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Molecular Mechanisms of Specific Target Organ Toxicity 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 3518

Special Issue Editor

Special Issue Information

Dear Colleagues, 

The field of toxicology is moving away from classical strategies that use animals to generate apical toxic outcomes assumed to be extrapolatable to humans toward more predictive human-based approaches devoid of animals. One of the historical milestones in this regard was the publication of the report “Toxicity testing in the 21st century: a vision and a strategy” by the US National Academy of Sciences in 2007, which fully embraces these novel approaches and that highlighted the importance of mechanistic toxicology. In this respect, human-based in vitro (cell culture) and in silico (computational) methodologies are strongly preferred over complex animal models to elucidate and predict mechanisms of toxicological action. This research field is still gaining momentum and has now evolved to become a multidisciplinary science feeding from various areas.

This Special Issue of the International Journal of Molecular Sciences focuses on the use of in vitro and in silico tools for the study and prediction of specific target organ toxicity at the mechanistic level. Submission of manuscripts, both original research papers and review papers, related to basic and applied animal-free and human-based toxicology involving a broad chemical space, such as pharmaceuticals, food ingredients, cosmetics, biocides, and industrial chemicals, is encouraged. The target audience includes undergraduates to full professionals in academic, industrial, and regulatory settings.

Prof. Dr. Mathieu Vinken
Guest Editor

Manuscript Submission Information

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Keywords

  • toxicity
  • mechanism
  • adverse outcome pathway
  • cell and tissue culture
  • computational modeling

Published Papers (1 paper)

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Review

30 pages, 2420 KiB  
Review
Linking Benzene, in Utero Carcinogenicity and Fetal Hematopoietic Stem Cell Niches: A Mechanistic Review
by Nur Afizah Yusoff, Zariyantey Abd Hamid, Siti Balkis Budin and Izatus Shima Taib
Int. J. Mol. Sci. 2023, 24(7), 6335; https://doi.org/10.3390/ijms24076335 - 28 Mar 2023
Cited by 3 | Viewed by 3295
Abstract
Previous research reported that prolonged benzene exposure during in utero fetal development causes greater fetal abnormalities than in adult-stage exposure. This phenomenon increases the risk for disease development at the fetal stage, particularly carcinogenesis, which is mainly associated with hematological malignancies. Benzene has [...] Read more.
Previous research reported that prolonged benzene exposure during in utero fetal development causes greater fetal abnormalities than in adult-stage exposure. This phenomenon increases the risk for disease development at the fetal stage, particularly carcinogenesis, which is mainly associated with hematological malignancies. Benzene has been reported to potentially act via multiple modes of action that target the hematopoietic stem cell (HSCs) niche, a complex microenvironment in which HSCs and multilineage hematopoietic stem and progenitor cells (HSPCs) reside. Oxidative stress, chromosomal aberration and epigenetic modification are among the known mechanisms mediating benzene-induced genetic and epigenetic modification in fetal stem cells leading to in utero carcinogenesis. Hence, it is crucial to monitor exposure to carcinogenic benzene via environmental, occupational or lifestyle factors among pregnant women. Benzene is a well-known cause of adult leukemia. However, proof of benzene involvement with childhood leukemia remains scarce despite previously reported research linking incidences of hematological disorders and maternal benzene exposure. Furthermore, accumulating evidence has shown that maternal benzene exposure is able to alter the developmental and functional properties of HSPCs, leading to hematological disorders in fetus and children. Since HSPCs are parental blood cells that regulate hematopoiesis during the fetal and adult stages, benzene exposure that targets HSPCs may induce damage to the population and trigger the development of hematological diseases. Therefore, the mechanism of in utero carcinogenicity by benzene in targeting fetal HSPCs is the primary focus of this review. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Specific Target Organ Toxicity 2.0)
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