Sidhu P, Garg M L, Dhawan D K
Department of Biophysics Panjab University Chandigarh, India.
Nutr Hosp. 2004 Nov-Dec;19(6):341-7.
This study was designed to evaluate the protective effects of zinc on the liver activities of antioxidant enzymes in protein-deficient rats. Zinc sulfate at a dose level of 227 mg/l in drinking water was administrated to Sprague Dawley normal control as well as to protein-deficient rats for a total duration of eight weeks. The effects of zinc treatment and protein deficiency alone as well as combined were studied on rat liver antioxidant enzymes which included catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic lipid peroxidation and in catalase, Gpx, GR and GST activity. A significant inhibition in the levels of SOD activity and reduced glutathione (GSH) was observed following protein deficiency in normal rats. Zn treatment to protein deficient animals lowered lipid peroxidation and catalase, Gpx and GST activities, and also resulted in a significant elevation in the levels of GSH and SOD activity. The concentration of zinc decreased significantly in protein deficient animals but returned to normal levels when zinc was administered.
本研究旨在评估锌对蛋白质缺乏大鼠肝脏抗氧化酶活性的保护作用。将饮用水中剂量为227毫克/升的硫酸锌给予斯普拉格-道利正常对照组以及蛋白质缺乏大鼠,持续时间共八周。研究了单独的锌处理、蛋白质缺乏以及两者联合对大鼠肝脏抗氧化酶的影响,这些抗氧化酶包括过氧化氢酶、谷胱甘肽过氧化物酶(GPX)、谷胱甘肽还原酶(GR)、超氧化物歧化酶(SOD)和谷胱甘肽S-转移酶(GST)。正常大鼠的蛋白质缺乏导致肝脏脂质过氧化以及过氧化氢酶、GPX、GR和GST活性显著增加。正常大鼠蛋白质缺乏后,观察到SOD活性水平和还原型谷胱甘肽(GSH)显著抑制。对蛋白质缺乏动物进行锌处理可降低脂质过氧化以及过氧化氢酶、GPX和GST活性,还导致GSH水平和SOD活性显著升高。蛋白质缺乏动物体内锌浓度显著降低,但给予锌后恢复到正常水平。