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971.
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凡纳滨对虾精氨酸激酶的分离纯化及性质研究 总被引:1,自引:0,他引:1
经过CM-纤维素批量层析、Separdex G-100柱层析、DEAE_纤维素柱层析等步骤,从凡纳滨对虾肌肉组织分离得到精氨酸激酶,经SDS-PAGE检测达到电泳纯,分子量约为40kDa.对该酶的性质进行分析结果表明,精氨酸激酶的最适作用温度为55℃,当温度高于65℃时,酶活力显著下降;pH 8时酶活力较高,低浓度的精氨酸对酶活力有促进作用,高浓度时表现抑制作用,而底物类似物精胺和氨基胍则对酶促反应表现出完全的抑制.NaCl,KCl对酶的活力具有促进作用,低浓度(10 mmol·L-1)MgCl2对酶活力表现出激活作用,而CuCl2与MnCl2则表现出完全抑制酶活力,CaCl2与ZnCl2在低浓度时对酶活力无明显影响,但是随着浓度升高,对酶具有抑制作用. 相似文献
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JIN Bei-fang LU Qin-zhen ZHANG Yan CUI Ya-lan QIANG Zheng LIAO Man-xi TAN Hui-yuan LIU Fang 《园艺学报》2000,36(9):1625-1630
AIM To explore the effects of oxidative stress and inflammatory response on kidney injury induced by hyperthyroidism in mice. METHODS Forty male Kunming mice were randomly divided into control group (n =20) and L-thyroxine (T4) group (n =20). The mice in T4 group were intraperitoneally injected with T4 diluent at a dose of 1 mg/kg to induce hyperthyroidism, and those in control group were injected with normal saline of the same volume. After 7 weeks, the mice were weighed and dissected, the kidneys were removed and weighed, and the length of tibia was also measured. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the kidney tissues were detected. The pathological changes of the kidney tissues were observed by HE staining. The levels of 4-hydroxynonenal (4-HNE)-modified proteins, interleukin-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor receptor-related factor 6 (TRAF6) were determined by Western blot and immunohistochemistry. RESULTS Compared with control group, the body weight of the mice was decreased, while the kidney size and weight were increased significantly in T4 group. In addition, the ratios of kidney weight/body weight and kidney weight/tibia length were also increased (P <0.05). In T4 group, the renal tubules were enlarged, and the epithelial cells of renal tubules were swollen and exfoliated, with vacuolar degeneration. Furthermore, reduced SOD activity, and increased MDA content and 4-HNE-modified proteins were found in T4 group, all of which were related to oxidative stress (P <0.05). The levels of inflammation-related proteins IRAK1 and TRAF6 were significantly increased in T4 group (P <0.05). CONCLUSION Excessive T4 may lead to kidney hypertrophy and injury in mice, and the mechanism may be related to oxidative stress and inflammatory response. 相似文献