高浓度铬对克氏原螯虾抗氧化酶系统的影响

Effects of High Level Chromium on Antioxidant Enzyme System in Gill and Hepatopancreas of Procambarus clarkia

采用毒性实验方法,研究了50mg·L^(-1)铬(Cr^(6+))在14d内对克氏原螯虾鳃和肝胰腺抗氧化酶系统的影响。结果表明,肝胰腺比鳃的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性、总抗氧化能力(T-AOC)和丙二醛(MDA)含量均要高。Cr6+对鳃和肝胰腺SOD和CAT活性的影响各异,鳃SOD活性先受抑制再被激活,最后再被抑制;而肝胰腺SOD活性始终受到抑制。鳃CAT活性先增高后下降,肝胰腺CAT活性先下降后上升,最后均下降至低于对照组。鳃和肝胰腺T-AOC随Cr^(6+)处理时间而出现的变化呈总体一致的趋势:在暴露的7d内,T-AOC与暴露时间呈正相关,在暴露14d后显著下降;而MDA含量几乎全部低于对照组。结果显示,肝胰腺比鳃对高浓度Cr^(6+)的毒性影响更为敏感,高浓度Cr^(6+)在短期内可能对抗氧化防御功能起促进作用;同时,高浓度下克氏原螯虾抗氧化能力的提高可能并非由抗氧化酶活性的提高引起,而主要通过调动机体的非酶促系统来完成。

A toxic experiment was conducted to investigate the effects of high concentration of Cr^6＋（50 mg· L^-1） on antioxidant defense system such as superoxide dismutase（SOD）, catalase （CAT）, malondialdehyde （MDA） and total antioxidative capacity （T-AOC） in gill and hepatopancreas of Procambarus clarkia. The results indicated that the level of all those antioxidant defenses in hepatopancreas were higher than those in gill. The effects of Cr^6＋ on SOD and CAT activities were different： the activity of SOD in gill was inhibited first and then induced, at last inhibited again; while which was inhibited in hepatopancreas all the time. The CAT activity in gill was induced first and then inhibited, while, in hepatopancreas it was inhibited first and then induced, but both were inhibited on the 14th day. Compared to the control groups, TAOC both in gill and hepatopancreas were induced significantly during the fist 7 d and had a positive relationship with the duration of exposure, but were markedly decreased and lowered to the control level （P〈0.01） after exposure for 14 d. The concentration of MDA was almost all lower than that of the control group in gill and hepatopancreas within the exposure time. These suggested that high concentration of Cr^6＋ may be an accelerant of antioxidant defense system in a short time and showed similarly pharmacological function to some extent, hepatopancreas was more sensitive to high concentration of Cr^6＋ than gill, and the enhancement of antioxidantive capacity was not due to the enzyme-induced system but mainly contributed to the non enzyme-induced substance.