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目的探讨亚慢性接触烹调油烟(COF)对大鼠卵巢的损伤作用及诱导卵巢细胞凋亡相关机制。方法将50只健康60日龄清洁级Wistar雌性大鼠按体重随机分为5组,分别为对照组和0.5、1、2、4 h/d COF暴露组,每组10只;采用吸入式暴露[油烟浓度为(32.21±5.11)mg/m3],连续暴露56 d。测定大鼠卵巢各级卵泡构成的情况及卵巢组织半胱氨酸天冬氨酸蛋白酶(caspase)-3,-8,-9及白细胞分化抗原95分子(Fas),B细胞淋巴瘤-2(Bcl-2),B细胞淋巴瘤-2相关X蛋白(Bax)m RNA表达水平。结果与对照组相比,0.5、1 h/d COF暴露组大鼠的原始/初级卵泡构成比下降,次级卵泡构成比上升;2、4 h/d COF暴露组的成熟卵泡构成比减少;各COF暴露组的闭锁卵泡构成比上升;仅1 h/d COF暴露组的黄体构成比升高;0.5、2、4 h/d COF暴露组大鼠卵巢组织中caspase-3 m RNA的表达水平和各剂量COF暴露组大鼠卵巢组织中caspase-9、Bax m RNA的表达水平升高,而2、4 h/d COF暴露组大鼠卵巢组织中Bcl-2 m RNA的表达水平下降,差异有统计学意义(P<0.05,P<0.01);而各剂量COF暴露组大鼠卵巢组织中Fas和caspase-8 m RNA的表达水平均无明显改变。结论亚慢性接触COF可导致卵泡正常生长发育与退化受损、线粒体及内质网损伤,并可能通过线粒体途径诱导细胞凋亡。
Objective To investigate the injury effect of sub-chronic exposure to cooking fume (COF) on ovary and the mechanism of ovarian cell apoptosis. Methods Fifty healthy Wistar female rats, aged 60 days, were randomly divided into five groups according to body weight: control group and 0.5, 1, 2, 4 h / d COF exposure group, with 10 in each group. Inhaled exposure [Fume concentration (32.21 ± 5.11) mg / m3], continuous exposure for 56 days. The levels of ovarian follicles and the expressions of caspase-3, -8, -9 and Fas, B-cell lymphoma-2 Bcl-2), B-cell lymphoma-2-related protein B (Bax) m RNA expression level. Results Compared with the control group, the ratio of primordial / primary follicle in 0.5 and 1 h / d COF exposure groups decreased and the ratio of secondary follicles increased. The ratio of mature follicles in COF exposed group at 2 and 4 h / d decreased. The proportion of atresia follicles increased in each COF exposure group; the luteinizing ratio of COF exposure group increased only in 1 h / d; the expression level of caspase-3 mRNA in ovary tissues of COF exposure group at 0.5, 2, 4 h / d The expression levels of caspase-9 and Bax m RNA in ovarian tissue of COF exposure group at each dose increased, while the expression of Bcl-2 m RNA in ovary tissue of COX exposure group decreased at 2 and 4 h (P <0.05, P <0.01). However, there was no significant change in the expression of Fas and caspase-8 mRNA in the ovariectomized rats exposed to all doses of COF. Conclusion Subchronic exposure to COF can lead to normal follicle growth and degeneration, damage to mitochondria and endoplasmic reticulum, and induce apoptosis through mitochondrial pathway.