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PMID: 

Environ Res. 2019 Nov 8:108902. Epub 2019 Nov 8. PMID: 31785779

Abstract Title: 

Phthalate exposure and prostate cancer in a population-based nested case-control study.

Abstract: 

BACKGROUND: Phthalic acid esters are established as endocrine disruptors. The study aimed to evaluate the association between urinary phthalate metabolites and prostate cancer occurrence.METHODS: The study was based on the Taiwan Community-Based Cancer Screening Program, which was set up in 1991-1992 and followed periodically. By 2010, 80 incident prostate cancer cases were identified in the 12,020 men. For each case, 2 controls were randomly selected, matched by age (±3 years), urine collection date (±3 months), and residential township. Frequently used phthalate metabolites from the urine samples were quantified by liquid chromatography/electrospray ionization tandem mass spectrometry. Logistic regression was conducted to assess the association between the exposure levels and prostate cancer occurrence.RESULTS: Exposure to di (2-ethylhexyl), butyl-benzyl and di-isobutyl phthalates (DEHP, BBzP, DiBP) was positively associated with prostate cancer in men with waist circumference (WC)≥90 cm but not in the leans. Odds ratio for the DEHP metabolite summary score (upper tertile compared to the rest) and prostate cancer were 7.76 (95% CI = 1.95-30.9) for WC ≥ 90 cm.CONCLUSIONS: DEHP, BBzP, and DiBP exposure were associated with prostate cancer occurrence in abdominally obese men. The main limitation remains the lack of mechanistic experiments and comparable toxicological data.

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PMID: 

Environ Sci Pollut Res Int. 2019 Dec 6. Epub 2019 Dec 6. PMID: 31808097

Abstract Title: 

Could phthalates exposure contribute to the development of metabolic syndrome and liver disease in humans?

Abstract: 

In the study, 305 patients of both genders were enrolled and divided into three groups: obese (BMI>30 kg/m), patients who were diagnosed type 2 diabetes mellitus (T2DM), and control, normal weight healthy volunteers. At least one of ten different phthalate metabolites was determined in the urine samples of 49.84% all enrolled participants. In the obese subgroup, the sum of all urinary phthalate metabolites was positively associated with TG levels (p = 0.031) together with derived TC/HDL and TG/HDL ratios (p = 0.023 and 0.015), respectively. Urinary MEP concentration was positively correlated with the HOMA-IR in T2DM subgroup (p = 0.016) while in the control subgroup, logMEP levels were negatively correlated with total cholesterol (p = 0.0051), and LDL serum levels (p = 0.0015), respectively. Also, in the control subgroup, positive linear correlations between urinary logMEP levels and TyG and TYG-BMI values (p = 0.028 and p = 0.027), respectively, were determined. Urinary MEHP levels were associated with glucose serum levels (p = 0.02) in T2DM subgroup, while in the control HDL values were negatively associated with logMEHP (p = 0.0035). Healthy volunteers exposed to phthalates had elevated AST levels in comparison to non-exposed ones (p = 0.023). In control subgroup, ALT and AST values were increased (p = 0.02 and p = 0.01, respectively) in MEP exposed while GGT levels were enhanced (p = 0.017) in MEHP exposed in comparison with non-exposed. Combined phthalates influence on glucose and lipid metabolism may increase the possibility for NAFLD and insulin resistance development among exposed individuals.

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PMID: 

mSystems. 2019 Dec 10 ;4(6). Epub 2019 Dec 10. PMID: 31822602

Abstract Title: 

Environmental Chemical Diethylhexyl Phthalate Alters Intestinal Microbiota Community Structure and Metabolite Profile in Mice.

