Saafi Emna Behija, Louedi Mouna, Elfeki Abdelfattah, Zakhama Abdelfattah, Najjar Mohamed Fadhel, Hammami Mohamed, Achour Lotfi
Laboratoire de Biochimie, UR Nutrition Humaine et Désordres Métaboliques, Faculté de Médecine, 5000 Monastir, Tunisia.
Exp Toxicol Pathol. 2011 Jul;63(5):433-41. doi: 10.1016/j.etp.2010.03.002. Epub 2010 Mar 31.
Nowadays, people's exposure to chemical compounds such as organophosphorus insecticides is continuously on the rise more and more. Theses compounds have induced an excessive production of free radicals which are responsible for several cell alterations in the organism. Recent investigations have proved the crucial role of nutritional antioxidants to prevent the damage caused by toxic compounds. In this study, we investigate the role of date palm fruit extract (Phoenix dactylifera L.) in protection against oxidative damage and hepatotoxicity induced by subchronic exposure to dimethoate (20mg/kg/day). Oral administration of dimethoate caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases, alkaline phosphatase, gamma-glutamyl transferase and lactate dehydrogenase), as well as in hepatic malondialdehyde thus causing drastic alteration in antioxidant defence system. Particularly, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were found increased by dimethoate while catalase (CAT) activity was reduced significantly. These biochemical alterations were accompanied by histological changes marked by appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in liver section. Pretreatment with date palm fruit extract restored the liver damage induced by dimethoate, as revealed by inhibition of hepatic lipid peroxidation, amelioration of SOD, GPx and CAT activities and improvement of histopathology changes. The present findings indicate that in vivo date palm fruit may be useful for the prevention of oxidative stress induced hepatotoxicity.
如今,人们接触有机磷杀虫剂等化合物的情况越来越多。这些化合物会诱导自由基过度产生,而自由基会导致机体出现多种细胞改变。最近的研究证明了营养抗氧化剂在预防有毒化合物造成损害方面的关键作用。在本研究中,我们探究了枣椰果提取物(Phoenix dactylifera L.)在预防由亚慢性接触乐果(20毫克/千克/天)引起的氧化损伤和肝毒性方面的作用。口服乐果会导致肝毒性,这可通过肝脏标志物酶(转氨酶、碱性磷酸酶、γ-谷氨酰转移酶和乳酸脱氢酶)水平的升高以及肝脏丙二醛水平的升高来监测,从而导致抗氧化防御系统发生剧烈改变。特别是,发现乐果会使超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)的活性增加,而过氧化氢酶(CAT)的活性则显著降低。这些生化改变伴随着组织学变化,肝脏切片中出现空泡化、坏死、充血、炎症以及肝血窦扩大。枣椰果提取物预处理可恢复乐果诱导的肝脏损伤,这表现为抑制肝脏脂质过氧化、改善SOD、GPx和CAT活性以及改善组织病理学变化。目前的研究结果表明,枣椰果在体内可能有助于预防氧化应激诱导的肝毒性。