目的：用微核试验评价生物羊膜引起遗传毒性的可能性。方法参照《GB/T16886.3-1997/ISO10993-3:1992》的方法及指导原则进行试验。结果：在研究过程中所有动物临床表现和体重变化都是正常的,生物羊膜浸提液与阴性对照嗜多染红细胞（PCEs）/红细胞（RBC）总数无显著性差异（P>0.05），没有出现遗传毒性的迹象。结论：生物羊膜用微核试验评价不会引起遗传毒性。

［目的］研究母鸡中枢神经组织ATP含量在磷酸三邻甲苯酯（TOCP）诱导迟发性神经毒性（OPIDN）过程的变化，进一步探讨TOCP诱发OPIDN的分子机制。［方法］成年罗曼母鸡40只，随机分为d0（正常对照组）、d5、d10、d15和d21组（每组8只），除d0组外，其余各组动物一次性经口灌胃TOCP750mg/kg。每天观察母鸡OPIDN症状并按8级评分标准进行评价，利用高效液相色谱法（HPLC）测定母鸡大脑、小脑和脊髓组织中ATP含量。［结果］母鸡在染毒后第5天即出现间或的双腿运动轻微不协调，第21天完全瘫痪。大脑组织中ATP含量在染毒后第5天升高了20.62%（P<0.01），第15天和第21天分别降低了15.5%和17.96%（均为P<0.01）；小脑组织中ATP含量在染毒后第5天和第10天分别升高了76.95%（P<0.01）和.36%（P<0.05），第21天降低了20.49%（P<0.05）；脊髓组织中ATP含量在染毒后第5天、第10天和第15天分别升高了32.45%、42.89%和87.1%（均为P（<0.01）。［结论］在母鸡表现出明显的OPIDN症状之前中枢神经组织ATP含量即出现明显的升高，提示能量的变化可能在OPIDN的发生过程中起重要作用。

To investigate the mechanisms and biomarker of the neuropathy induced by 2,5-hexanedione (HD), male Wistar rats were administrated HD at dosage of 200 or 400 mg/kg for 8 weeks (five-times per week). All rats were sacrificed after 8 weeks of treatment and the cerebrum cortex (CC), spinal cord (SC) and sciatic nerves (SN) were dissected, homogenized and used for the determination of cytoskeletal proteins by western blotting. The levels of neurofilaments (NFs) subunits (NF-L, NF-M and NF-H) in nerve tissues of 200 and 400 mg/kg HD rats significantly decreased in both the supernatant and pellet fractions. Furthermore, significant negative correlations between NFs levels and gait abnormality were observed. As for microtubule (MT) and microfilament (MF) proteins, the levels of-tubulin-tubulin and-actin in the supernatant and pellet fraction of SN significantly decreased in 200 and 400 mg/kg HD rats and correlated negatively with gait abnormality. However, the contents of MT and MF proteins in CC and SC were inconsistently affected and had no significant correlation with gait abnormality. The levels of NF-L and NF-H in serum significantly increased, while NF-M-tubulin-tubulin and-actin contents remain unchanged. A significant positive correlation (R=0.9427, P<0.01) was observed between gait abnormality and NF-H level in serum as the intoxication went on. These findings suggested that HD intoxication resulted in a progressive decline of cytoskeletal protein contents, which might be relevant to the mechanisms of HD-induced neuropathy. NF-H was the most sensitive index, which may serve as a good indicator for neurotoxicity of n-hexane or HD.

The protective effects of single dose of garlic oil (GO) on acute ethanol-induced fatty liver were investigated. Mice were treated with ethanol (4.8 g/kg bw) to induce acute fatty liver. The liver index, the serum and hepatic triglyceride (TG) levels and the histological changeswere examined to evaluate the protective effects. Hepatic malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) activities were determined for the antioxidant capacity assay. Acute ethanol exposure resulted in the enlargement of the liver index and the increase of the serum and hepatic TG levels (P<0.01), which were dramatically attenuated by GO pretreatment in a dose-dependent manner (P<0.01). GO treatment (simultaneously with ethanol exposure) exhibited similar effects to those of pretreatment, while no obviously protective effects were displayed when it was used at 2h after ethanol intake. Histological changes were paralleled to these indices. Beside this, GO dramatically prolonged the drunken time and shortened thewaking time, and these effects were superior to those of silymarin and tea polyphenol. In addition, GO dose-dependently suppressed the elevation of MDA levels, restored the GSH levels and enhanced the SOD, GR and GST activities. Compared with the ethanol group, the MDA levels decreased by 14.2% (P<0.05), 29.9% and 32.8% (P<0.01) in GO groups 50, 100 and 200 mg/kg, respectively. The GST activity increased by 9.97%, 19.94% (P<0.05) and 42.12% (P<0.01) of the ethanol group in GO groups 50, 100 and 200mg/kg, espectively, while the GR activity increased by 28.57% (P<0.05), 37.97% (P<0.01), 50.45% (P<0.01) of the ethanol group in GO groups 50, 100 and 200mg/kg, respectively. These data indicated that single dose ofGOpossessed ability to prevent acute ethanol-induced fatty liver, but may lose its capacity when used after ethanol exposure. The protective effects should be associated with its antioxidative activities.