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butyl phthalate/възпаление
Линкът е запазен в клипборда
Страница 1 от 27 резултата
Gestational and lactational exposition to Di-N-butyl-phthalate (DBP) increases inflammation and preneoplastic lesions in prostate of wistar rats after carcinogenic N-methyl-N-nitrosourea (MNU) plus testosterone protocol.
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In the present study, it was evaluated the susceptibility of prostatic lesions in male adult rats exposed to Di-N-butyl-phthalate during fetal and lactational periods and submitted to MNU plus testosterone carcinogenesis protocol. Pregnant females were distributed into four experimental groups: CN
Long-term effects of developmental exposure to di-n-butyl-phthalate (DBP) on rat prostate: proliferative and inflammatory disorders and a possible role of androgens.
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In the present study we evaluated the toxic effects on the male adult rat prostate of DBP exposure during fetal and lactational periods, because although many studies have addressed the influence of phthalates on the male reproductive system, only a few have discussed their possible effects on
Di-n-butyl phthalate causes antiestrogenic effects in female Murray rainbowfish (Melanotaenia fluviatilis).
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Di-n-butyl phthalate (DnBP) is an industrial pollutant with antiandrogenic effects reported in male mammals and fish. Little research has been done on the endocrine effects of DnBP in female fish. The present study investigated the changes in ovarian histology and serum vitellogenin concentrations
Histopathological alterations in the prostates of Mongolian gerbils exposed to a high-fat diet and di-n-butyl phthalate individually or in combination.
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Both high-fat diet and exposure to endocrine-disrupting chemicals have been implicated in susceptibility to pathological prostate lesions, but the consequences of combining the two have not yet been examined. We evaluated the effects of gestational and postnatal exposure to a high-fat diet (20% fat)
Exposure of DBP in gestation induces inflammation of testicular Sertoli cells in progeny by activating NLRP3 inflammasomes.
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Di-n-butyl phthalate (DBP), as one of the environmental chemicals, can cause male reproductive decline including testicular hypoplasia and impairments of spermatogenesis. Testicular inflammation is positively related to decline in male reproductive function. However, whether exposure to DBP in utero
Sex-specific difference in placental inflammatory transcriptional biomarkers of maternal phthalate exposure: a prospective cohort study.
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Previous epidemiologic research has shown that phthalate exposure in pregnant women is related to birth outcomes in a sex-specific manner. These outcomes may be mediated by placental inflammation, which is the proposed biological mechanism. This is the first study to address the relationship between
Mono-(2-ethylhexyl) Phthalate Aggravates Inflammatory Response via Sirtuin Regulation and Inflammasome Activation in RAW 264.7 Cells.
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Artificial environmental endocrine disrupting chemicals (EDCs) exert public health concerns. Exposure to EDCs may induce various disorders in the cardiometabolic system. However, the underlying mechanisms remain largely unknown. Over the past decade, an abundance of evidence has emerged
Neurochemical alterations following the exposure to di-n-butyl phthalate in rats.
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Due to its ability to cross blood brain barrier and placenta, dibutyl phthalate (di-n-butyl phthalate, DBP) is expected to cause severe side effects to the central nervous system of animals and humans. A little data is available about the potential DBP neurotoxicity; therefore, this work was
Hepatotoxic evaluation of Di- n-butyl phthalate in Wistar rats upon sub-chronic exposure: A multigenerational assessment
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The extensive use of di--n-butyl phthalate (DBP) as a plasticizer in medical devices, personal care products, and industries, which is a major threat to humankind as it leaches out easily from the plastic matrix into the environment. Health risks posed to adults and children from the broad
Exposure to phthalates aggravates pulmonary function and airway inflammation in asthmatic children.
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Curcumin inhibits adipogenesis induced by benzyl butyl phthalate in 3T3-L1 cells.
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Phthalates are a group of endocrine disrupting chemicals and may have contributed to the recent global obesity health crisis. Increased adipogenesis via the peroxisome proliferator-activated receptor γ (PPARγ)-CCAAT-enhancer binding protein α (C/EBPα) pathway could be one critical mechanism
Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications.
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BACKGROUND
Prenatal and early postnatal exposures to environmental factors are considered responsible for the increasing prevalence of allergic diseases. Although there is some evidence for allergy-promoting effects in children because of exposure to plasticizers, such as phthalates, findings of
Urinary phthalate metabolite associations with biomarkers of inflammation and oxidative stress across pregnancy in Puerto Rico.
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Phthalate exposure during pregnancy has been linked to adverse birth outcomes such as preterm birth, and inflammation and oxidative stress may mediate these relationships. In a prospective cohort study of pregnant women recruited early in gestation in Northern Puerto Rico, we investigated the
Phthalates and Phthalate Alternatives Have Diverse Associations with Oxidative Stress and Inflammation in Pregnant Women.
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Exposure to environmental chemicals such as phthalates has been linked to numerous adverse pregnancy outcomes, potentially through an oxidative stress mediated mechanism. Most research examined urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) as the oxidative stress biomarker.
The effects of di-butyl phthalate exposure from medications on human sperm RNA among men.
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Endocrine disruptors, such as phthalates, are suspected of affecting reproductive function. The Mesalamine and Reproductive Health Study (MARS) was designed to address the physiological effect of in vivo phthalate exposure on male reproduction in patients with Inflammatory Bowel Disease (IBD). As
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