2,3,7,8-tetrachlorodibenzo-p-dioxin induces multigenerational testicular toxicity and biosynthetic disorder of testosterone in BALB/C mice: Transcriptional, histopathological and hormonal determinants

Faiad, Walaa; Soukkarieh, Chadi; Hanano, Abdulsamie

doi:10.1016/j.ecoenv.2023.115233

Cited by 6 publications

(2 citation statements)

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“…As a prototype of halogenated aromatic compounds, TCDD is frequently employed to illustrate the toxicological effects of dioxins on organisms. Numerous studies have reported that TCDD induces a range of toxicological effects, encompassing reproductive, developmental, and carcinogenic impacts in both exposed individuals and a diverse array of experimental animal models ( White and Birnbaum, 2009 ; Faiad et al, 2022 ; Aldeli et al, 2023 ; Faiad et al, 2023 ; Hammoudeh et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Impact of dioxins on reproductive health in female mammals

Aldeli,

Murphy,

Hanano

2024

Front. Toxicol.

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Extensive research has been conducted to investigate the toxicological impact of dioxins on mammals, revealing profound effects on the female reproductive system in both humans and animals. Dioxin exposure significantly disrupts the intricate functions of the ovary, a pivotal organ responsible for reproductive and endocrine processes. This disruption manifests as infertility, premature ovarian failure, and disturbances in sex steroid hormone levels. Comprehensive studies, encompassing accidental human exposure and experimental animal data, have raised a wealth of information with consistent yet varied conclusion influenced by experimental factors. This review begins by providing an overarching background on the ovary, emphasizing its fundamental role in reproductive health, particularly in ovarian steroidogenesis and hormone receptor regulation. Subsequently, a detailed examination of the Aryl hydrocarbon Receptor (AhR) and its role in governing ovarian function is presented. The review then outlines the sources and toxicity of dioxins, with a specific focus on AhR involvement in mediating reproductive toxicity in mammals. Within this context, the impact of dioxins, notably 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on Folliculogenesis and Preimplantation embryos is discussed. Furthermore, the review delves into the disruptions of the female hormonal system caused by TCDD and their ramifications in endometriosis. Notably, variations in the effects of TCDD on the female reproductive and hormonal system are highlighted in relation to TCDD dose, animal species, and age. As a forward-looking perspective, questions arise regarding the potential involvement of molecular mechanisms beyond AhR in mediating the female reproductive toxicity of dioxins.

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Section: Introductionmentioning

confidence: 99%

Impact of dioxins on reproductive health in female mammals

Aldeli,

Murphy,

Hanano

2024

Front. Toxicol.

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“…Foremost among these is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), acknowledged as the most toxic member of the dioxin family. TCDD is a well-known substance for its detrimental effects on the immune system, its ability to cause cancer, disrupt the endocrine system, induce cardiovascular toxicity, and its potential to trigger abnormalities in reproduction and development [ 2 , 3 , 4 , 5 , 6 , 7 ]. Experiments on laboratory animals have unveiled various physiological responses to TCDD, including immunotoxicity, neurological and behavioral abnormalities, the potential to induce cancer, and significant alterations in biochemical indicators [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Boron Compounds Mitigate 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity in Human Peripheral Blood Mononuclear Cells

Arslan,

Baba,

Tozlu

2024

Toxics

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) stands as one of the most potent halogenated polycyclic hydrocarbons, known to inflict substantial cytotoxic effects on both animal and human tissues. Its widespread presence and recalcitrance make it an environmental and health concern. Efforts are being intensively channeled to uncover strategies that could mitigate the adverse health outcomes associated with TCDD exposure. In the realm of counteractive agents, boron compounds are emerging as potential candidates. These compounds, which have found applications in a spectrum of industries ranging from agriculture to pharmaceutical and cosmetic manufacturing, are known to modulate several cellular processes and enzymatic pathways. However, the dose–response relationships and protective potentials of commercially prevalent boron compounds, such as boric acid (BA), ulexite (UX), and borax (BX), have not been comprehensively studied. In our detailed investigation, when peripheral blood mononuclear cells (PBMCs) were subjected to TCDD exposure, they manifested significant cellular disruptions. This was evidenced by compromised membrane integrity, a marked reduction in antioxidant defense mechanisms, and a surge in the malondialdehyde (MDA) levels, a recognized marker for oxidative stress. On the genomic front, increased 8-OH-dG levels and chromosomal aberration (CA) frequency suggested that TCDD had the potential to cause DNA damage. Notably, our experiments have revealed that boron compounds could act as protective agents against these disruptions. They exhibited a pronounced ability to diminish the cytotoxic, genotoxic, and oxidative stress outcomes instigated by TCDD. Thus, our findings shed light on the promising role of boron compounds. In specific dosages, they may not only counteract the detrimental effects of TCDD but also serve as potential chemopreventive agents, safeguarding the cellular and genomic integrity of PBMCs.

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