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目的 :通过观察苯并[a]芘(Benzo(a)pyrene,B[a]P)对新生SD大鼠脑组织形态学、超微病理学和生化指标的改变,探讨B[a]P神经发育毒性的分子机制。方法 :将48只新生雄性SD大鼠随机分为溶剂对照组、低剂量组、中剂量组、高剂量组,每组各12只,从出生后第5天始,每天灌胃1次,持续14 d。染毒后制切片,光镜、电镜观察海马形态学改变,化学比色法测定生化指标变化。结果:与溶剂组比较,染毒组幼鼠可见不同程度的脑组织损伤;海马组织超氧化物歧化酶含量、Na~+-K~+-ATP酶和Ca~(2+)-Mg~(2+)-ATP酶的活性明显下降,丙二醛含量明显增高,差异均具有统计学意义(P<0.05)。结论 :B[a]P可致新生SD大鼠神经发育毒性,其机制可能与海马组织氧化应激产生、Na~+-K~+-ATP酶和Ca~(2+)-Mg~(2+)-ATP酶活性下降有关。
OBJECTIVE: To observe the morphological, ultrastructural and biochemical changes of brain in neonatal SD rats by observing Benzo (a) pyrene (B [a] P) Molecular mechanisms of developmental toxicity. Methods: 48 male Sprague-Dawley rats were randomly divided into solvent control group, low dose group, medium dose group and high dose group, with 12 rats in each group. The rats were orally administered once daily from the 5th day after birth 14 d. The sections were made after exposure to light. The morphological changes of hippocampus were observed under light microscope and electron microscope. The changes of biochemical indexes were determined by chemical colorimetry. Results: Compared with the solvent group, the damage of brain tissue was observed in the young rats in the exposure group. The levels of superoxide dismutase, Na ~ + -K ~ + -ATPase and Ca ~ (2 +) - Mg ~ (+ 2 +) - ATPase activity was significantly decreased, malondialdehyde content was significantly increased, the difference was statistically significant (P <0.05). CONCLUSION: B [a] P can cause neurodevelopmental toxicity in neonatal SD rats. The mechanism may be related to the generation of oxidative stress, Na ~ + -K ~ + -ATPase and Ca ~ (2 +) - Mg ~ +) - ATPase activity decreased.