■本研究旨在从下丘脑-垂体-睾丸轴的角度评估味精对小鼠睾丸精子发生的影响,以及这种破坏作用是否随时间减轻。
■将新生小鼠随机分为味精(MSG)组和对照组,出生后在肩胛骨间区域以下,用10微升味精递送4毫克/克(体重),或等量的0.9%盐水。涉及血液的样本,收集小鼠的大脑和睾丸,并在青春期60天和成年期90天进行测量。
■结果表明,GnRH神经纤维的荧光强度,卵泡刺激素(FSH)的水平,黄体生成素(LH),和生殖系统中的睾丸激素,睾丸切片中精母细胞和精子的数量,身体长度,体重,睾丸重量,味精组(MSG60组)和MSG90组60日龄小鼠睾丸指数均低于正常对照组(NC60组)60日龄小鼠睾丸指数(p<0.05),但睾丸切片凋亡细胞数高于NC60组(p<0.05)。味精组(MSG90组)90日龄小鼠与MSG60组比较,除了体重和睾丸重量增加(p<0.05),上述其他参数无显著差异(p>0.05)。
■味精通过损伤GnRH神经元对雄性小鼠产生生殖毒性,这种生殖毒性不能随时间自发缓解。观察到的组织学变化支持了这些发现。
UNASSIGNED: The present study aims to evaluate the effect of monosodium glutamate on testicular spermatogenesis in mice from the perspective of the hypothalamic-pituitary-testicular axis and whether this destructive effect is alleviated with time.
UNASSIGNED: Neonatal mice were randomly divided into a monosodium glutamate (MSG) group and a control group, just below the interscapular region after birth with 10 µL MSG to deliver 4 mg/g (body mass), or with equivalent volumes of 0.9% saline. Samples which involved blood, brains and testicles of mice were collected and measured at puberty at 60 days and adulthood at 90 days.
UNASSIGNED: The results show that the fluorescence intensity of GnRH nerve fibers, the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) hormones in the reproductive system, the number of spermatocytes and spermatozoa in testicular sections, the body length, body weight, testicular weight, and testicular index in the 60-day-old mice in monosodium glutamate group (MSG60 group) and the MSG90 group were lower than those in the 60-day-old mice in normal control group (NC60 group) (p < 0.05), but the number of apoptotic cells in the testicular section was higher than in the NC60 group (p < 0.05). When the 90-day-old mice in monosodium glutamate group (MSG90 group) was compared with the MSG60 group, except for body weight and testicular weight increase (p < 0.05), there is no significant difference in the other parameters mentioned above (p > 0.05).
UNASSIGNED: Monosodium glutamate can cause reproductive toxicity to male mice by damaging GnRH neurons, and this reproductive toxicity cannot be relieved spontaneously over time. These findings are supported by observed histological changes.