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The aim of this paper was to find any alterations in flash visual evoked potentials (FVEP) after pre- and postnatal exposure to Zn in rats. 18 white adult Wistar rats drank tap water containing 50ppm of ZnSO₄ x 7H₂O and ate pelleted food during 21 days of pregnancy. 14 pregnant rats of the control group drank only tap water. 10 newborn rats from pure (without prenatal Zn exposure) breeding had the oral Zn supplementation with the same dose of Zn for 21 postnatal days. The fluid consumption of each dam and each offspring rat was monitored daily. Every rat during the whole period consumed about 66.15mg of pure Zn. The offsprings were divided into three groups: prenatal Zn group (18 rats), postnatal Zn group (10 rats) and control group (14 rats). The FVEP recordings were made using the UTAS 1000 LKC electrophysiologically interfaced personal computer system (USA), with Ganzfield stimulation in all groups every 5 min for 30 min. The decrease in the latencies and increase in the amplitudes of N₁ and P₁ waves were observed in both Zn groups in comparison to the control, but only in the prenatal Zn group were the changes statistically significant. The maternal Zn supplementation may have a beneficial influence on visual cortical responses in newborn rats.
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.
Female adult Wistar rats were given tap warter (control), 10% (v/v) water solution of ethanol and/or cadmium (5 or 50 ppm) in tap water or in 10% ethanol ad libitum throughout their pregnacies. As soon as the offspring were born, the administration of all above solutions was discontinued and all females began drinking water only. Adult female and male offspring from each group were challenged with a single hypnotic dose of ethanol (3.5 g/kg IP) in the form of 20% (v/v) water solution. The latency from the time of injection until the loss of the righting reflex, as well as the latency for recovery of the reflex was recorded. The results showed that female rats exposed to cadmium after ethanol 3.5 g/kg IP challenge lose the righting reflex rapidly and recovery of it was later as compared to control animals. In female rats exposed during intrauteral development to cadmium jointly with ethanol measured parameters return to values as in the control group. No statistically significant differences in loss and recovery of the righting reflex in all groups of male rats after the ethanol 3.5 g/kg IP challenge was recorded.
The general exposure to endocrine disruptors, including phthalates, is considered as one of the reason diminished sperm count and deteriorated sperm quality, which may lead to infertility and higher incidence of congenital malformations of the genital tract. This article describes the effects of selected phthalates di(2-ethylhexyl)phthalate (DEHP), dibutyl phthalate (DBP); butylbenzyl phthalate (BBP), diethyl phthalate (DEP), di-isononyl phthalate (DINP) on the male gametes, reproduction and the offspring of exposed animals. Results of several papers in vitro showed that above mentioned phthalates are weakly estrogenic, whereas in vivo studies showed that they have rather antiandrogenic abilities. Review of papers regarding to laboratory animals confirmed that phthalates cause diminished sperm count, increased frequency of abnormal spermatozoa and DNA damage in germ cells, especially after chronic exposure and in case exposure of immature animals. Phthalates may induce in male gametes mutations leading to increased pre- and postnatal mortality of the offspring and to incidence of congenital malformations, growth retardation, delay in sexual development, shortening of anogenital distance in males, disturbances in sex ratio and diminished quality of semen in F1 generation. The sensitivity on mammalian life stages on phthalates seems to be as follows: fetal>peripubertal>adult. The human studies provided limited evidence of an association between phthalate exposure and semen quality. Concentration of phthalates in semen of men at the level from 0.08 to 1.32 mg/kg was related to declined semen quality and infertility. Majority of human data showed the connection of increased level of phthalates in urine and sperm quality, however on the basis results of other studies, the impact of environmental exposure on sperm parameters seems to be rather small.
Tobacco smoking during pregnancy is associated with a variety of negative consequences not only for the mother, but also for the developing fetus. Many studies have shown that carcinogens contained in tobacco smoke permeate across the placenta, and are found in fetus. The aim of the study was to determine the prenatal exposure to tobacco-specific carcinogenic N-nitrosamines on the basis of measurements of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine of smoking and second-hand smoke (SHS) exposed women and in the first urine of their newborns. A questionnaire documenting demographics and socio-economical data, smoking habits and exposure to SHS was completed by 121 delivering women near or at term. Maternal concentrations of cotinine and NNAL were measured in urine of the mother and the first urine of her newborn infant by liquid chromatography tandem mass spectrometry (LC/MS/MS). The mean concentration of cotinine was 439.2 ng/mg creatinine and NNAL concentration in urine of smoking women was 74.0 pg/mg creatinine, and for her newborn 78.6 pg/mg creatinine. Among mothers exposed to SHS, cotinine and NNAL mean concentration were 23.1 ng/mg creatinine, and 26.4 pg/mg creatinine. In newborns of SHS exposed mothers during pregnancy the mean concentration of NNAL was 34.1 pg/mg creatinine, respectively. Active tobacco smoking as well as passive exposure to smoking during pregnancy is an important source of tobacco specific N-nitrosamines to the fetuses as evidenced by increased concentrations of this carcinogen. Determination of NNAL in maternal urine samples can be a useful biomarker of prenatal exposure of newborn to carcinogenic nitrosamines.
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