Abstract: 

Exposure to environmental chemicals during windows of development is a potentially contributing factor in gut microbiota dysbiosis and linked to chronic diseases and developmental disorders. We used a community-level model of microbiota metabolism to investigate the effects of diethylhexyl phthalate (DEHP), a ubiquitous plasticizer implicated in neurodevelopmental disorders, on the composition and metabolite outputs of gut microbiota in young mice. Administration of DEHP by oral gavage increased the abundance of, while decreasingAddition of DEHP to-cultured cecal microbiota increased the abundance ofandUntargeted metabolomics showed that DEHP broadly altered the metabolite profile in the culture. Notably, DEHP enhanced the production of-cresol while inhibiting butyrate synthesis. Metabolic model-guided correlation analysis indicated that the likely sources of-cresol arespecies. Monoculture ofconfirmed that it is capable of producinghydroxyphenylacetic acid, the immediate precursor ofcresol, and that the species' growth is enhanced upon DEHP exposure. Taken together, these findings suggest a model where DEHP increases production of-cresol, a bacterial metabolite linked with neurodevelopmental disorders, by expanding the abundance of species that synthesize the metabolite's precursor.Several previous studies have pointed to environmental chemical exposure during windows of development as a contributing factor in neurodevelopmental disorders and correlated these disorders with microbiota dysbiosis; however, little is known about how the chemicals specifically alter the microbiota to interfere with development. The findings reported in this paper unambiguously establish that a pollutant linked with neurodevelopmental disorders can directly modify the microbiota to promote the production of a potentially toxic metabolite (-cresol) that has also been correlated with neurodevelopmental disorders. Furthermore, we used a novel modeling strategy to identify the responsible enzymes and bacterial sources of this metabolite. To the best of our knowledge, the present study is the first to characterize the functional consequence of phthalate exposure on a developed microbiota. Our results suggest that specific bacterial pathways could be developed as diagnostic and therapeutic targets against health risks posed by ingestion of environmental chemicals.

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PMID: 

Environ Sci Technol. 2019 Dec 20. Epub 2019 Dec 20. PMID: 31859481

Abstract Title: 

Feminine Hygiene Products-A Neglected Source of Phthalate Exposure in Women.

Abstract: 

Phthalates have been associated with reproductive toxicity and precocious puberty in females, but the occurrence of these toxicants in feminine hygiene products is rarely reported. In this study, eight phthalates were determined in 120 feminine hygiene products (56 feminine care products and 64 sanitary napkins) collected from China. Phthalates were found in 86% and 98% of feminine care products and sanitary napkins, respectively, with the total concentrations varying between not detectable and 813µg/g (median: 0.26 µg/g) and 0.25 and 8.76 μg/g (1.43 μg/g), respectively. Diethyl phthalate, dibutyl phthalate and bis(2-ethylhexyl)phthalate were the major compounds, accounting for>60% of the total concentrations. The plastic materials used on the top and bottom layers, as well as the hot melt adhesive used during the manufacturing process, are the potential sources of phthalates in sanitary napkins. The range of daily exposure doses of phthalates in women from the use of feminine care products and sanitary napkins were

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PMID: 

Environ Res. 2019 Dec 12 ;182:109020. Epub 2019 Dec 12. PMID: 31863942

Abstract Title: 

Prenatal exposure to di-(2-ethylhexyl) phthalate and decreased skeletal muscle mass in 6-year-old children: A prospective birth cohort study.

Abstract: 

