Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Toxicol Mech Methods. 2012 Oct;22(8):638-47. doi: 10.3109/15376516.2012.716090.
Diazinon (DZN) is an organophosphate pesticide widely used in agricultural to control insects and in veterinary medicine to control ectoparasites. This study investigated the induction of oxidative stress in the brain, heart, and spleen of Wistar and Norway rats treated with acute doses of DZN. Female Wistar and Norway rats were treated with 25, 50, 100, and 200 mg/kg of DZN by intraperitoneal injection. The animals were sacrificed 24 h after treatment, and tissues were isolated and analyzed. The result of this study shows that DZN at higher doses increased the level of malondialdehyde, superoxide dismutase and glutathione S-transferase activities and decreased glutathione (GSH) level, lactate dehydrogenase, and cholinesterase activities in the brain, heart, and spleen of both rat strains. At these concentrations, DZN toxicity also lead to a significant decrease in catalase (CAT) activity in all tissues of Wistar rat and brain of Norway rat, while it increased heart CAT activity in Norway rat. However, the alteration of these parameters was observed at lower doses of DZN in Wistar rat. These results suggest that DZN at higher doses induces the production of free radicals and oxidative stress in rat tissues and strains by alteration of antioxidant enzyme activity, depletion of GSH, and increasing lipid peroxidation. Induction of oxidative stress in DZN-treated rats is in the order of brain > heart > spleen. Wistar rats appear to be more sensitive to the effects of DZN on oxidative stress induction compared to Norway rat.
敌敌畏（DZN）是一种广泛应用于农业控制昆虫和兽医控制外寄生虫的有机磷农药。本研究调查了急性剂量敌敌畏处理的 Wistar 和挪威大鼠的大脑、心脏和脾脏的氧化应激诱导。雌性 Wistar 和挪威大鼠通过腹腔注射用 25、50、100 和 200mg/kg 的 DZN 处理。在处理后 24 小时，处死动物并分离和分析组织。该研究的结果表明，较高剂量的 DZN 增加了两种大鼠大脑、心脏和脾脏中丙二醛、超氧化物歧化酶和谷胱甘肽 S-转移酶活性的水平，并降低了谷胱甘肽（GSH）水平、乳酸脱氢酶和胆碱酯酶活性。在这些浓度下，DZN 毒性还导致 Wistar 大鼠所有组织和挪威大鼠大脑中的过氧化氢酶（CAT）活性显著降低，而 CAT 活性在挪威大鼠的心脏中增加。然而，在 Wistar 大鼠中，较低剂量的 DZN 观察到这些参数的改变。这些结果表明，较高剂量的 DZN 通过改变抗氧化酶活性、耗尽 GSH 和增加脂质过氧化，在大鼠组织和品系中诱导自由基产生和氧化应激。在 DZN 处理的大鼠中，诱导氧化应激的顺序为大脑>心脏>脾脏。与挪威大鼠相比，Wistar 大鼠似乎对 DZN 诱导氧化应激的影响更为敏感。
