Department of Basic Science, Physiology and Pharmacology, Federal Fluminense University, Nova Friburgo, Brazil.
Clin Toxicol (Phila). 2011 Mar;49(3):153-60. doi: 10.3109/15563650.2011.564587.
The toxicity of Dieffenbachia picta, an ornamental plant, arises from its ability to cause painful edema of oral mucous membranes, buccal ulcerations, and tongue hypertrophy after chewing on the stem or contact with the sap.
We compared the anti-inflammatory effect of eugenol (2-methoxy-4-(2-propenyl)phenol) to different drugs, and investigated the role of oxalate crystals in the development of the inflammation reaction.
Tongue edema in live mice were measured with a digital tachymeter, 2 h after topical application (0.1 mL) or tissue injection (0.05 mL) of D. picta sap. The mice were treated by intraperitoneal or topical application of drugs, 15 min after edema induction. Vascular permeability was quantified based on abdominal skin plasma extravasation of Evans blue dye in response to intradermal administration of D. picta sap. The proteolytic assay was carried out as previously described (Kunitz M. Crystalline soybean trypsin inhibitor. General properties. J Gen Physiol 1947; 30:291-310.).
Arachidonate cascade antagonists and eugenol showed anti-edematogenic effects. High doses of eugenol (50 μg/kg) and sodium cromoglycate (100 mg/kg), but not a combination of the two, inhibited plasma extravasations. The sap without crystals, its methanol extract, or the ethanol-washed crystals in saline-reconstituted solution did not reproduce the tongue edema seen with the original sap. Topical application of 10% sodium bicarbonate completely abolished the tongue edema.
The inflammatory response induced by D. picta may be due to mechanical tissue damage resulting from the physical presence of calcium oxalate crystals. We were, however, unable to exclude the possibility of an insoluble toxicity present within the sap as an etiological agent. We realized that emergency treatment should also aim to inhibit antidromic vasodilation and axon reflex flare, reducing mastocyte degranulation and release of tachykinins from nerve endings. We speculate that eugenol showed better antiedematogenic results because it seems to function not only as a classic non-steroidal anti-inflammatory drug, but also as a local anesthetic, blocking neurotransmission in the damaged tissue.
观赏植物五彩千年木的毒性来自其茎部咀嚼或汁液接触后造成口腔黏膜疼痛性水肿、口腔溃殇和舌体肥大的能力。
我们比较了丁香酚（2-甲氧基-4-（2-丙烯基）苯酚）与不同药物的抗炎作用，并研究了草酸晶体在炎症反应发展中的作用。
在舌部肿胀的活鼠模型中，使用数字测时仪测量经皮（0.1 mL）或组织内注射（0.05 mL）五彩千年木汁液后 2 h 的肿胀程度。在诱导水肿 15 min 后，通过腹腔或局部应用药物进行治疗。根据皮内注射五彩千年木汁液后腹部皮肤伊文思蓝染料渗出量，量化血管通透性。蛋白酶分析如前所述（Kunitz M. 结晶大豆胰蛋白酶抑制剂。一般特性。J Gen Physiol 1947；30：291-310.）进行。
花生四烯酸级联拮抗剂和丁香酚具有抗水肿作用。高剂量丁香酚（50 μg/kg）和色甘酸钠（100 mg/kg），但不是两者的组合，可抑制血浆渗出。无晶体的汁液、其甲醇提取物或在生理盐水重悬的晶体乙醇洗脱物不能复制原汁液引起的舌水肿。局部应用 10%碳酸氢钠可完全消除舌水肿。
五彩千年木引起的炎症反应可能是由于草酸钙晶体的物理存在导致的组织机械损伤。然而，我们不能排除汁液中存在不溶性毒性物质作为病因的可能性。我们意识到，紧急治疗还应旨在抑制逆行血管扩张和轴突反射性扩张，减少肥大细胞脱颗粒和神经末梢释放速激肽。我们推测丁香酚显示出更好的抗水肿效果，因为它不仅似乎作为一种经典的非甾体抗炎药，而且作为一种局部麻醉剂，阻断受损组织中的神经传递。
