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Toxics
Special Issues
Effects of Chemical-Induced Organ Damage via Inducing Antioxidant Defense Responses
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Effects of Chemical-Induced Organ Damage via Inducing Antioxidant Defense Responses

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6260

Special Issue Editors

Prof. Dr. Fatma M. El-Demerdash

E-Mail Website
Guest Editor
Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, Alexandria 21526, Egypt
Interests: environmental toxicology and biochemistry; oxidative stress; medicinal plants; molecular toxicology; nanotechnology
Prof. Dr. Mohamed M. Abdel-Daim

E-Mail Website
Guest Editor
1. Department of Pharmaceutical Sciences, Pharmacy Program, Batterjee Medical College, P.O. Box 6231, Jeddah 21442, Saudi Arabia
2. Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, Egypt
Interests: pharmacology; drug toxicology; alternative medicine; environmental pharmacology and toxicology
Special Issues, Collections and Topics in MDPI journals
Dr. Yanzhu Zhu

E-Mail Website
Guest Editor
Animal Science and Technology College, Jilin Agriculture Science and Technology University, Changchun, China
Interests: pharmacology; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Living organisms are continuously and inadvertently exposed to an array of insults that produce reactive oxygen species, eventually predisposing them to oxidative stress. Oxidative stress, an imbalance in the redox homeostasis of the cell, impacts almost all acute and chronic progressive disorders and, on a cellular basis, is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism, and neurodegeneration. A large body of evidence supports the notion that dietary antioxidants are useful protectors against oxidative stress and play an important role in preventing human diseases. Since oxidative stress is a complex condition, new insights into its cellular and molecular mechanisms in several organ systems and techniques and markers for assessing it are void areas that need to be filled by scientific contributions in these aspects.

Potential topics include, but are not limited to, the following:

  • Cellular and molecular insights into oxidative stress;
  • Antioxidant defense system;
  • New sources of antioxidants;
  • Xenobiotics toxicity;
  • Toxicological aspects in oxidative stress;
  • Oxidative stress and disease relation;
  • Biomarkers of oxidative stress;
  • Interactions among antioxidants.

The purpose of this Special Issue is to encourage researchers to submit original research and review articles that address all aspects of environmental pollutants and their mechanisms of action linked with oxidative stress, inflammation, and cell death in human diseases or using animal models. This Special Issue aims to attract research that will translate this knowledge into new public strategies.

Prof. Dr. Fatma M. El-Demerdash
Prof. Dr. Mohamed M. Abdel-Daim
Dr. Yanzhu Zhu
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

  • environmental toxicology and biochemistry
  • oxidative stress
  • antioxidants
  • medicinal plants
  • xenobiotics
  • molecular biology
  • living organisms

Published Papers (3 papers)

