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Exposure to Dibutyl Phthalate and Reproductive-Related Outcomes in Animal Models: Evidence From Rodents Study.

ABSTRACT: Background: Dibutyl phthalate (DBP) was an endocrine disruptor, which may lead to cancer and affects reproductive function when accumulated in the body. But the precise role of DBP in the reproductive system remained controversial. Objective: We employed the meta-analysis to explore the relationship between DBP and reproductive-related outcomes. Methods: We searched relevant literature in PubMed, EMBASE, and Web of Science databases. The standardized mean differences (SMDs) and their 95% CIs were measured by random-effects models. Funnel plots and Egger's regression test were applied to assess publication bias. Results: Finally, 19 literatures were included in this research. The outcomes revealed that DBP was negatively correlated with reproductive organs weight (testis weight: SMD: -0.59; 95% Cl: -1.23, -0.23; seminal vesicles weight: SMD: -0.74; 95% Cl: -1.21, -0.27; prostate weight: SMD: -0.46; 95% Cl: -0.76, -0.16) and sperm parameters (sperm morphology: SMD: 1.29; 95% Cl: 0.63, 1.94; sperm count: SMD: -1.81; 95% Cl: -2.39, -1.23; sperm motility: SMD: -1.92; 95% Cl: -2.62, -1.23). Conclusion: Our research demonstrated that DBP may be negatively associated with reproductive-related indicators, especially at Gestation exposure period and middle dose (100-500 mg/kg/day).

SUBMITTER: Wang J

PROVIDER: S-EPMC8692859 | biostudies-literature |

REPOSITORIES: biostudies-literature

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A crossover-crossback prospective study of dibutyl-phthalate exposure from mesalamine medications and serum reproductive hormones in men.

Project description:BACKGROUND:Phthalates, such as dibutyl phthalate (DBP), are endocrine disruptors used in some medication coatings e.g., mesalamine to treat inflammatory bowel disease (IBD). OBJECTIVES:Taking advantage of different mesalamine formulations with/without DBP, we assessed whether DBP from mesalamine (>1000x background) altered serum hormones. METHODS:Men (N=73) with IBD participated in a crossover-crossback prospective study and provided up to 6 serum samples (2:baseline, 2:crossover, 2:crossback). Men on non-DBP mesalamine (background) at baseline crossed-over for 4 months to DBP-mesalamine (high) and then crossed-back for 4 months to non-DBP mesalamine (B1HB2-arm) and vice versa for men on DBP-mesalamine at baseline (H1BH2-arm). We divided H1BH2-arm at the median (H1<3yrs or H1?3yrs). We estimated crossover and crossback % changes in serum reproductive hormones using multivariable linear mixed effect models. RESULTS:When B1HB2-arm (26 men,134 samples) crossed-over, luteinizing hormone decreased 13.9% (95% confidence interval(CI): -23.6,-3.0) and testosterone, inhibin-B, and follicle-stimulating hormone (FSH) marginally decreased; after crossback all increased 8-14%. H1BH2-arm, H1?3yrs (25 men,107samples) had no changes at crossover or crossback whereas in H1BH2-arm,H1<3yrs (22 men,100 samples) after crossover, inhibin-B increased 13.2% (CI: 4.2,22.9), FSH decreased 9.9% (CI: -17.9,-1.1) and after crossback, inhibin-B further increased 11.3%, and FSH marginally increased. CONCLUSIONS:High-DBP exposure may disrupt pituitary-gonadal hormones that largely reversed after exposure removal, but only in men with no or short previous high-exposure history. Paradoxically, men with longer duration of high-DBP exposure, exposure removal did not change hormone levels, suggesting that long-term high-DBP exposure may alter the pituitary-gonadal axis and make it insensitive to exposure changes.

| S-EPMC5705343 | biostudies-literature

Dibutyl-phthalate exposure from mesalamine medications and serum thyroid hormones in men.

Project description:BACKGROUND:Dibutyl phthalate (DBP) is an endocrine disruptor and used in some medication coatings, such as mesalamine for treatment inflammatory bowel disease (IBD). OBJECTIVES:To determine whether high-DBP from some mesalamine medications alters thyroid function. METHODS:Seventy men with IBD, without thyroid disease or any radiation history participated in a crossover-crossback prospective study and provided up to 6 serum samples (2:baseline, 2:crossover, 2:crossback). Men on non-DBP mesalamine (background exposure) at baseline crossed-over to DBP-mesalamine (high exposure) then crossed-back to non-DBP mesalamine (B1HB2-arm) and vice versa for men on DBP-mesalamine at baseline (H1BH2-arm). Serum concentrations of total triiodothyronine (T3), total thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH) and thyroid peroxidase antibody (TPOAb), and thyroglobulin antibody (TgAb). RESULTS:After crossover in B1HB2-arm (26 men, 134 samples), T3 decreased 10% (95% confidence interval (CI): 14%,-5%), T3/T4 ratio decreased 8% (CI: 12%,-3%), TPOAb, and TgAb concentrations decreased, 11% (-20%, -2%) and 15% (-23%, -5%), respectively; after crossback, they increased. When men in the H1BH2-arm (44 men, 193 samples) crossed-over, T3 decreased 7% (CI: -11%, -2%) and T3/T4 ratio decreased 6% (CI: -9%, -2%). After crossback, only TgAb increased and FT4 decreased. CONCLUSIONS:High-DBP novel exposure or removal from chronic high-DBP exposure could alter elements of the thyroid system, and most probably alters the peripheral T4 conversion to T3 and thyroid autoimmunity, consistent with thyroid disruption. After exposure removal, these trends were mostly reversed.

