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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Behavioral and neurochemical effects induced by subchronic exposure to 40 ppm toluene in rats.
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Behavioral and neurochemical effects induced by subchronic exposure to 40 ppm toluene in rats.

机译：亚慢性暴露于大鼠40 ppm甲苯诱导的行为和神经化学作用。

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Chronic toluene inhalation at concentrations above occupational exposure limits (e.g., 100 ppm; NIOSH) has been repeatedly shown to induce neurotoxic effects. In contrast, although few clinical and experimental data are available on the effects of toluene exposure at concentrations below occupational exposure standards, some of these data may support adverse effects of long-term exposure to low toluene concentrations. To test this hypothesis, we investigated the neurobehavioral and neurochemical effects of 40 ppm inhaled toluene in a rat model of 16-week subchronic exposure, examining locomotor and rearing activities; adaptation/sensitization to narcosis produced by acute exposure to toluene at high concentration; and tyrosine hydroxylase and tryptophan hydroxylase activities, and dopamine (DA) and serotonin (5-HT) turnovers in the caudate-putamen, nucleus accumbens, hippocampus, prefrontal cortex, and cerebellum. Our results mainly show that subchronic exposure to 40 ppm toluene significantly resultedin a sensitization to toluene-induced narcosis, a decrease in rearing activity, and alterations in DA and 5-HT transmissions. This demonstrates that subchronic toluene exposure at a low concentration may lead to adverse changes in neurobehavioral and neurochemical functioning, and further questions in a public health perspective the actual neurotoxic potential of toluene and other organic compounds, because deficits in functioning are generally viewed as precursors of more serious adverse effects.
机译：反复吸入浓度超过职业接触限值（例如100 ppm; NIOSH）的慢性甲苯会引起神经毒性作用。相反，尽管在低于职业接触标准的浓度下可获得很少的关于甲苯接触影响的临床和实验数据，但其中一些数据可能支持长期接触低甲苯浓度的不利影响。为了检验这一假设，我们研究了在16周亚慢性暴露的大鼠模型中40 ppm吸入甲苯的神经行为和神经化学作用，研究了运动和饲养活动。急性暴露于高浓度甲苯引起的对麻醉的适应/敏化;和酪氨酸羟化酶和色氨酸羟化酶的活性，以及​​尾状-丘脑，伏核，海马，前额叶皮层和小脑中的多巴胺（DA）和5-羟色胺（5-HT）转换。我们的结果主要表明，亚慢性暴露于40 ppm的甲苯显着导致了对甲苯诱导的麻醉的致敏作用，饲养活性的降低以及DA和5-HT传递的改变。这表明低浓度的亚慢性甲苯暴露可能导致神经行为和神经化学功能发生不良变化，并在公共卫生角度进一步质疑甲苯和其他有机化合物的实际神经毒性潜力，因为功能缺陷通常被认为是甲苯的前体。不良反应更为严重。

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