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Research

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19 pages, 3095 KiB  
Article
Punica granatum (Pomegranate) Peel Extract Pre-Treatment Alleviates Fenpropathrin-Induced Testicular Injury via Suppression of Oxidative Stress and Inflammation in Adult Male Rats
by Ali B. Jebur, Raghda A. El-Sayed, Mohamed M. Abdel-Daim and Fatma M. El-Demerdash
Toxics 2023, 11(6), 504; https://doi.org/10.3390/toxics11060504 - 03 Jun 2023
Cited by 4 | Viewed by 1605
Abstract
Fenpropathrin (FNP) is one of the commonly used insecticides in agriculture and domestically, leading to environmental and health problems. The goal of the current investigation was to determine how well pomegranate peel extract (PGPE) could prevent the testicular toxicity and oxidative stress induced [...] Read more.
Fenpropathrin (FNP) is one of the commonly used insecticides in agriculture and domestically, leading to environmental and health problems. The goal of the current investigation was to determine how well pomegranate peel extract (PGPE) could prevent the testicular toxicity and oxidative stress induced by FNP. Four groups of male Wistar rats were randomly assigned: negative control (corn oil), PGPE (500 mg/kg BW), positive control (FNP; 15 mg/kg BW, 1/15 LD50), and PGPE + FNP. For four weeks, the rats received their doses daily and orally via gavage. The major phytochemical components (total phenolic, flavonoids, and tannins contents) detected in PGPE by GC-MS included ellagic acid, hydroxymethylfurfurole, guanosine, and pyrogallol with high total phenolic, flavonoids, and tannin contents. FNP-treated rats showed a marked elevation in testicular levels of thiobarbituric acid-reactive substances, hydrogen peroxide, and protein carbonyl content, as well as the activity of aminotransferases and phosphatases. Meanwhile. a significant decline in body weight, gonadosomatic index, glutathione, protein contents, enzymatic antioxidants, and hydroxysteroid dehydrogenase (3β HSD, and 17β HSD) activity was observed. In addition, significant alterations in testicular P53, Cas-3, Bcl-2, IL-β, IL-10, testosterone, follicle-stimulating and luteinizing hormones, and sperm quality were detected. Furthermore, biochemical and molecular changes were corroborated testicular histological abnormalities. Moreover, PGPE-pretreated FNP-intoxicated rats demonstrated considerable improvement in the majority of the studied parameters, when compared to FNP-treated groups. Conclusively, PGPE provided a potent protective effect against the testicular toxicity caused by FNP, due to its antioxidant-active components. Full article
(This article belongs to the Special Issue Effects of Chemical-Induced Organ Damage via Inducing Antioxidant Defense Responses)
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28 pages, 8455 KiB  
Article
Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay
by Farooq A. Wani, Mahrous A. Ibrahim, Shimaa H. Ameen, Amira E. Farage, Zinab Abd-Elhady Ali, Khaldoon Saleh, Medhat M. Farag, Mohammed U. Sayeed, Muhannad A. Y. Alruwaili, Abdulsalam H. F. Alruwaili, Ahmad Z. A. Aljared and Rania A. Galhom
Toxics 2023, 11(5), 398; https://doi.org/10.3390/toxics11050398 - 22 Apr 2023
Cited by 1 | Viewed by 2425
Abstract
Background: the nephrotoxicity of methotrexate (MTX) is observed in high-dose therapy. Moreover, low-dose MTX therapy for rheumatic diseases is debatable and claimed to cause renal impairment. This study aimed at studying the effect of methotrexate in repeated low doses on rat kidneys and [...] Read more.
Background: the nephrotoxicity of methotrexate (MTX) is observed in high-dose therapy. Moreover, low-dose MTX therapy for rheumatic diseases is debatable and claimed to cause renal impairment. This study aimed at studying the effect of methotrexate in repeated low doses on rat kidneys and assessing the efficacy of adipose-derived mesenchymal stem cells (AD-MSCs) and platelet rich plasma (PRP) for attenuating this effect. Methods: Forty-two male Wistar rats were used, 10 rats were donors of AD-MSCs and PRP, 8 rats served as control, and the remaining rats were subjected to induction of nephrotoxicity by MTX intraperitoneal injection once weekly for successive 8 weeks and then assigned into 3 groups of 8 animals each: Group II: received MTX only. Group III: received MTX + PRP. Group IV: received MTX + AD-MSCs. After one month, rats were anaesthetized, serum-sampled, and renal tissue removed for biochemical, histological, and ultrastructural evaluation. Results: there was significant tubular degeneration, glomerulosclerosis, fibrosis, decreased renal index, along with increased levels of urea and creatinine in the MTX group compared to the control group. Immunohistochemical expression of caspase-3 and iNOS in the renal tissue was significantly increased in group II compared to groups III and IV. Biochemical results revealed higher tissue malondialdehyde (MDA) concentration in the MTX-injected group which decreased significantly in co-treatment with either AD-MSC or PRP + MTX. MSC promoted the activation of the Nrf2/PPARγ/HO-1 and NF-κB/Keap1/caspase-3 pathways, increased antioxidant enzyme activities, reduced lipid peroxidation levels, and alleviated oxidative damage and apoptosis. PRP showed therapeutic effects and molecular mechanisms similar to MSC. Furthermore, MSC and PRP treatment significantly reduced MTX-induced upregulation of the pro-inflammatory (NF-κB, interleukin-1ß, and TNF-α), oxidative stress (Nrf-2, hemoxygenase-1, glutathione, and malondialdehyde), and nitrosative stress (iNOS) markers in the kidney. Conclusion: repeated administration of low-dose MTX resulted in massive renal tissue toxicity and deterioration of renal function in rats which proved to be attenuated by PRP and AD-MSCs through their anti-inflammatory, anti-apoptotic and anti-fibrotic properties. Full article
(This article belongs to the Special Issue Effects of Chemical-Induced Organ Damage via Inducing Antioxidant Defense Responses)
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Review

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19 pages, 9227 KiB  
Review
Advances in Antioxidant Applications for Combating 131I Side Effects in Thyroid Cancer Treatment
by Li Yang, Jiahui Ma, Pengyu Lei, Jia Yi, Yilei Ma, Zhongke Huang, Tingjue Wang, Haiyan Ping, Danping Ruan, Da Sun and Hongying Pan
Toxics 2023, 11(6), 529; https://doi.org/10.3390/toxics11060529 - 13 Jun 2023
Cited by 3 | Viewed by 1792
Abstract
Thyroid cancer is the most common endocrine cancer, and its prevalence has been increasing for decades. Approx. 95% of differentiated thyroid carcinomas are treated using 131iodine (131I), a radionuclide with a half-life of 8 days, to achieve optimal thyroid residual [...] Read more.
Thyroid cancer is the most common endocrine cancer, and its prevalence has been increasing for decades. Approx. 95% of differentiated thyroid carcinomas are treated using 131iodine (131I), a radionuclide with a half-life of 8 days, to achieve optimal thyroid residual ablation following thyroidectomy. However, while 131I is highly enriched in eliminating thyroid tissue, it can also retain and damage other body parts (salivary glands, liver, etc.) without selectivity, and even trigger salivary gland dysfunction, secondary cancer, and other side effects. A significant amount of data suggests that the primary mechanism for these side effects is the excessive production of reactive oxygen species, causing a severe imbalance of oxidant/antioxidant in the cellular components, resulting in secondary DNA damage and abnormal vascular permeability. Antioxidants are substances that are capable of binding free radicals and reducing or preventing the oxidation of the substrate in a significant way. These compounds can help prevent damage caused by free radicals, which can attack lipids, protein amino acids, polyunsaturated fatty acids, and double bonds of DNA bases. Based on this, the rational utilization of the free radical scavenging function of antioxidants to maximize a reduction in 131I side effects is a promising medical strategy. This review provides an overview of the side effects of 131I, the mechanisms by which 131I causes oxidative stress-mediated damage, and the potential of natural and synthetic antioxidants in ameliorating the side effects of 131I. Finally, the disadvantages of the clinical application of antioxidants and their improving strategies are prospected. Clinicians and nursing staff can use this information to alleviate 131I side effects in the future, both effectively and reasonably. Full article
(This article belongs to the Special Issue Effects of Chemical-Induced Organ Damage via Inducing Antioxidant Defense Responses)
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