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Pregnant Wistar rats received 50 ppm of zinc (ZnSO4 • 7H2O) in their drinking water for the entire duration of pregnancy. On the day of delivery zinc was removed from the drinking water. Another group, dams, received 50 ppm of zinc in drinking water during the suckling period (from delivery until the 21st day of postnatal life). Their offspring were weaned on the 21st day, at which time zinc was removed from the drinking water. The control group drank tap water only. In 8-12-week-old offspring of all three groups the DA, DOPAC, HVA, 3-MT, 5-HT, 5-HIAA, NA, and MOPEG synthesis rate in the brain was estimated by HPLC/ED technique. Independent behavioral exam were performed such as locomotor and exploratory activity, irritability, yawning and oral activity, stereotype behavior, catalepsy and others. For the above, cen­tral DA receptor agonists (quinpirole, SKF 38393, apomorphine, 7-OH-DPAT) or antagonists (haloperidol, SCH 23390) were used. It was found that exposure to zinc during early stages of ontogenic development produce changes in the central dopaminergic system activity of adult offspring. From the above we con­cluded that uncontrolled supplementation with zinc during pregnancy or lactation can induce disturbance of the central dopaminergic system in adult mammal.
Galactosamine (GalN), a well-known hepatotoxin that depletes the cellular pool of uracil nucleotides, was previously shown to have greater impact on the inhibition of protein synthesis in hepatocytes of old rats as compared with young animals (Kmiec 1994, Ann. N.Y. Ac. Sci. 717, 216-225). In the present study we compared the effects of GalN on the nucleotide content (measured by ion-exchange HPLC) in the livers of young (4 months), adult (12 months), and old (24-26 months old) rats two hours after its intraperitoneal administration. UTP content of the livers of old control rats was significantly lower (by 28%) than that of young animals. GalN administration decreased the UTP content in the livers of young, adult and old rats by, respectively, 55%, 65% and 89%, and increased the content of UDP-sugars by 189%, 175% and 305%. The hepatic content of ATP, ADP, AMP, NAD, GTP except CTP did not differ significantly among the age groups of rats studied, and was not changed by GalN treatment. The content of CTP was significantly higher in old rats (P < 0.03) upon GalN treatment. The lower hepatic content of UTP may partially explain the increased sensitivity of hepatocytes and livers of old rats to the action of galactosamine, and pos­sibly to other hepatotoxic compounds that decrease transcription in the liver.
To determine the susceptibility of developing brain and other tissues to accumulate zinc, rats were exposed to zinc at different periods of ontogeny. For the prenatal group, pregnant Wistar rats received 50 ppm of zinc (ZnSO₄ · 7H₂O) in drinking for the entire duration of pregnancy. On the day of delivery zinc was removed from the drinking water. Another group, dams, received 50 ppm of zinc in drinking water only during the suckling period (from delivery until the 21st day of postnatal life). Their offspring were weaned on the 21st day, at which time zinc was removed from the drinking water. The control group drank tap water only. At 3 weeks after birth, the level of zinc was estimated in the brain, liver, mandibular bone and kidney of offspring from all groups. At 8 weeks after birth 6-[³H]D-glucose (500 µCi/kg) was administered IP to male offspring, 15 minutes before sacrifice. By liquid scintillation spectroscopy, ³H-activity (expressed as disintegrations per minute [DPM]) was determined in discrete parts of the brain and some peripheral tissues, and expressed as DPM/100 mg of tissue, wet weight. It was found that the highest amount of zinc was accumulated in the brain and liver of rat offspring that were exposed to zinc postnatally. [³H]-activity was at lower levels, in comparison, in nearly all other parts of the brain of rats exposed to zinc postnatally. In offspring receiving zinc prenatally, zinc levels were at similar or lower amounts in the brain and peripheral tissues, vs. the group with postnatal exposure. From this study in rats we conclude that zinc accumulates to the highest extent in brain, following a later ontogenetic (postnatal) exposure period, and by this, there is also greater disturbance of metabolic processes associated with glucose utilization.
In this study we examined the mechanism of action of Dieldrin on the reproductive function in adult male rats. Experimental data suggest that exposure to pesticide at 3 and 6mg/kg/day for 10 consecutive days, induced a dose-dependant decrease of the number and the mobility of epididymal spermatozoa. Tes­ticle histological analysis shows alteration of spermatogenesis with marked reduce of gametes production combined with reduction in the seminiferous tubule diameters in treated relative to control. Concentration of plasma testosterone dropped significantly in a dose-dependent manner after exposure to Dieldrin, while circulating levels of Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) and weight of accessory sex glands were not affected significantly. Thus, it may be concluded that Dieldrin exposure can impair both testicle gametogenesis and steroidogenesis in adult rats.
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