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Association between environmental contaminant TBOEP and hepatic metabolism

ABSTRACT: tris(2-butoxyethyl) phosphate (TBOEP) is a common organophosphorus compound widely used in industrial production as a plasticizer and flame retardant. In recent years, studies have shown that TBOEP may pose potential threats to human health, particularly its association with liver metabolic function has attracted widespread attention. The liver, as the most important metabolic organ in the human body, plays a crucial role in detoxification, synthesis, and decomposition of various biomolecules. After entering the human body, TBOEP is mainly metabolized and detoxified by the liver. However, TBOEP and its metabolites may interfere with the normal function of the liver, leading to metabolic disorders. Research has shown that TBOEP exposure may affect the activity of enzymes in the liver, such as the cytochrome P450 enzyme system, which plays an important role in drug metabolism and endogenous substance synthesis. Long-term exposure to TBOEP may also lead to liver inflammation and fatty degeneration, further affecting liver metabolic function. In addition, TBOEP may also affect liver metabolic pathways by influencing gene expression. For example, TBOEP exposure may activate or inhibit genes related to lipid metabolism, glucose metabolism, and oxidative stress, thereby altering the metabolic state of the liver. These changes not only affect the function of the liver itself but may also have a chain reaction on the health of other organs and systems through the interaction of the systemic metabolic network. In summary, as an environmental pollutant, the potential impact of TBOEP on liver metabolic function cannot be ignored. Future research needs to further explore the toxicological mechanisms of TBOEP and its long-term effects on human health in order to develop effective prevention and intervention measures to protect public health.

ORGANISM(S): Mus musculus

PROVIDER: GSE299130 | GEO | 2026/03/18

REPOSITORIES: GEO

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Project description:Humans are chronically exposed to a mixture of environmental chemicals (ECs), many with endocrine disrupting potential, contributing to the development of non-communicable diseases. The adverse health effects of exposure to single ECs have been extensively studied but less is known about the impact of chronic exposure to low levels of a mixture of ECs, which is the real-life exposure scenario. Biosolids, derived from human wastewater treatment, closely reflects the human exposome in both the array and concentration of ECs and is a novel, real-life model to investigate the health risks posed by developmental exposure to mixtures of ECs. Previous studies using the prenatal biosolids exposure model found an increased accumulation of the endocrine disrupting chemical diethylhexylphthalate in the fetal liver and metabolic perturbations including increased thyroid gland weight in the male fetus and reduced bodyweight in prepubertal male lambs. To understand the basis of this sexually dimorphic metabolic phenotype we investigated the transcriptome of liver, the primary metabolic organ, in lambs of both sexes. Since many liver genes show sexual dimorphism, with sex-biased genes playing a pivotal role in lipid and drug metabolism, sex-differences in liver gene expression and the impact of prenatal biosolids exposure on it was examined. We hypothesized that maternal preconceptional and gestational exposure of sheep to biosolids programs sex-specific transcriptional changes in the offspring liver. Ewes (F0) were grazed on either inorganic fertilizer (Control) or biosolids-treated pastures (Biosolids) from 1 month before mating till parturition. All lambs (F1) were raised on control pastures after lambing until euthanasia at 9.5 weeks of age. RNA from liver from Control male (n=7), Control female (n=8), BTP male (n=7) and BTP female (n=8) lambs were subjected to next generation sequencing and DESeq2 R package was used to identify differentially expressed genes due to prenatal biosolids exposure and sex-differentially expressed genes .

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Association between environmental contaminant TBOEP and hepatic metabolism

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