| S-EPMC6221978 | biostudies-literature

Identification of Rat foreskin biomarkers of in utero dibutyl phthalate exposure

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-07-12 | GSE48803 | GEO

Identification of Rat foreskin biomarkers of in utero dibutyl phthalate exposure [Illumina]

Project description:Dibutyl phthalate was administered to pregnant Sprague Dawley rats from gestational days 16-20 at either a 100 mg/kg/day or 500 mg/kg/day dose level. This timeframe covers the reproductive masculinization window which corresponds to increased androgen signalling. Dibutyl phthalate has been shown to disrupt testosterone production leading to male reproductive abnormalities. As such, we selected this exposure window for our study and examined gene expression changes in the male rat foreskin, which expresses the androgen receptor. We collected tissue samples at both gestational day 20 to identify gene expression changes immediately after exposure, and postnatal day 5 to identify gene expression changes persisting after birth using microarray analysis (Illumina RatRef 12 Bead Chips). To determine whether gene expression changes were brought on by decreased androgen signalling or additional effects of dibutyl phthalate exposure, we exposed rats to the potent androgen receptor antagonist flutamide (5 mg/kg/day) during the same period of development. Gene expression changes were compared to determine which were brought on by disruption of androgen signalling and which were the result of other aspects of chemical exposure.

2013-07-12 | GSE48802 | GEO

Identification of Rat foreskin biomarkers of in utero dibutyl phthalate exposure [Affymetrix]

2013-06-04 | GSE47618 | GEO

Fetal Rat Testis mRNA Expression after 50 mg/kg Dibutyl Phthalate Exposure

Project description:High dose level dibutyl phthalate (DBP) exposure of fetal rat testes in vivo inhibits testosterone production (i.e. endocrine disruption). Here, fetal testis mRNA levels were profiled following exposure to a DBP dose level that did not significantly reduce testosterone levels. The goal was to identify the constellation of gene expression changes that do not correlate with endocrine disruption.

2011-04-25 | GSE25196 | GEO

Identification of Rat foreskin biomarkers of in utero dibutyl phthalate exposure

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-12 | E-GEOD-48803 | biostudies-arrayexpress

Identification of Rat foreskin biomarkers of in utero dibutyl phthalate exposure

2013-06-04 | E-GEOD-47618 | biostudies-arrayexpress

Environmentally relevant exposure to dibutyl phthalate disrupts DNA damage repair gene expression in the mouse ovary†.

Project description:Phthalates have a history of reproductive toxicity in animal models and associations with adverse reproductive outcomes in women. Human exposure to dibutyl phthalate (DBP) occurs via consumer products (7-10 ?g/kg/day) and medications (1-233 ?g/kg/day). Most DBP toxicity studies have focused on high supraphysiological exposure levels; thus, very little is known about exposures occurring at environmentally relevant levels. CD-1 female mice (80 days old) were treated with tocopherol-stripped corn oil (vehicle control) or DBP dissolved in oil at environmentally relevant (10 and 100 ?g/kg/day) or higher (1000 ?g/kg/day) levels for 30 days to evaluate effects on DNA damage response (DDR) pathway genes and folliculogenesis. DBP exposure caused dose-dependent effects on folliculogenesis and gene expression. Specifically, animals exposed to the high dose of DBP had more atretic follicles in their ovaries, while in those treated with environmentally relevant doses, follicle numbers were no different from vehicle-treated controls. DBP exposure significantly reduced the expression of DDR genes including those involved in homologous recombination (Atm, Brca1, Mre11a, Rad50), mismatch repair (Msh3, Msh6), and nucleotide excision repair (Xpc, Pcna) in a dose-specific manner. Interestingly, staining for the DNA damage marker, ?H2AX, was similar between treatments. DBP exposure did not result in differential DNA methylation in the Brca1 promoter but significantly reduced transcript levels for the maintenance DNA methyltransferase, Dnmt1, in the ovary. Collectively, these findings show that oral exposure to environmentally relevant levels of DBP for 30 days does not significantly impact folliculogenesis in adult mice but leads to aberrant ovarian expression of DDR genes.

| S-EPMC6930367 | biostudies-literature

Oral exposure to dibutyl phthalate exacerbates chronic lymphocytic thyroiditis through oxidative stress in female Wistar rats.

Project description:Chronic lymphocytic thyroiditis (CLT) is a common autoimmune disorder. The possible pathogenic role and mechanism of dibutyl phthalate (DBP) in CLT is still controversial. Experiments were conducted after 35-days of oral exposure to the three concentrations of DBP or saline, and three immunizations with thyroglobulin (TG). Healthy female Wistar rats were randomly divided into ten exposure groups (n?=?8 each): (A) saline control, (B) 0.5?mg/kg/d DBP, (C) 5?mg/kg/d DBP, (D) 50?mg/kg/d DBP, (E) TG-immunized group, (F) TG- combined with 0.5?mg/kg/d DBP, (G) TG- combined with 5?mg/kg/d DBP, (H) TG- combined with 50?mg/kg/d DBP, (I) TG- combined with 50?mg/kg/d DBP plus 100?mg/kg/d vitamin C; (J) 100?mg/kg/d vitamin C. We showed that oral exposure DBP can aggravate CLT in rats. This deterioration was concomitant with increased thyroid auto antibodies, Th1/Th2 imbalance and Th17 immune response, activated pro-inflammatory and apoptosis pathways, and increased thyroid dysfunction in rats. Our results also suggested that DBP could promote oxidative damage. The study also found that vitamin C reduced the levels of oxidative stress and alleviated CLT. In short, the study showed that DBP exacerbated CLT through oxidative stress.

| S-EPMC5684247 | biostudies-literature

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