Pubertal exposure to the endocrine disruptor mono-2-ethylhexyl ester at body burden level caused cholesterol imbalance in mice

Wang, Cui; Yue, Siqing; Hao, Zhengliang; Ren, Guangyan; Lu, Dezhao; Zhang, Quan; Zhao, Meirong

doi:10.1016/j.envpol.2018.08.091

Cited by 37 publications

(15 citation statements)

References 56 publications

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“…Our study revealed that exposure to DEHP during pregnancy alters the cecal microbial population in mice. Several previous studies also showed that phthalate exposure (DEHP, mono-ethylhexyl phthalate, or diethyl phthalate) modified the gut microbiome [42][43][44], and these changes were associated with obesity [43] and neurodevelopmental disorders [42]. One study showed that phthalate exposure was linked to dysbiosis in newborns, as the newborns exposed to higher levels of DEHP had significantly altered immune responses to vaccinations later in life compared with controls [45].…”

Section: Discussionmentioning

confidence: 99%

“…Although different phthalates, species, and exposure time periods were used, one study in female rats also showed that phthalate (DEP) exposure decreased the F/B ratio compared with the control [44]. In contrast to these results, MEHP exposure in male mice increased the relative abundance of Firmicutes [43]. The F/B ratio was used as a marker of obesity, such that obese individuals have an increased F/B ratio, whereas normal and lean individuals have a decreased F/B ratio.…”

Section: Discussionmentioning

confidence: 99%

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Subacute Exposure to an Environmentally Relevant Dose of Di-(2-ethylhexyl) Phthalate during Gestation Alters the Cecal Microbiome, but Not Pregnancy Outcomes in Mice

Bashir

Gao

Gutiérrez

et al. 2021

Toxics

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Di-2-ethylhexyl phthalate (DEHP) is a plasticizer commonly found in polyvinyl chloride, medical equipment, and food packaging. DEHP has been shown to target the reproductive system and alter the gut microbiome in humans and experimental animals. However, very little is known about the impact of DEHP-induced microbiome changes and its effects during pregnancy. Thus, the objective of this study was to investigate the effects of DEHP exposure during pregnancy on the cecal microbiome and pregnancy outcomes. Specifically, this study tested the hypothesis that subacute exposure to DEHP during pregnancy alters the cecal microbiome in pregnant mice, leading to changes in birth outcomes. To test this hypothesis, pregnant dams were orally exposed to corn oil vehicle or 20 µg/kg/day DEHP for 10 days and euthanized 21 days after their last dose. Cecal contents were collected for 16S Illumina and shotgun metagenomic sequencing. Fertility studies were also conducted to examine whether DEHP exposure impacted birth outcomes. Subacute exposure to environmentally relevant doses of DEHP in pregnant dams significantly increased alpha diversity and significantly altered beta diversity. Furthermore, DEHP exposure during pregnancy significantly increased the relative abundance of Bacteroidetes and decreased the relative abundance of Firmicutes and Deferribacteres compared with controls. The affected taxonomic families included Deferribacteraceae, Lachnospiraceae, and Mucisprillum. In addition to changes in the gut microbiota, DEHP exposure significantly altered 14 functional pathways compared with the control. Finally, DEHP exposure did not significantly impact the fertility and birth outcomes compared with the control. Collectively, these data indicate that DEHP exposure during pregnancy shifts the cecal microbiome, but the shifts do not impact fertility and birth outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Subacute Exposure to an Environmentally Relevant Dose of Di-(2-ethylhexyl) Phthalate during Gestation Alters the Cecal Microbiome, but Not Pregnancy Outcomes in Mice

Bashir

Gao

Gutiérrez

et al. 2021

Toxics

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“…A review by Chiu et al summarizes many of the phthalate exposure studies that alter the gut microbiome [3]. Briefly, DEHP, DEP, MEHP, DMP, and DBP exposure have been shown to alter the gut microbiota in a variety of models including rats [35], mice [7,8], and fish [5,6]. Human infant data have also shown that medically relevant doses of DEHP altered the gut microbiota in males and females [9].…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to environmental chemicals such as heavy metals, pesticides, persistent organic pollutants, and plasticizers all perturb the gut microbiome [3]. In particular, phthalate exposures impact the gut microbiome in newborn infants, rats, mice, and fish during puberty, birth, and pregnancy [4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Isolation of DiNP-Degrading Microbes from the Mouse Colon and the Influence DiNP Exposure Has on the Microbiota, Intestinal Integrity, and Immune Status of the Colon

