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目的探讨湿热环境下氰化物毒性作用变化规律及其对组织氧化应激反应的影响。方法以小动物湿热环境试验箱模拟高温高湿环境,测定不同温、湿度[温度(Ta)(20±0.5)℃、相对湿度(50±5)%,温度36℃及38℃、相对湿度(RH)(60±3)%]条件下氰化钠经腹腔注射KM小鼠的LD50。另将30只SD大鼠随机分为常温对照、常温中毒、湿热对照、湿热中毒及药物预防组,各组受试动物分别按以下因素单一或联合处理:(1)湿热应激:模拟箱内[温度(38±0.5)℃,相对湿度(60±3)%]60 min;(2)氰中毒:动物腹腔注射氰化钠3.6 mg/kg;(3)药物预防:给予谷胱甘肽、维生素C灌胃5 d。各组受试动物于热应激后60 min和(或)中毒30 min后测定脑、肝组织匀浆超氧化物歧化酶(superoxide dismutase,SOD)活性和丙二醛(malondialdehyde,MDA)含量。结果与20℃,RH50%时KM小鼠氰化钠中毒LD50(4.77 mg/kg)相比,(36±0.5)℃或(38±0.5)℃,RH 60%湿热环境中毒动物的LD50分别下降至4.66 mg/kg(P>0.05)及4.17 mg/kg(P<0.05)。20℃RH 50%条件下NaCN中毒后肝、脑组织SOD活力下降(P<0.01),MDA含量增加(P<0.01),而38℃RH 60%环境下NaCN中毒所致氧化应激改变更明显(P<0.01)。药物预防可缓解相同条件下上述指标的改变(P<0.01)。结论暴露于湿热环境下,小鼠氰化纳中毒的LD50可随环境温度的升高而降低。湿热环境和(或)氰化钠中毒两因素均可导致氧化应激指标的明显改变,二者同时作用可能具有联合效应。服用抗氧化药物可提高组织抗氧化应激能力。
Objective To investigate the change of cyanide toxicity and its effect on the tissue oxidative stress in hot and humid environment. Methods The temperature and humidity (Ta (20 ± 0.5) ℃, relative humidity (50 ± 5)%, temperature 36 ℃ and 38 ℃, relative humidity ( RH) (60 ± 3)%] sodium cyanide intraperitoneal injection of KM mice LD50. Another 30 SD rats were randomly divided into room temperature control, room temperature poisoning, damp heat control, damp heat poisoning and drug prevention group, the animals in each group were treated individually or in combination according to the following factors: (1) (2) cyanosis: intraperitoneal injection of sodium cyanide 3.6 mg / kg; (3) drug prevention: given glutathione, Vitamin C orally 5 d. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in brain homogenate and liver homogenate were measured at 60 min and / or 30 min after heat stress in each group. Results LD50 of (36 ± 0.5) ℃ or (38 ± 0.5) ℃, RH 60% of damp heat environment poisoning animals were lower than that of KM mice sodium cyanide poisoning LD50 (4.77 mg / kg) To 4.66 mg / kg (P> 0.05) and 4.17 mg / kg (P <0.05) respectively. The activity of SOD in liver and brain decreased (P <0.01) and the content of MDA increased (P <0.01) after NaCN poisoning at 20 ℃ RH 50%, while the change of oxidative stress induced by NaCN poisoning was more obvious under the condition of 38 ℃ RH 60% (P <0.01). Drug prevention can alleviate the above conditions under the same conditions (P <0.01). Conclusion The LD50 of mouse sodium cyanide poisoning decreased with the increase of ambient temperature when exposed to hot and humid environment. Both hot and humid environment and (or) sodium cyanide poisoning can lead to significant changes in the indicators of oxidative stress, both of which may have a combined effect. Taking anti-oxidant drugs can improve tissue antioxidant capacity.