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butyl phthalate/atrofia
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Pagina 1 a partire dal 53 risultati
Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes.
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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was
Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 5. Testicular iron depletion and levels of ferritin, haemoglobin and transferrin in the bone marrow, liver and spleen.
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This study reports changes in levels of ferritin, haemoglobin and transferrin in the bone marrow, liver and spleen as an attempt to determine the causes of testicular iron depletion. A single oral dose of di-n-butyl phthalate (DBP) to male rats caused a sloughing of the germ cells (at 6 h) prior to
Short-time exposure to mono-n-butyl phthalate (MBP)-induced oxidative stress associated with DNA damage and the atrophy of the testis in pubertal rats.
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Phthalates are widely used as plasticizer in various consumer domestic products and are known to disturb the male reproductive function in rodents. This study investigated the involvement of oxidative stress and the atrophy of the testes in pubertal rats exposed to mono-n-butyl phthalate (MBP).
Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 1.
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Repeated oral doses of di-n-butyl phthalate (DBP) to male rats caused a decrease in testicular fructose and glucose and a sloughing of the germ cells on the first day of treatment. On day 2, more severe sloughing was seen and was accompanied by decreases in testicular iron and zinc levels and
Mechanism of testicular atrophy induced by Di-n-butyl phthalate in rats. VI. A possible origin of testicular iron depletion.
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In previous studies we have described mechanisms of testicular atrophy whereby di-n-butyl phthalate (DBP) caused a sloughing of the germ cells, prior to the testicular atrophy; this sloughing might be attributed to iron depletion in the blood and the testicular interstitial cells. To determine
Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 4. Changes in the activity of succinate dehydrogenase and the levels of transferrin and ferritin in the Sertoli and germ cells.
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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused a sloughing of the germ cells at 6 h both with a decrease in the activity of succinate dehydrogenase (SDH) in the Sertoli cells and in the Sertoli-germ connection and with an increase in the activity of lactate dehydrogenase (LDH)
Differences in urinary metabolic profile from di-n-butyl phthalate-treated rats and hamsters. A possible explanation for species differences in susceptibility to testicular atrophy.
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A high-performance liquid chromatographic method for the direct analysis of the urinary metabolites of di-n-butyl phthalate (DBP) is described. In both rats and hamsters the major urinary metabolite found after treatment with either DBP or mono-n-butyl phthalate (MBP) was MBP glucuronide and not MBP
Mechanisms of testicular atrophy induced by di-n-butyl phthalate in rats. Part 3. Changes in the activity of some enzymes in the Sertoli and germ cells, and in the levels of metal ions.
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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused a sloughing of the germ cells at 6 h, with more severe sloughing at 24 and 48 h. DBP is metabolized to mono-n-butyl phthalate (MBP), which is transported through the blood-tubular barrier into the seminiferous lumen. MBP is
Structure-activity requirements for the induction of testicular atrophy by butyl phthalates in immature rats: effect on testicular zinc content.
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Induction of spermatogenic cell apoptosis in prepubertal rat testes irrespective of testicular steroidogenesis: a possible estrogenic effect of di(n-butyl) phthalate.
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Although di(n-butyl) phthalate (DBP), a suspected endocrine disruptor, induces testicular atrophy in prepubertal male rats, whether it exerts estrogenic activity in vivo remains a matter of debate. In the present study, we explored the estrogenic potency of DBP using 3-week-old male rats, and then
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
Dose-dependent effects on cell proliferation, seminiferous tubules, and male germ cells in the fetal rat testis following exposure to di(n-butyl) phthalate.
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Adult male rats gestationally exposed to di(n-butyl)phthalate (DBP) have dysgenetic testes characterized by seminiferous epithelial degeneration, clustering of Leydig cells, and decreased spermatogenesis. Cell proliferation and apoptosis are key processes regulating development of the testis, and
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
The effects on steroidogenesis and histopathology of adult male Japanese quails (Coturnix coturnix japonica) testis following pre-pubertal exposure to di(n-butyl) phthalate (DBP).
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In the present study, we have investigated the effects of 30-day dietary (pre-pubertal) exposure to different doses (0 (control), 1, 10, 50, 200 and 400 mg/kg bodyweight/day) of di(n-butyl) phthalate (DBP) on Leydig cells of adult male Japanese quails by quantifying the transcript levels for P450
Effects of di-n-butyl phthalate on male rat reproduction following pubertal exposure.
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Di-n-butyl phthalate (DBP) is an endocrine-disrupting chemical that has the potential to affect male reproduction. However, the reproductive effects of low-dose DBP are still not well known, especially at the molecular level. In the present study, pubertal male Sprague-Dawley rats were orally
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