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Scope of the Problem
Published in Jason W. Birkett, John N. Lester, Endocrine Disrupters in Wastewater and Sludge Treatment Processes, 2002
An androgen is defined as “a class of male sex hormones related to the steroid androstane and produced in the adrenal cortex and the testes; includes testosterone, androsterone, and androstenolone responsible for the development of secondary male characteristics, such as a deep voice and facial hair.”
Evaluation of the carcinogenicity of carbon tetrachloride
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Samuel M. Cohen, Christopher Bevan, Bhaskar Gollapudi, James E. Klaunig
A critical component of the MOA analysis is an evaluation of possible alternative MOA. The MOA for liver carcinogenesis (Table 8) in rodents and in humans was delineated in various reviews (Cohen 2010; Holsapple et al. 2006; Klaunig and Wang 2018). These include DNA reactive and non-DNA reactive MOA. The non-DNA reactive MOA is either receptor-mediated or non-receptor-mediated. Receptor-mediated MOA includes estrogen stimulation and cytotoxicity secondary to specific reactions, such as those related to HMG-CoA reductase inhibition of various enzyme in the porphyrin-heme synthesis pathway. Other MOA that are receptor-mediated appear to be rodent-specific and include PPARα activation (peroxisome proliferation) and cytochrome enzyme induction (constitutive androstane receptor (CAR), pregnane X receptor (PXR), aryl hydrocarbon receptor (AHR)). Non-receptor mediated MOA includes cytotoxicity, infections, iron or copper overload and increased apoptosis (for example, fumonisin B1), as well as several inherited disorders in humans (Cohen 2010).
A critical review on the bioaccumulation, transportation, and elimination of per- and polyfluoroalkyl substances in human beings
Published in Critical Reviews in Environmental Science and Technology, 2023
Yao Lu, Ruining Guan, Nali Zhu, Jinghua Hao, Hanyong Peng, Anen He, Chunyan Zhao, Yawei Wang, Guibin Jiang
Human studies consistently demonstrated the association between exposure to PFOA, PFOS, and perfluorononanoic acid (PFNA) and the disturbance of liver injury markers (alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase) (Costello et al., 2022). The hepatic and metabolic toxicity mechanisms of PFAS exposure are the most widely investigated, with results showing that nuclear receptors involved in lipid and glucose metabolism, such as peroxisome proliferator–activated receptors (e.g., PPARα and PPARγ), pregnane X-receptor (PXR), and constitutive androstane receptor (CAR), are regulated by PFAS exposure (Consoer et al., 2016). PPARα and PPARγ are also highly expressed in the kidney proximal tubules that regulate adipogenesis and cell growth and differentiation. Other pathogenic pathways affected by PFAS have also been investigated. For example, NF-E2-related factor 2 (Nrf2) pathways can combat oxidative stress damage by PFAS in kidney. Nrf2 and its target genes have been found to be upregulated following PFAS exposure (Fenton et al., 2021).
Windows of sensitivity to toxic chemicals in the development of the endocrine system: an analysis of ATSDR’s toxicological profile database
Published in International Journal of Environmental Health Research, 2022
Chemicals that affect the normal function of the endocrine system are called endocrine-disrupting chemicals (EDCs). These are defined by the US Environmental Protection Agency (EPA) as ‘exogenous agents that interfere with synthesis, secretion, transport, metabolism, binding action or elimination of natural blood-borne hormones that are present in the body and are responsible for homeostasis, reproduction, and developmental process’ (US EPA 1997). Anin-depth review and scientific statement from the Endocrine Society focused on seven different topics, which strengthens the knowledgebase of EDCs’ actions on endocrine health-related effects (Gore et al. 2015). Considering the impact on several different toxicokinetics/toxicodynamic processes listed above, it is not surprising that the mechanism of action of these chemicals is complex. It was established that there are at least five important mechanisms, four of which involve induction of receptors (the aryl hydrocarbon [Ah] receptor, the peroxisome proliferator activated receptor [PPAR], the constitutive androstane receptor [CAR, phenobarbital induction], the pregnane X receptor [PXR, rifampicin induction]) (Fuhr 2000). The end result is increased expression of various enzymes. Another type of induction (ethanol-like) is mediated by ligand stabilization of the CYP2E1 enzyme. A detailed discussion on the mechanism of action of EDCs is beyond the scope of this paper; interested readers should consult a literature review of the topic (Fuhr 2000; Gore et al. 2015).