BACKGROUND/AIM: Phthalate is a well-known endocrine-disrupting chemical that has anti-androgenic effects. Although there are several studies on the relationship between body composition and phthalate, studies that investigated the effects of phthalate on skeletal muscle during childhood are lacking.METHODS: We analyzed data from 481 mother-and-child pairs enrolled in the Environment and Development of Children cohort in South Korea. We examined the association between phthalate metabolites (mono [2-ethyl-5-hydroxyhexyl] phthalate [MEHHP], mono [2-ethyl-5-oxohexyl] phthalate [MEOHP], molar sum of MEHHP and MEOHP [Σ DEHP], and mono-n-butyl phthalate [MnBP]) in prenatal maternal urine and children's urine at the age of 6, and body composition indices (body mass index [BMI] z-score, percentage of fat mass, fat mass index, percentage of skeletal muscle, and the skeletal muscle index [SMI]) measured when the child was 6 years using a bioelectrical impedance analyzer.RESULTS: A 2-fold increase inΣ DEHP and MnBP in the prenatal maternal urine was significantly associated with a -0.07 unit (95% CI: -0.11, -0.03) and -0.09 unit (95% CI: -0.14, -0.03) change in SMI, respectively, in 6-year old girls alone. BMI z-score was also negatively associated with a 2-fold increase in MEHHP and MnBP in prenatal maternal urine as -0.11 unit (95% CI: -0.22, -0.01) and -0.15 unit (95% CI: -0.28, -0.02) change, respectively, only among girls. Among boys, phthalate metabolites in the prenatal and children's urine were not significantly associated with any body composition indices.CONCLUSIONS: Our longitudinal study shows that high levels of prenatal exposure to phthalates are significantly associated with decreased SMI among girls. We can postulate that anti-androgenic effects of phthalates during pregnancy may affect girl offspring's muscle growth.

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PMID: 

Environ Int. 2019 Dec 18 ;135:105342. Epub 2019 Dec 18. PMID: 31864031

Abstract Title: 

Maternal bisphenol and phthalate urine concentrations and weight gain during pregnancy.

Abstract: 

BACKGROUND: Insufficient or excessive gestational weight gain are associated with increased risks of adverse birth and childhood outcomes. Increasing evidence suggests that exposure to bisphenols and phthalates may disrupt hormonal pathways and thereby influence gestational weight gain.OBJECTIVE: To examine the associations of early and mid-pregnancy bisphenol and phthalate urine concentrations with gestational weight gain.METHODS: In a population-based prospective cohort study among 1,213 pregnant women, we measured early and mid-pregnancy bisphenol and phthalate urine concentrations. Maternal anthropometrics before pregnancy were obtained by questionnaire and repeatedly measured at our research center during pregnancy. We used linear and logistic regressions to evaluate the associations of bisphenols and phthalates with total and period-specific gestational weight gain.RESULTS: Higher maternal total bisphenols and bisphenol S were associated with a lower total gestational weight gain at nominal level. Stratification by body mass index group showed that higher total bisphenols and bisphenol S were associated with lower total gestational weight gain specifically in normal weight women (respectively -509 g [95% CI -819, -198] and -398 g [95% CI -627, -169]). Each log unit increase in early pregnancy total bisphenol and bisphenol A urine concentrations were associated with lower mid- to late pregnancy gestational weight gain in the whole group (effect estimates -218 g/log unit increase [95% CI -334, -102] and -132 g/log unit increase [95% CI -231, -34], respectively). These associations were independent of mid-pregnancy compounds. Mid-pregnancy bisphenols and phthalates concentrations were not associated with gestational weight gain.DISCUSSION: Higher maternal bisphenol urine concentrations in early pregnancy may lead to reduced gestational weight in second half of pregnancy. Further research is needed to assess the effects of maternal bisphenols and phthalates urine concentrations on placental and fetal growth and development.

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PMID: 

Free Radic Biol Med. 2018 08 20 ;124:1-11. Epub 2018 May 26. PMID: 29807160

Abstract Title: 

Nano-liposomes of lycopene reduces ischemic brain damage in rodents by regulating iron metabolism.

Abstract: 