Bashir

Abdelhamid

Clark

et al. 2022

Toxics

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Di-isononyl phthalate (DiNP) is a plasticizer used to impart flexibility or stability in a variety of products including polyvinyl chloride, cable coatings, artificial leather, and footwear. Previous studies have examined the impact of DiNP on gut integrity and the colonic immune microenvironment, but this study further expands the research by examining whether DiNP exposure alters the colonic microbiota and various immune markers. Previous studies have also revealed that environmental microbes degrade various phthalates, but no studies have examined whether anaerobic gut bacteria can degrade DiNP. Thus, this study tested the hypothesis that DiNP exposure alters the gut microbiota and immune-related factors, and that anaerobic bacteria in the gut can utilize DiNP as the sole carbon source. To test this hypothesis, adult female mice were orally dosed with corn oil or various doses of DiNP for 10–14 consecutive days. After the treatment period, mice were euthanized during diestrus. Colonic contents were collected for full-length 16S rRNA gene sequencing to identify the bacteria in the colon contents. Sanger sequencing of the 16S rRNA gene was used to identify bacteria that were able to grow in Bacteroides minimal media with DiNP as the sole carbon source. Colon tissues were collected for immunohistochemistry of immune(-related) factors. An environmentally relevant dose of DiNP (200 µg/kg) significantly increased a Lachnoclostridium taxon and decreased Blautia compared to the control. Collectively, minimal changes in the colonic microbiota were observed as indicated by non-significant beta-diversities between DiNP treatments and control. Furthermore, three strains of anaerobic bacteria derived from the colon were identified to use DiNP as the sole carbon source. Interestingly, DiNP exposure did not alter protein levels of interleukin-6, tumor necrosis factor alpha, claudin-1, and mucin-1 compared to the control. Collectively, these findings show that DiNP exposure alters the gut microbiota and that the gut contains DiNP-degrading microbes.

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“…Quantitative PCRs were run on a Step One Plus Real-Time PCR system (Applied Biosystems, Foster City, California, USA). The protocol containing melt curve steps was set as described in our previous report (Wang et al, 2019). The relative expression of the target genes was calculated using the 2 -△△Ct method.…”

Section: Methodsmentioning

confidence: 99%

Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway

Zhu

et al. 2019

Toxicol Ind Health

Self Cite

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This study aims to investigate the role of Toll-like receptors (TLRs) on fine particulate matter (PM2.5)-induced inflammatory responses of vascular endothelial cells. Inflammatory factors and TLRs were examined in the aorta of mice after nonsurgical intratracheal instillation of PM2.5 as well as in the human umbilical vein endothelial cells (HUVECs) treated with PM2.5. In addition, the effects of TLR2 and TLR4 inhibitors in the secretion of interleukin 6 (IL-6) and IL-1β and the expression of TLRs were determined in the HUVECs. The results showed that PM2.5 could increase the expression of IL-1β, IL-6, TLR2, and TLR4 in vitro and in vivo. Anti-TLR2 IgG or TAK242, an inhibitor of TLR4, decreased the secretion of IL-1β and IL-6 by HUVECs and reduced the expression of corresponding TLRs. In conclusion, we demonstrate that both TLR2 and TLR4 are involved in PM2.5-induced inflammatory responses of vascular endothelial cells. Inhibition of TLR2 and TLR4 expression has the potential to prevent PM2.5-induced cardiovascular diseases.

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Pubertal exposure to the endocrine disruptor mono-2-ethylhexyl ester at body burden level caused cholesterol imbalance in mice

Cited by 37 publications

References 56 publications

Subacute Exposure to an Environmentally Relevant Dose of Di-(2-ethylhexyl) Phthalate during Gestation Alters the Cecal Microbiome, but Not Pregnancy Outcomes in Mice

Subacute Exposure to an Environmentally Relevant Dose of Di-(2-ethylhexyl) Phthalate during Gestation Alters the Cecal Microbiome, but Not Pregnancy Outcomes in Mice

Isolation of DiNP-Degrading Microbes from the Mouse Colon and the Influence DiNP Exposure Has on the Microbiota, Intestinal Integrity, and Immune Status of the Colon

Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway

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