury Marker Mediated by Oxidative Stress: Examples in Patients with Urolithiasis and Occupational Workers
by Chu-Chih Chen, Chia-Chu Liu, Yin-Han Wang, Chia-Fang Wu, Yi-Chun Tsai, Sih-Syuan Li, Tusty-Jiuan Hsieh and Ming-Tsang Wu
Toxics 2024, 12(8), 584; https://doi.org/10.3390/toxics12080584 - 11 Aug 2024
Viewed by 2674
Abstract
Establishing a safe exposure level from epidemiological studies while providing direct hazard characterization in humans often faces uncertainty in causality, especially cross-sectional data. With advances in molecular epidemiology, it is reasonable to integrate identified intermediate biomarkers into health risk assessment. In this study, [...] Read more.
Establishing a safe exposure level from epidemiological studies while providing direct hazard characterization in humans often faces uncertainty in causality, especially cross-sectional data. With advances in molecular epidemiology, it is reasonable to integrate identified intermediate biomarkers into health risk assessment. In this study, by considering the mediation of the oxidative stress marker malondialdehyde (MDA), we explored the exposure threshold of melamine on the early renal injury marker N-acetyl-β-D glucosaminidase (NAG). The benchmark dose (BMD) was derived from model averaging of the composite direct effect of melamine exposure and the indirect effect through the mediation of MDA on NAG levels. As illustrative examples, we analyzed 309 adult patients with calcium urolithiasis and 80 occupational workers for the corresponding exposure thresholds. The derived threshold was subpopulation-dependent, with the one-sided lower bound BMDL10 for the patients with urolithiasis with (without) the mediator MDA for the patients with kidney stones and the occupational workers being 0.88 (0.96) μg/kg_bw/day and 22.82 (18.09) μg/kg_bw/day, respectively. The derived threshold levels, considering the oxidative stress marker MDA, were consistent with those without adjusting for the mediation effect. However, the study outcomes were further supported by the suggested mechanism pathway. The threshold for the patients with urolithiasis was up to two orders lower than the current tolerable daily intake level of 200 μg/kg_bw/day recommended by the WHO (EFSA). Full article
(This article belongs to the Special Issue Nephrotoxicity Induced by Drugs and Chemicals in the Environment)
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16 pages, 3457 KiB  
Article
The Flavoring Agent Ethyl Vanillin Induces Cellular Stress Responses in HK-2 Cells
by Ashley J. Cox, Kathleen C. Brown and Monica A. Valentovic
Toxics 2024, 12(7), 472; https://doi.org/10.3390/toxics12070472 - 29 Jun 2024
Viewed by 1113
Abstract
Flavored e-cigarettes are a popular alternative to cigarette smoking; unfortunately, the extrapulmonary effects are not well-characterized. Human proximal tubule cells were cultured for 24 or 48 h with 0–1000 µM ethyl vanillin (ETH VAN) and cytotoxicity evaluated. Mitochondrial health was significantly diminished following [...] Read more.
Flavored e-cigarettes are a popular alternative to cigarette smoking; unfortunately, the extrapulmonary effects are not well-characterized. Human proximal tubule cells were cultured for 24 or 48 h with 0–1000 µM ethyl vanillin (ETH VAN) and cytotoxicity evaluated. Mitochondrial health was significantly diminished following 48 h of exposure, accompanied by significantly decreased spare capacity, coupling efficiency, and ATP synthase expression. ETH VAN at 24 h inhibited glycolysis. The endoplasmic reticulum (ER) stress marker C/EBP homologous protein (CHOP) was increased at 100 μM relative to 500–1000 μM. The downstream proapoptotic marker cleaved caspase-3 subsequently showed a decreasing trend in expression after 48 h of exposure. The autophagy biomarkers microtubule-associated proteins 1A/1B light chain 3 (LC3B-I and LC3B-II) were measured by Western blot. LC3B-II levels and the LC3B-II/LC3B-I ratio increased at 24 h, which suggested activation of autophagy. In contrast, by 48 h, the autophagy biomarker LC3B-II decreased, resulting in no change in the LC3B-II/LC3B-I ratio. Mitophagy biomarker PTEN-induced putative kinase 1 (PINK1) expression decreased after 48 h of exposure. The downstream marker Parkin was not significantly changed after 24 or 48 h. These findings indicate that the flavoring ETH VAN can induce energy pathway dysfunction and cellular stress responses in a renal model. Full article
(This article belongs to the Special Issue Nephrotoxicity Induced by Drugs and Chemicals in the Environment)
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Review

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25 pages, 2798 KiB  
Review
Unveiling the Mysteries of Contrast-Induced Acute Kidney Injury: New Horizons in Pathogenesis and Prevention
by Zhong Wang, Qiuhan Wang and Xuezhong Gong
Toxics 2024, 12(8), 620; https://doi.org/10.3390/toxics12080620 - 22 Aug 2024
Cited by 1 | Viewed by 2360
Abstract
The utilization of contrast media (CM) in clinical diagnostic imaging and interventional procedures has escalated, leading to a gradual increase in the incidence of contrast-induced acute kidney injury (CI-AKI). Presently, the scarcity of effective pharmacological treatments for CI-AKI poses significant challenges to clinical [...] Read more.
The utilization of contrast media (CM) in clinical diagnostic imaging and interventional procedures has escalated, leading to a gradual increase in the incidence of contrast-induced acute kidney injury (CI-AKI). Presently, the scarcity of effective pharmacological treatments for CI-AKI poses significant challenges to clinical management. Firstly, we explore the pathogenesis of CI-AKI in this review. Beyond renal medullary ischemia and hypoxia, oxidative stress, cellular apoptosis, and inflammation, emerging mechanisms such as ferroptosis, release of neutrophil extracellular traps (NETs), and nitrosative stress, which offer promising avenues for the management of CI-AKI, are identified. Secondly, a comprehensive strategy for the early prevention of CI-AKI is introduced. Investigating the risk factors associated with CI-AKI is essential for the timely identification of high-risk groups. Additionally, exploring early sensitive biomarkers is crucial for early diagnosis. A synergistic approach that combines these sensitive biomarkers, CI-AKI risk factors, and disease risk prediction models enhances both the accuracy and efficiency of early diagnostic processes. Finally, we explore recent pharmacological and non-pharmacological interventions for the management of Cl-AKI. Beyond the traditional focus on the antioxidant N-acetylcysteine (NAC), we look at active compounds from traditional Chinese medicine, including tetramethylpyrazine (TMP), salvianolic acid B (Sal B), as well as emerging preventive medications like N-acetylcysteine amide (NACA), alprostadil, and others, which all showed potential benefits in animal and clinical studies for CI-AKI prevention. Furthermore, innovative strategies such as calorie restriction (CR), enhanced external counterpulsation (EECP), and mesenchymal stem cell therapy are highlighted as providing fresh insights into Cl-AKI prevention and management. Full article
(This article belongs to the Special Issue Nephrotoxicity Induced by Drugs and Chemicals in the Environment)
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