In order to discover new drug delivery approaches and to understand the mechanism of iron overload in cerebral ischemia/reperfusion (I/R), we aimed to investigate the effects of lycopene (LYC) in the form of nano-liposomes (L-LYC) on iron-regulating proteins and ischemic brain injury. We found that L-LYC significantly increased the LYC content in serum and the brain. Adult male Sprague-Dawley rats treated with L-LYC for 14 days were subjected to 60 min of ischemia and 7 days of reperfusion. The effects of L-LYC were evaluated by infarction volume, neurological score, neuronal apoptosis, and markers for oxidative stress. Levels of iron-regulating protein such as hepcidin and ferroportin (FPN1) were examined. L-LYC reduced cerebral infarctionand improved neurobehavior of the rats more efficiently than"naked"LYC. L-LYC reduced protein levels of oxidases (e.g. nitric oxide synthase and NOX2), increased the level of Bcl-2, lowered caspase-3, and suppressed apoptosis through inhibiting MAPK-JNK. Furthermore, L-LYC suppressed hepcidin-mediated decrease in FPN1, a sole iron exporter, and normalized the levels of iron. We further demonstrated that the effect of L-LYC on hepcidin expression might result from its ability to attenuate the release of the inflammatory factor interleukin 6. The results demonstrated that nano-liposomal encapsulation significantly improved LYC efficacy in providing neuronal protection against I/R injury. The data also revealed a novel mechanism of L-LYC's neuroprotection by regulating iron metabolism in an ischemic brain.

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PMID: 

Life Sci. 2018 Aug 15 ;207:265-271. Epub 2018 Jun 7. PMID: 29886059

Abstract Title: 

Lycopene abrogates di-(2-ethylhexyl) phthalate induced testicular injury by modulating oxidative, endocrine and inflammatory changes in mice.

Abstract: 

Di (2-ethylhexyl) phthalate (DEHP) is one of the environmental pollutants that causes testicular damage. Lycopene (LYCO), the main active carotenoid in red fruits and vegetables, has well-known antiinflammatory and antioxidant activities. The present study aimed to investigate the effects of LYCO on DEHP-induced testicular injury in male mice. DEHP (2 g/kg, p.o.) was given for two weeks to mice. LYCO was given at 4 mg/kg, p.o., for two weeks, starting the same day of DEHP insult. Serum testosterone, luteinizing hormone and follicle stimulating hormone and testicular total antioxidant status, malondialdehyde, nitric oxide, glutathione, superoxide dismutase, glutathione peroxidase, catalase, tumor necrosis factor-α, interleukin-1β were measured. Also, testicular histopathological examination and sperm analysis were evaluated. Results showed that administration of LYCO significantly attenuated the DEHP-induced gonadotoxicity. Also, thegonadoprotective effects of LYCO were confirmed by the histopathological examination of the testes. Our results suggested that LYCO has produced attenuation of inflammatory, oxidative stress and hormonal parameters against DEHP-induced gonadotoxicity.

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PMID: 

Wei Sheng Yan Jiu. 2018 Mar ;47(2):281-306. PMID: 29903284

Abstract Title: 

[Lycopene's protective effect on oxidative damage of L02 cells and its mechanism].

Abstract: 

OBJECTIVE: To explore lycopene 's protective effect on H_2O_2 induced oxidative damage of L02 cells and its mechanism.METHODS: L02 cells were cultured by H_2O_2 to build the model of cellular oxidative damage. Different dose of lycopene was used to pretreat the cells, and cell survival rate was detected to verify the appropriate concentration. Then cellular ROS level, activity of cellular SOD and GSH-Px, cellular MDA content, and activity of ALT, AST and LDH in the culture medium were detected to observe lycopene 's effect on cellular oxidant damage. Finally, to observe lycopene 's activating effect on nuclear-translocation of Nrf2, L02 cells' nuclear protein was extracted to detect Nrf2 protein content, and also, mRNA expression level of Nrf2 target genes HO-1 and NQO1 was assayed to verify this mechanism.RESULTS: Pretreatment of 10μmol/Llycopene raised cellular viability of L02 cells on H_2O_2 culturing condition, reduced cellular ROS, enhanced enzymatic activity of cellular SOD and GSH-Px, reduced cellular MDA content, and depressed the activity of ALT, AST and LDH in culture medium. Lycopene also increased nuclear Nrf2 protein content and enhanced the expression of its target genes HO-1 and NQO1.CONCLUSION: Lycopene could protect L02 cells from H_2O_2 induced oxidative damage, probably by promoting nuclear-translocation of Nrf2 and activating expression of its target antioxidant genes.

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