Chelation in Metal-Induced Diseases

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

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 2666

Special Issue Editor


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Guest Editor
1. Institute of Pharmacy, Era Medical University, Lucknow, India
2. Ex-Director, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research-Raebareli, Transit Campus, Lucknow, India
Interests: chemical toxicity; toxicity of metals; arsenic poisoning; drug development; organ toxicity; mechanism of toxicity; oxidative medicine; chelation therapy

Special Issue Information

Dear Colleagues,

Occupational and environmental risks for human health derived from metal exposure are of concern. Hereditary conditions such as Wilson’s disease caused by excess copper accumulation, or patients with secondary iron overload (thalassemia major), require treatment because of the excess accumulation of these metals. The  reduction of aluminum accumulation and toxicity following chelation may also prove beneficial in end-stage renal disease patients, and perhaps those suffering from neurodegenerative disorders such as Alzheimer's disease (AD). Chelation therapy has been practiced in various forms for more than five decades. The development of organic compounds capable of reducing body toxic burden continues to be an area of general importance. Metal complexes formed with these metal ions and chelating agents in vivo are readily excreted in the urine or feces, leading to the reduction of toxic metal burden. Neurodegenerative disorders are a group of heterogeneous diseases characterized by protein deposition within neurons or brain parenchyma and oxidative stress. Although most neurodegenerative, hepatic, renal, cardiovascular, and bone disorders have distinct and characteristic etiologies, they share striking similarity with respect to metal discrepancies. Recognizing the metal-based hypothesis of diseases, chelation therapy has been proposed to break bonds between metals and proteins/enzymes etc. and reduce organ toxicity along with the possible restoration of metal homeostasis.

We welcome manuscripts focused on the effect of chelation in various metal/metalloid-induced diseases. Manuscripts should fall within one or more of the following topics of interest:

Synthesis and characterization of new chelating agents; isolation and characterization of phytochemicals against metal-induced neurological disorders; effectiveness of conventional chelators against metal-induced neurodegenerative/hepatic/renal/cardiovascular diseases; chelation therapy against cardiovascular diseases like Wilson’s disease, Alzheimer’s, and Parkinsonism; effectiveness against carcinogenesis etc.; clinical studies describing the efficacy of chelation in the recovery of numerous metal-induced human diseases; recent discoveries about natural-based molecules with potential organ protective activity; alternative strategies such as pharmaceutical engineering approaches explored for enhancing the efficacy of natural-based molecules; preclinical and clinical studies of phyto-pharmaceuticals; toxicity assessment of these synthetic and natural-based products; as well as regulatory challenges or considerations for natural-based products.

The present Special Issue thus welcomes high-quality manuscripts/review papers on the above theme. There is still a substantial lack of relevant and reliable data as well as definitive conclusions regarding the clinical advantages of chelation in neurodegenerative conditions. Such papers will be given priority.

Dr. Swaran J. S. Flora
Guest Editor

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Keywords

  • neurodegerative diseases
  • cardiovascular diseases
  • organ toxicity
  • toxic metals/metalloids
  • phytochemicals
  • chelation therapy
  • clinical trials
  • synthesis of new chelating agents

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Published Papers (1 paper)

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Research

21 pages, 5847 KiB  
Article
Alpha Lipoic Acid and Monoisoamyl-DMSA Combined Treatment Ameliorates Copper-Induced Neurobehavioral Deficits, Oxidative Stress, and Inflammation
by Jayant Patwa, Ashima Thakur and Swaran Jeet Singh Flora
Toxics 2022, 10(12), 718; https://doi.org/10.3390/toxics10120718 - 24 Nov 2022
Cited by 4 | Viewed by 2308
Abstract
Copper (Cu), being an essential trace metal, plays several roles in biological processes, though exposure to Cu can be potentially toxic to the brain and a few other soft organs. In the present study, we investigated the effects of the combined administration of [...] Read more.
Copper (Cu), being an essential trace metal, plays several roles in biological processes, though exposure to Cu can be potentially toxic to the brain and a few other soft organs. In the present study, we investigated the effects of the combined administration of monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA), which is a new chelator, and alpha lipoic acid (ALA) and an antioxidant that is made naturally in the body and is also found in foods, against Cu-induced oxidative stress in rats. Rats were exposed to 20 mg/kg copper sulfate for 16 weeks once a day via the oral route. After 16 weeks of exposure, animals were divided into different sub-groups. Group I was divided into three subgroups: Group IA, control; Group IB, MiADMSA (75 mg/kg, oral); Group IC, ALA (75 mg/kg, oral), while Group II was divided into four subgroups: Group IIA, Cu pre-exposed; Group IIB, Cu+ MiADMSA; Group IIC, Cu+ ALA; Group IID, Cu+ ALA+ MiADMSA. Exposure to Cu led to significant neurobehavioral abnormalities; treatment with MiADMSA, and in particular MiADMSA + ALA, significantly ameliorated the neurobehavioral parameters and restored the memory deficits in rats. Oxidative stress variables (ROS, nitrite, TBARS, SOD, catalase) and inflammatory markers (TNF-α, and IL-1β), which were altered on Cu exposed rats, also responded favorably to ALA+ MiADMSA combined treatment. Thus, combined administration of MiADMSA and ALA might be a better treatment strategy than monotherapy with MiADMSA or ALA against Cu-induced neurotoxicity, particularly in reducing oxidative stress, neurobehavioral abnormalities, and inflammatory markers. Full article
(This article belongs to the Special Issue Chelation in Metal-Induced Diseases)
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