Objective To elucidate the etiology of DNA impairment of type Ⅱ alveolar epithelial cells(AT-II) of the rats fed with low selenium and high cadmium fodder，and the effect of Vitamin C.Methods With single cell gel electrophoresis technique，we observed the joint action of selenium，cadmium and vitamin C on DNA damage in AT-II cells of the eight groups of rats fed separately with：normal （2 groups），high Cd，high Cd+high VC，low Se+high Cd，low Se+high Cd+high VC，high Se+high Cd and high Se+high Cd+high VC fodder for 14 weeks.Results Compared with the control，there was no DNA changes have been observed in the high Se+high Cd+high VC group.However，in the high Se+high Cd group and high Cd+high VC group，DNA damage of AT-II cells can be detected clearly；in the low Se+high Cd+high VC group and high Cd group，the degree of the DNA damage is more serious than the above two groups；in the low Se+high Cd group，the extent of the DNA damage was the most serious on all of the groups be studied.Conclusion It is suggested that Se deficiency and simultaneously Cd overabundance may damaged DNA of AT-II cells of the rats significantly，however，Vitamin C may protect AT-II against the injury effectively.
Objective To investigate the time l imit of repairing old sciatic nerve defect in rats and observe the repair effect of autogenous nerve transplantation on old sciatic nerve defect in rats. Methods Thirty-six SD rats of clean grade wererandomized into 6 groups (n=6 per group). The animal model of nerve defect was made by transecting left sciatic nerve at the mid-thigh level. For groups A1, B1 and C1, defects were repaired by the contralateral autogenous nerve transplantation 1, 3 or 6 months after nerve damage and for the control groups of A2, B2 and C2, defects were not repaired. After operation, the gait, toe skin and leg muscle were examined weekly. Three months after autograft, a combination of electrophysiology examination, fluoro gold (FG) retrograde tracing and histological assessment including l ight microscopy, TEM was util ized to investigate the nerve functional recovery. Results Lameness and foot skin ulcers were observed in each group after nerve damage. At 2 months after autograft, such denervation symptoms were only improved in groups A1 and B1. At 3 months after autograft, the motor conduction velocity was (21.84 ± 6.74), (20.02 ± 4.17) and (16.09 ± 8.21) m/s in groups A1, B1 and C1, respectively, showing no statistically significant difference between them (P gt; 0.05). The ampl itude of compound muscle action potential (CAMP) was (12.68 ± 4.38), (9.20 ± 3.43) and (1.22 ± 0.39) mV in groups A1, B1 and C1, respectively, indicating significant differences between groups A1, B1 and group C1 (P lt; 0.05). No CAMP was evident in groups A2, B2 and C2. FG retrograde tracing conducted 3 months after autograft showed that the positive cells were most common in group A1 with big soma, mild in group B1 and lest in group C1 with smallest soma. Gastrocnemius Masson staining showed that the fiber morphology of gastrocnemius in groups A1 and B1 was close to normal, while the rest 4 groups had an obvious atrophy of muscle fiber. The fiber cross-section area was (340.73 ± 118.46), (299.88 ± 119.75), (54.33 ± 53.43), (78.60 ± 51.38), (65.62 ± 25.36), and (40.93 ± 28.22) μm2 in groups A1, B1, C1, A2, B2 and C2, respectively, indicating a significant difference between groups A1, B1 and groups C1, A2, B2 (P lt; 0.05). Neurohistology observation showed that more regenerated nerve fibers were observed in group A1 and B1, but less in group C1. The myel in sheath was thick in groups A1 and B1, while it was thin in group C1. Only SCs and hyperplastic collagen fiber were found in groups A2, B2 and C2. Conclusion Autogenous nerve transplantation is capable of repairing 1- and 3- month sciatic nerve defect to some degree in rat, but repair effect is not obvious on 6-month sciatic nerve defect in rats.