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作为补钙剂的钙尔奇对有机磷化合物所致迟发性神经毒性的影响。

The effect of Calcicol as calcium tonic on delayed neurotoxicity induced by organophosphorus compounds.

作者信息

Piao Fengyuan, Yamauchi Toru, Ma Ning

机构信息

Department of Public Health, School of Medicine, Mie University, 2-174 Edobashi, Tsu, Mie-Pref. 514-8507, Japan.

出版信息

Toxicol Lett. 2003 Jun 5;143(1):65-71. doi: 10.1016/s0378-4274(03)00072-9.

DOI:10.1016/s0378-4274(03)00072-9
PMID:12697382
Abstract

To examine whether delayed neuropathy is prevented or alleviated when Ca is administered to experimental animals before or after organophosphorus compounds (OPs) dosing, we observed the effects of Calcicol administration as a calcium tonic on delayed neurotoxicity by OPs in hens. The hens (n=28) were randomly divided into seven groups (four in each group). One group received glycerol formal as vehicle group, two groups received 30 mg/kg leptophos or 40 mg/kg triortho-cresyl phosphate (TOCP) (L group and T group), two groups received 2.4 mg/kg Ca(2+) (0.3 ml/kg Calcicol) 24 h before leptophos or TOCP administration, and the last two groups received 2.4 mg/kg Ca after leptophos or TOCP administration, respectively. Although delayed polyneuropathy induced by OPs could not be prevented completely by Calcicol, the clinical signs of organophosphorus-induced delayed neuropathy (OPIDN) in hens that received Calcicol soon before or after OPs administration were less severe than those in hens that received only OPs and there were significant differences in OPIDN score between groups (P<0.05). This shows that polyneuropathy and the recovery function of nerves and muscles suffering from polyneuropathy can be alleviated, as long as calcium tonic is administered before the clinical signs develop. This study offers hope of recovery to humans who are exposed to these OPs because of work, attempted suicide, accidental ingestion or other accidents, etc. Meanwhile, our results indicate further that there is a relationship between a decrease in Ca(2+) concentration in tissues and induction of delayed neuropathy.

摘要

为了研究在给实验动物施用有机磷化合物(OPs)之前或之后给予钙,是否可以预防或减轻迟发性神经病变,我们观察了作为钙补充剂的Calcicol对母鸡中OPs所致迟发性神经毒性的影响。将母鸡(n = 28)随机分为七组(每组四只)。一组接受福尔马林甘油作为赋形剂组,两组分别接受30mg/kg的溴苯磷或40mg/kg的磷酸三邻甲苯酯(TOCP)(L组和T组),两组在给予溴苯磷或TOCP前24小时接受2.4mg/kg的Ca²⁺(0.3ml/kg Calcicol),最后两组分别在给予溴苯磷或TOCP后接受2.4mg/kg的Ca。虽然Calcicol不能完全预防OPs诱导的迟发性多发性神经病,但在OPs给药之前或之后不久接受Calcicol的母鸡中,有机磷诱导的迟发性神经病(OPIDN)的临床症状比仅接受OPs的母鸡轻,并且组间OPIDN评分存在显著差异(P<0.05)。这表明,只要在临床症状出现之前给予钙补充剂,多发性神经病以及患有多发性神经病的神经和肌肉的恢复功能就可以得到缓解。这项研究为因工作、自杀未遂、意外摄入或其他事故等接触这些OPs的人类带来了康复的希望。同时,我们的结果进一步表明,组织中Ca²⁺浓度的降低与迟发性神经病的诱导之间存在关联。

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