Objectives: Methylmercury (MeHg) and polychlorinated biphenyls (PCBs) are ubiquitous and persistent environmental pollutants and food contaminants. Both are neurotoxic, especially for the developing nervous system. Material and Methods: Female rats were exposed from day 7 of pregnancy up to day 21 after the delivery to MeHg in drinking water, PCB 153 per os or MeHg+PCB 153. Assessment of the exposure effects in mothers included food and water intake, body weight and reproduction success. Assessment of the progeny comprised determination of body weight, time of pinna detachment, eye opening, incisor eruption, and the negative geotaxis, grip strength and righting reflex. Results: The following effects of the exposures were observed: A) MeHg: 0.5 mg/kg/day -no effect on maternal health status and reproduction. In the progeny: faster incisor eruption and hastened negative geotaxis development. MeHg 2.0 mg/kg/day: In mothers: signs of MeHg toxicity (reduced food intake and body weight, ataxia) during lactation. In the progeny: reduced rate of body weight increase, accelerated incisor eruption but delayed development of the righting reflex. B) PCB 153 exposure: 1.0 mg/kg/day: no effect on maternal health status, reproduction success or morphological and physical development of the progeny; 5.0 mg/kg/day: no effect on maternal health status and reproduction. In the progeny: accelerated growth in females, faster pinna detachment and incisor eruption but delayed development of the grip strength. C) MeHg+PCB153 exposure: none overt effect was noted in mothers or in their progeny. Conclusion: The results confirm the ability of a low level perinatal exposure to MeHg or PCB 153 to affect the early development in the rat. They have not provided, however, an evidence of a synergistic interaction of these contaminants. To the contrary, the results suggest that, at least under the conditions prevailing in the present study, MeHg and PCB 153 interact antagonistically.

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Objectives: Exposure to organophosphorus (OP) pesticides, irreversible inhibitors of acetylcholinesterase (AChE), may result in long-lasting alterations in the functional state of the central nervous system. In earlier studies, we found that a single exposure of the rat to chlorphenvinphos (CVP), an OP pesticide, made the animal hyposensitive to amphetamine (AMPH) three weeks posttreatment. A repeated administration of AMPH is known to result in a progressive increase in the behavioral sensitivity to the psychostimulant. It makes it likely that treatment with AMPH after the CVP exposure may result in amelioration of the CVP-induced hyposensitivity to the psychostymulant. The purpose of the present experiment was to check out this supposition. Materials and Methods: At the first stage, the relationship between the CVP dose and the effect on sensitivity to AMPH was tested. The rats were given CVP once intraperitoneally (i.p.) at a dose of 0.0, 1.0 or 3.0 mg/kg. Three weeks later their open field behavior was assessed before and after i.p. administration of 0.25, 0.5 or 1.0 mg/kg of AMPH. At the subsequent stage, the susceptibility of the CVP-treated rats to AMPH sensitization by repeated AMPH treatment was investigated. For this purpose each of the rats was repeatedly treated with AMPH in its home cage (one injection/day for five days). At stage two, the daily AMPH dose received by each animal was of the same magnitude as that received at stage one. Two weeks after the last AMPH treatment dose, the motor response to a test AMPH dose (0.5 mg/kg) was measured in all rats. Results: The results of stage one confirmed a significant reduction of behavioral sensitivity to AMPH in the CVP-treated rats. The results of stage two indicated that the CVP-induced decrease in sensitivity to AMPH was not ameliorated by a repeated treatment with AMPH at any of the used doses. In fact, in the rats exposed to the high CVP dose, repeated treatment with AMPH resulted, dose dependently, in augmenting of the depressive effect of the pesticide. Conclusions: It appears then that treatment to an OP pesticide reduces the rat's sensitivity to AMPH and makes the animal resistant to sensitization by repeated treatment with the psychostimulant.

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Objectives: Methylmercury (MeHg) and polychlorinated biphenyls (PCBs) are ubiquitous environmental pollutants. Both are neurotoxic, especially for the developing brain. The main source of human exposure to MeHg and PCBs is seafood. The aim of the present work was to find out whether and how separate or combined perinatal exposure to these neurotoxicants affects neurobehavioural functions in maturity. Materials and Methods: The study was performed on adult Wistar rats, the progeny of rat mothers exposed to MeHg (0.5 mg/kg/day or 2.0 mg/kg/day), PCB 153 (1.0 mg/kg/day or 5.0 mg/kg/day), or to MeHg 0.5 mg/kg/day + PCB 153 5.0 mg/kg/day, from day 7 of pregnancy to day 21 post partum. The following functions were assessed: spontaneous locomotor activity (open field test), spatial short-term memory (radial maze test), long-term memory (passive avoidance test), sensitivity to pain and vulnerability to stress (hot plate test), efficiency of the sensorimotor gating (startle response test), and sensorimotor coordination (the rotarod test). Results:The results obtained in the MeHg part of the study showed a reduced locomotor activity in the female progeny of both exposed groups, an impaired passive avoidance in the male progeny of the high and low exposure group and a faster recovery from the effects of the stressful experience (hot plate test) in the male progeny of the high dose group. Results obtained in the PCB part showed an increased locomotor activity in the female progeny of both exposure groups and impairment in rotarod performance in males of the high dose group. Neurobehavioural alterations were not found in either the females or males exposed jointly to MeHg and PCB 153. Conclusions: The results suggest that in condition of the combined exposure, MeHg may protect against the effects of PCB 153 and vice versa.

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Objectives: The aim of the study was to obtain quantitative data on the effect of inhalation exposure to benzalkonium chloride (BAC) on the concentration of catecholamines and their metabolites in selected brain structures. Additionally, concentration of corticosterone (CORT) in plasma was estimated. Material and Methods: Wistar rats were subjected to a single (6-hour) or repeated (3 days, 6 h/day) exposure to BAC aerosol at ca. 30 mg/m 3 . The Waters integrated analytical system of HPLC was used to determine the plasma corticosterone. Qualitative and quantitative determinations of catecholamines and their metabolites: 3,4-dihydroxyphenylacetic (DOPAC) and homovanillic (HVA) acids were performed with the use of the Waters integrity HPLC. Results: The determinations have shown that in the BAC-exposed rats the plasma CORT concentration was several times higher than in the control rats. A significant increase of the concentration of dopamine (DA) (striatum and diencephalon) and noradrenaline (NA) (hippocampus and cerebellum) and a significant reduction of adrenaline (A) level (cortex, hippocampus, striatum and mesencephaloon) was found to occur in the brain of rats exposed to BAC compared to control. In the animals exposed to BAC, the concentration of DOPAC, a DA metabolite, was significantly reduced, but the change occurred mainly in the striatum. This resulted in a significant decrease of the DOPAC/DA and HVA/DA metabolic ratio in this structure. Conclusion: It is assumed that the alterations in the concentration of catecholamines and their metabolites in the BAC-exposed rats were related to the unexpectedly strong and persistent activation of the hypothalamo-pituitary-adrenocortical (HPA) axis evidenced by the high plasma CORT concentration.