Xiao Ping, Jia Xiao-Dong, Zhong Wei-Jian, Jin Xi-Peng, Nordberg Gunnar
Laboratory of Toxicology, Shanghai Municipal Center for Disease Control and Prevention, 1380 Zhong-Shan West Road, Shanghai 200336, China.
Biomed Environ Sci. 2002 Mar;15(1):67-74.
To investigate whether cadmium-induced oxidative stress in the kidney is influenced by zinc and selenium.
Five groups of rats were maintained: (A) Cd (CdCl2, 400 micrograms.kg-1.day-1 intraperitoneal injection); (B) Cd + Zn (ZnCl2, 20 mg.kg-1.day-1 hypodermic injection); (C) Cd + Se (Na2SeO3, 350 micrograms.kg-1.day-1 via a stomach tube); (D) Cd + Zn + Se; (E) treated with physiological saline as a sham-handled control. The rats were given treatment for a period of 4 weeks. The activities of superoxide dismutase (SOD), glutathione peroxidase (GH-Px), catalase (CAT), and the level of malondialdehyde (MDA) in the kidney tissue were measured to assess the oxidative stress. Urinary lactate dehydrogenase (LDH) activity was used as an indicator of tubular cell damage caused by lipid peroxidation.
In group C and D, activities of SOD (110.5 +/- 5.2, 126.8 +/- 7.0; P < 0.05) and GSH-Px (85.7 +/- 4.9, 94.6 +/- 7.3; P < 0.05) were higher than those in group A (84.7 +/- 3.3; 56.9 +/- 3.8); and in group B, only the activity of GSH-Px (80.0 +/- 4.3, P < 0.01) increased in comparison with that in group A (56.9 +/- 3.8). Significant increase of MDA (P < 0.05) was seen in group B (31.1 +/- 4.7) and C (35.0 +/- 4.1) when compared with control values (17.2 +/- 1.8). No difference was found in the level of MDA between group D (18.9 +/- 2.6) and control. The activity of LDH in urine of control group (0.06 +/- 0.02) was lower than that of group A (0.46 +/- 0.19, P < 0.05), B (0.10 +/- 0.05, P < 0.05) and C (0.14 +/- 0.07, P < 0.05), and there was no significant change between control (0.06 +/- 0.02) and group D (0.08 +/- 0.02).
Zinc or selenium could partially alleviate the oxidative stress induced by cadmium in kidney, but administration cadmium in combination with zinc and selenium efficiently protects kidney from cadmium-induced oxidative damage.
研究锌和硒是否会影响镉诱导的肾脏氧化应激。
将大鼠分为五组：（A）镉组（腹腔注射CdCl₂，400微克·千克⁻¹·天⁻¹）；（B）镉+锌组（皮下注射ZnCl₂，20毫克·千克⁻¹·天⁻¹）；（C）镉+硒组（经胃管给予Na₂SeO₃，350微克·千克⁻¹·天⁻¹）；（D）镉+锌+硒组；（E）用生理盐水处理作为假手术对照。对大鼠进行为期4周的治疗。测量肾脏组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GH-Px）、过氧化氢酶（CAT）的活性以及丙二醛（MDA）的水平，以评估氧化应激。尿乳酸脱氢酶（LDH）活性用作脂质过氧化引起的肾小管细胞损伤的指标。
C组和D组中，SOD（110.5±5.2，126.8±7.0；P<0.05）和GSH-Px（85.7±4.9，94.6±7.3；P<0.05）的活性高于A组（84.7±3.3；56.9±3.8）；B组中，与A组（56.9±3.8）相比，仅GSH-Px活性（80.0±4.3，P<0.01）增加。与对照值（17.2±1.8）相比，B组（31.1±4.7）和C组（35.0±4.1）中MDA显著增加（P<0.05）。D组（18.9±2.6）与对照组之间MDA水平无差异。对照组尿液中LDH活性（0.06±0.02）低于A组（0.46±0.19，P<0.05）,B组（0.10±0.05，P<0.05）和C组（0.14±0.07，P<0.05），对照组（0.06±0.02）与D组（0.08±0.02）之间无显著变化。
锌或硒可部分减轻镉诱导的肾脏氧化应激，但镉与锌和硒联合使用可有效保护肾脏免受镉诱导的氧化损伤。
