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目的探讨氧化应激-炎性因子在燃煤型氟中毒致雌鼠卵巢早衰机制。方法模拟贵州燃煤污染型疫区,煤烘烤玉米为雌鼠饮食氟饲料。体重均等,24只清洁级SD雌性大鼠构建动物模型,随机分为对照组、低氟组(25 mg/Kg)、中氟组(50 mg/Kg)、高氟组(100 mg/Kg)。染氟90 d处死雌鼠,分离双侧卵巢。检测致卵巢早衰氧化应激和炎性因子,谷胱甘肽过氧化物酶(GSH-Px)、总抗氧化能力(T-AOC)、活性氧簇(ROS)活性和白细胞介素6(IL-6)、白细胞介素8(IL-8)含量;透射电镜观察卵巢早衰超微结构变化。结果各模型组与对照组比较,GSH-Px、T-AOC、ROS和IL-6、IL-8均有统计学意义(P<0.05)。各模型组间比较,随染氟剂量的增加,卵巢GSH-Px、T-AOC逐渐降低,ROS和IL-6、IL-8逐渐增高,差异均有统计学意义(P<0.05)。透射电镜下,低氟组卵巢颗粒细胞超微结构电镜结果未见明显损伤。中氟组:颗粒细胞核膜轻微皱缩,少部分细胞核染色质聚集、边集,核仁消失,线粒体轻微肿胀。间质细胞核膜轻微皱缩,核染色质边集,呈现早衰现象。高氟组:颗粒细胞的核固缩,大量染色质成块状,边集,核仁消失,大量的线粒体肿胀,脂滴增多,呈现早衰现象,与染氟剂量呈正相关。结论燃煤型氟中毒卵巢氧化应激水平和炎性机制发生紊乱,抗氧化GSH-Px、T-AOC明显降低,促氧化ROS和促炎性因子IL-6、IL-8明显增高,卵巢超微结构的明显损伤,呈现早衰现象,与染氟剂量呈正相关。
Objective To investigate the mechanism of oxidative stress - inflammatory cytokines in premature ovarian failure induced by coal-burning fluorosis in female rats. Method to simulate coal-borne pollution-affected areas in Guizhou, corn bake corn diet fluoride feed. The rats were divided into control group, low fluoride group (25 mg / Kg), medium fluoride group (50 mg / Kg) and high fluoride group (100 mg / Kg) . Fluoride 90 d killed female rats, ovaries were isolated. The levels of oxidative stress, inflammatory factors, glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), reactive oxygen species (ROS) and interleukin 6 -6) and interleukin-8 (IL-8) were detected by transmission electron microscopy and ultrastructural changes of premature ovarian failure. Results Compared with the control group, the levels of GSH-Px, T-AOC, ROS, IL-6 and IL-8 in the model group were significantly increased (P <0.05). The levels of GSH-Px and T-AOC in ovary gradually decreased and the levels of ROS, IL-6 and IL-8 gradually increased with the increase of fluoride dose in each model group. The difference was statistically significant (P <0.05). Under the transmission electron microscope, the ultrastructure of ovarian granulosa cells in the low fluoride group showed no obvious damage. Fluoride group: granular nuclear membrane slightly shrunk, a small part of nuclear chromatin aggregation, edge set, nucleolus disappear, mitochondria slight swelling. Slight contraction of stromal nuclear membrane, nuclear chromatin edge set, showing the phenomenon of premature aging. In the high fluoride group, nuclear condensation of granular cells, a large number of chromatin into massive, edge sets, nucleoli disappear, a large number of mitochondria swelling, lipid droplets increased, showing the phenomenon of premature aging, and fluoride dose was positively correlated. Conclusion The levels of oxidative stress and inflammatory mechanism in ovary induced by coal-burning fluorosis are disorderly. The levels of GSH-Px and T-AOC in serum are significantly decreased, the levels of pro-oxidant ROS and proinflammatory cytokines IL-6 and IL-8 are significantly increased, Significant damage to the microstructure, showing the phenomenon of premature aging, and fluoride dose was positively correlated.