Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants created by incomplete combustion. Benzo(a)pyrene (BaP), the prototypic PAH, is known to exert toxicity through oxidative stress which is thought to occur through inhibition of antioxidant scavenging systems. The use of agents that reduce oxidative stress may be a valuable route for ameliorating the adverse effects of PAHs on neural development and behavior. This study was conducted to determine if tocofersolan (a synthetic water-soluble analog of vitamin E) supplementation can prevent or reduce neurobehavioral deficits in zebrafish embryos exposed to BaP during early development. Newly hatched zebrafish were assessed on locomotor activity and light responsivity. Zebrafish embryos were exposed to vehicle (DMSO), tocofersolan (0.3 μM–3 μM), and/or BaP (5 μM) from 5−120 hours post-fertilization. This concentration range was below the threshold for producing overt dysmorphogenesis or decreased survival. One day after the end of exposure the larval fish were tested for locomotor activity under alternating light and dark 10 min periods, BaP (5 μM) was found to cause locomotor hypoactivity in larval fish. Co-exposure of tocofersolan (1 μM) restored control-like locomotor function. Based on the findings of this study, this model can be expanded to assess the outcome of vitamin E supplementation on other potential environmental neurotoxicants, and lead to determination if this rescue persists into adulthood.

多环芳烃 (PAHs) 是由不完全燃烧产生的广泛存在的环境污染物。已知苯并(a)芘 (BaP) 是原型 PAH，它通过氧化应激产生毒性，这种氧化应激被认为是通过抑制抗氧化剂清除系统而发生的。使用减少氧化应激的药物可能是改善 PAHs 对神经发育和行为的不利影响的重要途径。进行这项研究的目的是确定补充 tocofersolan（维生素 E 的合成水溶性类似物）是否可以预防或减少在早期发育过程中暴露于 BaP 的斑马鱼胚胎的神经行为缺陷。对新孵化的斑马鱼进行了运动活动和光反应性评估。斑马鱼胚胎暴露于载体 (DMSO)、tocofersolan (0.3 μM–3 μM)、和/或受精后 5-120 小时的 BaP (5 μM)。该浓度范围低于产生明显畸形发生或存活率降低的阈值。暴露结束后一天，在光照和黑暗交替 10 分钟期间测试幼鱼的运动活动，发现 BaP (5 μM) 会导致幼鱼的运动减退。tocofersolan (1 μM) 的共同暴露恢复了控制样运动功能。根据本研究的结果，该模型可以扩展以评估补充维生素 E 对其他潜在环境神经毒物的结果，并确定这种拯救是否持续到成年期。暴露结束后一天，在光照和黑暗交替 10 分钟期间测试幼鱼的运动活动，发现 BaP (5 μM) 会导致幼鱼的运动减退。tocofersolan (1 μM) 的共同暴露恢复了控制样运动功能。根据本研究的结果，该模型可以扩展以评估补充维生素 E 对其他潜在环境神经毒物的结果，并确定这种拯救是否持续到成年期。暴露结束后一天，在光照和黑暗交替 10 分钟期间测试幼鱼的运动活动，发现 BaP (5 μM) 会导致幼鱼的运动减退。tocofersolan (1 μM) 的共同暴露恢复了控制样运动功能。根据本研究的结果，该模型可以扩展以评估补充维生素 E 对其他潜在环境神经毒物的结果，并确定这种拯救是否持续到成年期。