Singh Mohan, Sandhir Rajat, Kiran Ravi
Department of Biochemistry, Panjab University, Chandigarh 160 014, India.
J Biochem Mol Toxicol. 2008 Sep-Oct;22(5):363-9. doi: 10.1002/jbt.20249.
Erythrocytes are a convenient model to understand oxidative damage to the membranes induced by various xenobiotics. The objective of the present study was to investigate the propensity of atrazine to induce oxidative stress and its possible attenuation by vitamin E. Experimental animals were orally administered atrazine (300 mg kg(-1) body weight, daily) and vitamin E (100 mg kg(-1) body weight, daily) for a period of 7, 14, and 21 days. Erythrocyte membranes were prepared and analyzed for acetylcholinesterase (AChE) activity, lipid peroxidation (LPO), and lipid composition. Susceptibility of erythrocytes to atrazine exposure was further investigated in terms of morphological alterations by scanning electron microscopy (SEM). Results indicate that atrazine exposure caused a significant inhibition of AChE activity and induction of oxidative stress in terms of increased malondialdehyde (MDA) levels. Atrazine treatment significantly decreased total lipid, cholesterol, and phospholipid content of erythrocyte membranes. SEM revealed varying degrees of distortion depending on duration of atrazine exposure. However, administration of vitamin E ameliorated the oxidative stress and changes in the erythrocyte membranes induced by atrazine.
红细胞是理解各种异源生物对膜造成氧化损伤的便利模型。本研究的目的是调查莠去津诱导氧化应激的倾向以及维生素E对其可能的缓解作用。给实验动物口服莠去津（300毫克/千克体重，每日）和维生素E（100毫克/千克体重，每日），持续7、14和21天。制备红细胞膜并分析乙酰胆碱酯酶（AChE）活性、脂质过氧化（LPO）和脂质组成。通过扫描电子显微镜（SEM）从形态学改变方面进一步研究红细胞对莠去津暴露的易感性。结果表明，莠去津暴露导致AChE活性显著抑制，并在丙二醛（MDA）水平升高方面诱导氧化应激。莠去津处理显著降低了红细胞膜的总脂质、胆固醇和磷脂含量。SEM显示，根据莠去津暴露持续时间不同，红细胞膜有不同程度的变形。然而，维生素E的给药改善了莠去津诱导的氧化应激和红细胞膜变化。
