866 resultados para CHLOROFORM EXPOSURE
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The aim of this study was to determine the consequent reproductive developmental and immunotoxic effects due to exposure to fenvalerate during pregnancy and lactation in male offspring of maternal-treated rats. Pregnant rats were treated daily by oral gavage with 40 or 80 mg/kg of fenvalerate or corn oil (vehicle, control), from d 12 of pregnancy to d 21 of lactation. Immune and reproductive developmental effects were assessed in male offspring at postnatal days (PND) 40 (peripuberty), 60 (postpuberty), and 90 (sexual maturity). Treatment with the higher dose (80 mg/kg) resulted in convulsive behavior, hyperexcitability, and mortality in 45% of the dams. Fenvalerate was detected in the fetus due to placental transfer, as well as in pups due to breast-milk ingestion, persisting in male offspring until PND 40 even though pesticide treatment was terminated on PND 20. However, fenvalerate did not produce marked alterations in age of testicular descent to the scrotum and prepucial separation, parameters indicative of puberty initiation. In contrast, at puberty, there was a reduction in testicular weight and sperm production in male offspring of maternal-treated rats. At adulthood, the sperm counts and fertility did not differ between control and treated groups. Testosterone levels were not changed at any time during reproductive development. Similarly, no apparent exposure-related effects were detected in the histological structures of the lymphohematopoietic system. Data indicate that fenvalerate, in this experimental model, interfered with initial development of the male reproductive system, but that these effects on sperm production or fertility did not persist into adulthood. There was no apparent evidence that fenvalerate altered testosterone levels or produced a disruption in male endocrine functions.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Contamination with cadmium compounds poses high potential risk for the health of populations and for this reason the treatment of their toxic effects should urgently be established. The present study was carried out to determine whether or-tocopherol intake can protect tissues against damage induced by cadmium, and to clarify the contribution of superoxide radicals (O-2(-)) in this process. Cadmium chloride was tested for tissue damage by a single intraperitoneal injection of Cd2+ ions (2 mg Kg(-1)). To determine the potential therapeutic effect of Vitamin E, a group of Cd2+-treated rats received a drinking solution of or-tocopherol (40 mg l(-1)) for 15 days. Cadmium induced increased serum creatinine and total lactate dehydrogenase, reflecting renal and cardiac damage. The increased lipoperoxide and decreased Cu-Zn superoxide dismutase levels indicated the generation of superoxide radicals in cadmium-treated rats. Tocopherol induced increased serum high-density lipoprotein and depressed the toxic effects of Ca2+ alone, since creatinine and lactate dehydrogenase determinations were recovered to the control values. Tocopherol decreased lipoperoxide and led the superoxide dismutase activities to approach those of the control values. We concluded that superoxide radicals are produced as mediators of cadmium toxicity. Tocopherol possesses a significant anti-radical activity and inhibits the cadmium effect on superoxide dismutase activity. Tocopherol also protected tissues from the toxic effects of cadmium by a direct antioxidant action which decreased lipoperoxide formation.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Single high doses of estrogen (35 mg/kg body weight) were administered to young rats aiming to exacerbate its effects on germ cell populations. The short-term (1 week) and medium-term (7 weeks) consequences of this estrogenic treatment (ET) on the testis were evaluated using light and electron microscopies, quantitative methods and TUNEL reaction. Short-term ET led to 50% atrophy of the testis, however, in the medium term the gonado-somatic index was recovered. No histopathological alterations were found at seminiferous epithelium except for short-term severe degeneration of elongated spermatids (EL) and low frequency of these cells in both time intervals. Two morphologically distinct patterns of degeneration were observed: (1) clusters of EL which were TUNEL-negative and exhibited bizarre appearance and nuclear fragmentation, (2) isolated apoptotic EL within the cytoplasm of Sertoli cells (SC). Both degenerative phenomena were more frequent in stages III - VIII of seminiferous cycle, whereas at stages I and II only coiling of flagellum was observed. One week after ET, small amounts of EL were detected in stages IX - XII, suggesting spermiation failure. Signs of functional SC damage such as an accumulation of myelin-like inclusions in their cytoplasm were observed in the short but not medium-term. However, the apoptotic rates still remained five times higher and the number of elongated spermatids was three-fold lower. Our data indicate that exposure to a high dose of estrogen around puberty has stage-specific effects on the testis and causes massive degeneration of elongated spermatids. (c) 2007 Elsevier Ltd. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)