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butyl phthalate/царевица
Линкът е запазен в клипборда
Страница 1 от 40 резултата
Maternal supplementation with corn oil associated or not with di-n-butyl phthalate increases circulating estradiol levels of gerbil offspring and impairs sperm reserve.
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This study evaluated the consequences of gestational exposure to di-n-butyl phthalate (DBP) for testicular steroidogenesis and sperm parameters of the adult gerbil and the interference of corn oil (co), a vehicle widely used for administration of liposoluble agents, on DBP effects. Pregnant gerbils
Uptake and phytotoxicity of di-n-butyl phthalate in corn (Zea mays).
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Differential expression of peroxiredoxin 6, annexin A5 and ubiquitin carboxyl-terminal hydrolase isozyme L1 in testis of rat fetuses after maternal exposure to di-n-butyl phthalate.
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OBJECTIVE
To isolate and identify differentially expressed proteins in testis of rat fetuses after maternal exposure to di-n-butyl phthalate (DBP).
METHODS
Pregnant rats were daily treated by gavage with 1 ml/kg corn oil or 750 mg/kg DBP from GD14 to GD18. We used the technique of proteomic analysis
Protection of male reproductive toxicity in rats exposed to di-n-butyl phthalate during embryonic development by testosterone.
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Di-n-butyl phthalate (DBP) widely spread industrial chemical that made drastic alteration in male reproductive system. The present study elucidates the protective role of testosterone on reproductive toxicity in prenatal DBP exposed adult male rats. Pregnant rats were injected with corn oil or 100
Effects of di-iso-butyl phthalate on testes of prepubertal rats and mice.
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Di-iso-butyl phthalate (DiBP), a special plasticizer, is used as a substitute for di(n-butyl) phthalate (DBP). The effects of DiBP on testes in prepubertal rodents still remain to be obscure. Testicular toxicity of DiBP was investigated in 21-day-old Sprague-Dawley rats and C57BL/6N mice, using with
Quantitative changes in gene expression in fetal rat testes following exposure to di(n-butyl) phthalate.
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Di(n-butyl) phthalate (DBP) alters male reproductive development by decreasing testicular testosterone (T) production when fetuses are exposed on gestation days (GD) 12-21. Previous studies have shown altered gene expression for enzymes in the T biosynthetic pathway following exposure to DBP. The
Di-n-butyl phthalate prompts interruption of spermatogenesis, steroidogenesis, and fertility associated with increased testicular oxidative stress in adult male rats.
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Di-n-butyl phthalate (DBP) is extensively used as plasticizer, and it was ubiquitary released into the environment. The present study was aimed to investigate the effect of DBP on reproductive competence in adult male rats. Adult male rats were received corn oil or DBP injection intraperitoneally
[Effects of di-butyl phthalate on the reproductive system of adolescent male rats].
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OBJECTIVE
To explore the effects of di-butyl phthalate (DBP) on the reproductive system of adolescent male rats.
METHODS
Sprague-Dawley (SD) rats aged 5 weeks were assigned to receive corn oil (vehicle control) or DBP orally at 10, 100 and 500 mg/(kg x d) for 30 days. After the exposure, the testis,
Prepubertal Di-n-Butyl Phthalate Exposure Alters Sertoli and Leydig Cell Function and Lowers Bone Density in Adult Male Mice.
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Phthalate exposure impairs testis development and function; however, whether phthalates affect nonreproductive functions is not well understood. To investigate this, C57BL/6J mice were fed 1-500 mg di-n-butyl phthalate (DBP) in corn oil, or vehicle only, daily from 4 to 14 days, after which tissues
Di(n-butyl) phthalate impairs cholesterol transport and steroidogenesis in the fetal rat testis through a rapid and reversible mechanism.
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In utero exposure to di(n-butyl) phthalate (DBP) leads to a variety of male reproductive abnormalities similar to those caused by androgen receptor antagonists. DBP demonstrates no affinity for the androgen receptor, but rather leads to diminished testosterone production by the fetal testis. The
Nuclear Morphometric Analysis of Leydig Cells of Male Pubertal Rats Exposed In Utero to Di(n-butyl) Phthalate.
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We recently reported that prenatal rat exposure to di(n-butyl) phthalate (DBP) induced Leydig cell (LC) hyperplasia after nine weeks (wks) of age, yet the number of LCs was similar to that of the vehicle group until seven weeks. Nuclear pleomorphism of hyperplastic LCs is common and is considered to
Di-n-Butyl Phthalate Induces Multinucleated Germ Cells in the Rat Fetal Testis Through a Nonproliferative Mechanism.
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In utero exposure to some phthalate esters adversely affects the development of the rat seminiferous cord, causing germ cell loss and increasing the number of multinucleated germ cells (MNGs). To understand the timing of MNG formation and determine whether it requires nuclear division, timed
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
Identification of differentially expressed genes in the testis of Sprague-Dawley rats treated with di(n-butyl) phthalate.
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The aim of this study was to identify the di(n-butyl) phthalate (DBP)-induced differentially expressed genes (DEGs) using a novel annealing control primer system in the testes of Sprague-Dawley male rats. Animals (4 weeks of age) were administered orally either corn oil only (vehicle control) or DBP
Kinetics of selected di-n-butyl phthalate metabolites and fetal testosterone following repeated and single administration in pregnant rats.
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Human exposure to phthalic acid diesters occurs through a variety of pathways as a result of their widespread use in consumer products and plastics. Repeated doses of di-n-butyl phthalate (DBP) from gestation day (GD) 12 to 19 disrupt testosterone synthesis and male sexual development in the fetal
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