Łukaszewicz-Hussain Anna
Zakład Toksykologii, Uniwersytet Medyczny w Białymstoku, Białystok, Poland.
Med Pr. 2012;63(5):559-64.
Toxicity of organophosphate insecticides is mainly due to the inhibition of acetylcholinesterase (AChE). However, organophosphate insecticides in acute, as well as in chronic and subchronic intoxication may lead to oxidative stress causing the enhancement of lipid peroxidation and changing the activities of antioxidative enzymes. Paraoxonase PON1 is synthesized by the liver. This enzyme hydrolyzes organophosphate compounds, phospholipid hydroperoxides and cholesterol ester hydroperoxides. Its role as an antioxidant has also been suggested. For this reason the aim of the work was to estimate the activity of paraoxonase and the level of serum lipid peroxides in the rats subchronically intoxicated with chlorpyrifos.
The animals received chlorpyrifos at a single daily dose of 0.2, 2 or 5 mg/kg b.w./day for 14 days. For biochemical determinations of paraoxonase activity in serum of rats, Aryloesterase/Paraoksonase Assay Kit (ZeptoMetrix Corporation Buffalo, USA) and for lipid peroxides level, LPO-586 (OXIS International, Foster City, Calif., USA) were used.
Chlorpyrifos administration resulted in a decreased activity of paraoxonase in serum. The highest decrease was observed after administration of chlorpyrifos in doses 2 and 5 mg/kg b.w./day. In the intoxication with the highest insecticide dose under study the decreased paraoxonase activity was accompanied by the increased level of lipid peroxides.
In view of the literature data, the finding that low doses of chlorpyrifos lead to statistically significant decrease in paraoxonase activity in serum of rats provides evidence that exposure to organophosphate insecticides induces oxidative stress. It also suggests the need to take into consideration a possible development of arteriosclerosis, hypercholesterolemia and diabetes mellitus in people exposed to these compounds.
有机磷杀虫剂的毒性主要源于对乙酰胆碱酯酶（AChE）的抑制作用。然而，有机磷杀虫剂在急性、慢性及亚慢性中毒时，均可能导致氧化应激，从而增强脂质过氧化作用，并改变抗氧化酶的活性。对氧磷酶PON1由肝脏合成。该酶可水解有机磷化合物、磷脂氢过氧化物及胆固醇酯氢过氧化物。其作为抗氧化剂的作用也已得到证实。因此，本研究旨在评估亚慢性毒死蜱中毒大鼠的对氧磷酶活性及血清脂质过氧化物水平。
动物每日单次接受剂量为0.2、2或5mg/kg体重/天的毒死蜱，持续14天。对于大鼠血清中对氧磷酶活性的生化测定，使用了芳基酯酶/对氧磷酶检测试剂盒（美国纽约州布法罗市ZeptoMetrix公司）；对于脂质过氧化物水平的测定，使用了LPO - 586（美国加利福尼亚州福斯特城OXIS国际公司）。
毒死蜱给药导致血清中对氧磷酶活性降低。在给予2和5mg/kg体重/天剂量的毒死蜱后，观察到对氧磷酶活性下降最为明显。在研究的最高杀虫剂剂量中毒时，对氧磷酶活性降低伴随着脂质过氧化物水平升高。
根据文献数据，低剂量毒死蜱导致大鼠血清中对氧磷酶活性出现统计学显著下降这一发现，证明了接触有机磷杀虫剂会引发氧化应激。这也表明，对于接触这些化合物的人群，需要考虑动脉粥样硬化、高胆固醇血症和糖尿病等疾病可能的发展情况。
