dibutyl phthalate/atrofi

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Zinc metabolism and dibutyl phthalate-induced testicular atrophy in the rat.

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Studies on dibutyl phthalate-induced testicular atrophy in the rat: effect on zinc metabolism.

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

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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

NTP technical report on the toxicity studies of Dibutyl Phthalate (CAS No. 84-74-2) Administered in Feed to F344/N Rats and B6C3F1 Mice.

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Dibutyl phthalate is a phthalate ester with extensive use in industry in such products as plastic (PVC) piping, various varnishes and lacquers, safety glass, nail polishes, paper coatings, dental materials, pharmaceuticals, and plastic food wrap. Concomitant with this extensive worldwide use is the

[Effects of prepubertal continuous exposure to dibutyl phthalate on testicular development in rats].

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OBJECTIVE To investigate the effects of prepubertal continuous exposure to dibutyl phthalate (DBP) on the testis development in SD rats. METHODS Twenty-one-day-old weanling prepubertal male SD rats were randomly divided into a control (n = 24) and an experiment group (n = 54), gavaged daily with

Dibutyl phthalate induces oxidative stress and impairs spermatogenesis in adult rats.

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Phthalates are abundantly produced plasticizers, and dibutyl phthalate (DBP) is the most widely used derivative in various consumer products and medical devices. This study was conducted to further explore the potential testicular toxicity of DBP in adult rats and to elucidate the underlying

The p-eIF2α/ATF4 pathway links endoplasmic reticulum stress to autophagy following the production of reactive oxygen species in mouse spermatocyte-derived cells exposed to dibutyl phthalate.

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Dibutyl phthalate (DBP) is a widely used plasticizer that has been shown to induce germ cell apoptosis-related testicular atrophy and cause reproductive toxicity. Our previous results indicated that endoplasmic reticulum (ER) stress-activated autophagy served as a self-defense mechanism against

A new pharmacological activity of dibutyl phthalate (DBP) on selective elimination of tumor cells from bone marrow.

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DBP possesses a new pharmacological activity leading to selective deterioration of leukemic cells, with less harmful effect on the growth of normal hematopoietic progenitors.

Dibutyl phthalate purged autologous bone marrow transplant in the treatment of leukemia.

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It has been proved that di-N-butyl phthalate (DBP) is singular in killing leukemic cells selectively or accelerating the deterioration of residual leukemic cells in long-term marrow culture in vitro. Based on this principle, the DBP-purged autologous bone marrow transplant has been applied to the

Preparation and characterization of molecularly imprinted polymer for di(2-ethylhexyl) phthalate: application to sample clean-up prior to gas chromatographic determination.

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The molecularly imprinted polymer (MIP) selective for di(2-ethylhexyl) phthalate (DEHP) an environmental endocrine disruptor was prepared by suspension polymerization using methacrylamide as functional monomer and N,N'-methylene-bis-acrylamide as cross-linker. The imprinted polymer was employed for

Inhibin B response to testicular toxicants hexachlorophene, ethane dimethane sulfonate, di-(n-butyl)-phthalate, nitrofurazone, DL-ethionine, 17-alpha ethinylestradiol, 2,5-hexanedione, or carbendazim following short-term dosing in male rats.

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BACKGROUND Inhibin B is a heterodimer glycoprotein that downregulates follicle-stimulating hormone and is produced predominantly by Sertoli cells. The potential correlation between changes in plasma Inhibin B and Sertoli cell toxicity was evaluated in male rats administered testicular toxicants in

DBP-induced endoplasmic reticulum stress in male germ cells causes autophagy, which has a cytoprotective role against apoptosis in vitro and in vivo.

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Recently, spermatogenic cell apoptosis was shown to play a key role in the induction of testicular atrophy by dibutyl phthalate (DBP), thus causing reproductive toxicology. However, the molecular events induced by DBP in apoptotic germ cells remain unclear. In the present study, the mouse

Administration of potentially antiandrogenic pesticides (procymidone, linuron, iprodione, chlozolinate, p,p'-DDE, and ketoconazole) and toxic substances (dibutyl- and diethylhexyl phthalate, PCB 169, and ethane dimethane sulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in the male rat.

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Antiandrogenic chemicals alter sexual differentiation by a variety of mechanisms, and as a consequence, they induce different profiles of effects. For example, in utero treatment with the androgen receptor (AR) antagonist, flutamide, produces ventral prostate agenesis and testicular nondescent,

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