Dai Xu-feng, Zhou Zhi-jun, Gu Xi-an, Sun Yun-guang, Zheng Guang, Zheng Jie
School of Public Health, Fudan University, Shanghai 200032, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2004 Feb;22(1):11-4.
To study the protective effect of memantine on the regulation of N-methyl-D-aspartate (NMDA) receptor in dichlorvos-poisoned rat brain, and to understand the mechanism of its role in organophosphate poisoning.
SD rats were administrated dichlorvos (25 mg/kg, ip) then three groups were treated with memantine at doses of 5, 15 and 45 mg/kg respectively. The activity of acetylcholinesterase (AChE) and binding capacity of NMDA receptor with [(3)H]MK-801 were determined 16 h after dichlorvos injection.
The time of onset of toxic symptoms in 15, 45 mg memantine treated groups [(18.40 +/- 1.14) and (21.40 +/- 1.52) min respectively] was higher than that in dichlorvos alone group [(16.75 +/- 1.62) min]; the intensity of muscle fasciculation (1.60 +/- 1.14 and 0.80 +/- 0.84, respectively) was less than that in control group (2.85 +/- 0.37); the total score of poisoning symptoms (8.80 +/- 1.79 and 9.00 +/- 2.24 respectively) was also less than that in dichlorvos group (14.60 +/- 1.70). The AChE activities both in blood and brain of memantine treated groups were not significantly different from those in dichlorvos alone group. The affinity (Kd value) and density (Bmax value) of brain NMDA receptor in dichlorvos exposed rats [(75.55 +/- 7.87) nmol/L, (0.46 +/- 0.06) pmol/mg pro respectively] were higher and lower respectively than those in control group [(37.37 +/- 4.17) nmol/L, (0.62 +/- 0.04) pmol/mg pro respectively]. Lower level of memantine (5 and 25 mg/kg) could antagonize the dichlorvos-evoked down-regulation of [(3)H]MK-801 binding to NMDA receptor in rat brain [Bmax value: (0.55 +/- 0.07) and (0.64 +/- 0.07) pmol/mg pro; Kd value: (38.68 +/- 4.54) and (32.58 +/- 3.90) nmol/L respectively] while higher dose of memantine (45 mg/kg), the Bmax (0.45 +/- 0.06) pmol/mg pro and Kd (22.88 +/- 4.42) nmol/L of NMDA receptor were significantly decreased (P < 0.01).
Memantine in certain dose range could protect against the down-regulation of NMDA receptor in rat brain, and alleviate organophosphorus poisoning symptoms to some extent. The recovery of AChE activity inhibition wasn't involved in the treatment with memantine on dichlorvos poisoning, therefore, atropine and a proper AChE reactivator (an oxime) should be used clinically.
研究美金刚对毒死蜱中毒大鼠脑内N-甲基-D-天冬氨酸(NMDA)受体调节的保护作用,探讨其在有机磷中毒中的作用机制。
给SD大鼠腹腔注射毒死蜱(25mg/kg),然后将大鼠分为三组,分别给予5、15和45mg/kg剂量的美金刚。在注射毒死蜱16小时后,测定乙酰胆碱酯酶(AChE)活性以及NMDA受体与[³H]MK-801的结合能力。
15mg/kg和45mg/kg美金刚治疗组的中毒症状出现时间[分别为(18.40±1.14)分钟和(21.40±1.52)分钟]长于单用毒死蜱组[(16.75±1.62)分钟];肌肉震颤强度[分别为1.60±1.14和0.80±0.84]低于对照组(2.85±0.37);中毒症状总分[分别为8.80±1.79和9.00±2.24]也低于毒死蜱组(14.60±1.70)。美金刚治疗组血液和脑内的AChE活性与单用毒死蜱组相比无显著差异。毒死蜱染毒大鼠脑内NMDA受体的亲和力(Kd值)[(75.55±7.87)nmol/L]高于对照组[(37.37±4.17)nmol/L],密度(Bmax值)[(0.46±0.06)pmol/mg蛋白]低于对照组[(0.62±0.04)pmol/mg蛋白]。低剂量美金刚(5mg/kg和25mg/kg)可拮抗毒死蜱引起的大鼠脑内[³H]MK-801与NMDA受体结合下调[Bmax值:(0.55±0.07)和(0.64±0.07)pmol/mg蛋白;Kd值:(38.68±4.54)和(32.58±3.90)nmol/L],而高剂量美金刚(45mg/kg)则使NMDA受体的Bmax(0.45±0.06)pmol/mg蛋白和Kd(22.88±4.42)nmol/L显著降低(P<0.01)。
美金刚在一定剂量范围内可保护大鼠脑内NMDA受体下调,并在一定程度上减轻有机磷中毒症状。美金刚治疗毒死蜱中毒未涉及AChE活性抑制的恢复,因此临床上应使用阿托品和适当的AChE复活剂(肟类)。