Research On The Mechanism Of Ascorbic Acid Inhibits Cadmium Induced Testis Damage Of Rats

PART?Effect of cadmium on the testis and the antagonism of ascorbic acidObjective:To explore the destructive effect of acute exposure to cadmium on the blood-testis barrier?BTB?and the protective effect of ascorbic acid.Methods:twenty-four healthy adult male Sprague-Dawley rats of 250±10g were housed in cagas with free access to drink water and food under controlled temperature?22-25°C?,lighting schedule was maintained at 12 h of light per day.Animals were allowed to acclimatize for 1 week before experiments began.Rats were randomly divided into 4 groups.Each group consisted of 6 rats:the Cd-treated group received a single dose?s.c.?of Cdcl₂ 2mg/kg BW;in AA antagonism group,rats were s.c.injected with AA at the dose of 400 mg/kg BW?200 mg at 24 h prior to Cd-treatment and 200 mg at 24h after Cd-treatment?;the control rats received an equal volume of saline or an equal dose of AA.After 48 hours after Cd treatment,under drugged state all rats were killed to gain materials.Result:1.A significant decrease in occludin and claudin-11 expression were observed in the Cd-treated rats,whereas,AA administration attenuated this.Moreover,Testicular histopathology and transmission electron microscopy results strengthen the protective effects of AA against Cd-induced the BTB damage.Conclusion:Ascorbic acid could antagonize the toxicity of cadmium to the blood testis barrier in SD rats.PART ? Research on the mechanism of ascorbic acid inhibits cadmium induced disruption of the blood-testis barrierObjective: To explore the mechanism of protective effects of ascorbic acid on blood-testis barrier injury evoked by cadmium.Methods: twenty-four healthy adult male Sprague-Dawley rats of 250 ± 10 g were housed in cagas with free access to drink water and food under controlled temperature?22-25°C?,lighting schedule was maintained at 12 h of light per day.Animals were allowed to acclimatize for 1 week before experiments began.Rats were randomly divided into 4 groups as follows.Each group consisted of 6 rats: the Cd-treated group received a single dose?s.c.?of Cdcl2 2mg/kg BW;in AA antagonism group,rats were s.c.injected with AA at the dose of 400 mg/kg BW?200 mg at 24 h prior to Cd-treatment and 200 mg at 24 h after Cd-treatment?;the control rats received an equal volume of saline or an equal dose of AA.After 48 hours after Cd treatment,under drugged state all rats were killed to gain materials.Result: As expected,ROS expression was upregulated in Cd-treated rats,accompanied by elevated content of malondialdehyde?MDA?.Interestingly,AA suppressed Cd-induced oxidative stress by decreasing the level of ROS and MDA and increasing the activity of superoxide dismutase?SOD?and catalase?CAT?.In addition,AA also reduced BTB disruption by inhibition of TGF-?3 activation and p38 MAPK phosphorylation.Conclusion: the results of the present study suggest AA protects rats from Cd-evoked the BTB destruction via inhibiting oxidative stress and TGF-?3/p38 MAPK signaling pathway in testes.