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.
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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