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目的通过研究大鼠急性羰基镍中毒后肺脏、肝脏和心脏Ca2+-Mg2+-ATP酶活性变化,探讨急性羰基镍中毒对脏器损伤的机制。方法 SD大鼠静态吸入方式染毒一次,染毒时间为30 min,其中羰基镍染毒低剂量组为20 mg/m3、中剂量组为135 mg/m3、高剂量组为250 mg/m3,并设氯气染毒组,染毒浓度为250 mg/m3,并设正常对照组,染毒后分别于1、2、3和7 d应用化学显色法测定肺脏、肝脏和心脏Ca2+-Mg2+-ATP酶活性变化。结果低、中、高剂量羰基镍染毒后,肺脏、肝脏和心脏Ca2+-Mg2+-ATP酶活性均有下降,以高剂量组下降最为明显(P<0.05);氯气染毒组也显著下降(P<0.05);羰基镍染毒不同的时间段下,肺脏、肝脏、心脏Ca2+-Mg2+-ATP酶活性于1 d时已开始降低、3 d降低最为明显,7 d时渐升高;氯气染毒组大鼠肝脏和心脏以2 d时降低最为明显。结论羰基镍可通过抑制肺脏、肝脏和心脏Ca2+-Mg2+-ATP酶活性导致细胞内钙稳态失调,引起组织器官细胞损伤。
OBJECTIVE: To investigate the mechanism of acute carbonyl nickel poisoning on the organ injury in rats by studying the changes of Ca2 + -Mg2 + -ATPase activity in lung, liver and heart after acute carbonyl nickel poisoning in rats. Methods SD rats were exposed to static inhalation once and the exposure time was 30 min, in which the low-dose nickel carbonyl group was 20 mg / m 3, the middle-dose group was 135 mg / m 3, the high-dose group was 250 mg / m 3, The rats in the control group were treated with chlorine. The concentration of the Ca2 + -Mg2 + - ATPase in the lung, liver and heart was measured at 1, 2, 3 and 7 d after exposure. ATPase activity changes. Results The activity of Ca2 + -Mg2 + -ATP in lung, liver and heart decreased after administration of carbonyl nickel in low, medium and high doses, and decreased most significantly in high-dose group (P <0.05). Chlorine exposure also significantly decreased P <0.05). The activity of Ca2 + -Mg2 + -ATPase in the lung, liver and heart started to decrease at 1 d after the nickel carbonyl treatment and decreased most significantly at 3 d and gradually increased at 7 d. The toxicity of the liver and heart in rats at 2 d decreased the most obvious. Conclusion Carbonyl nickel can cause the imbalance of intracellular calcium homeostasis by inhibiting the activity of Ca2 + -Mg2 + -ATP in the lung, liver and heart, resulting in cell injury of tissues and organs.