Laboratório de Toxinologia, Departamento de Ciências Fisiológicas, Universidade de Brasília, Instituto de Ciências Biológicas, Brasília 70910-900, DF, Brazil.
Toxicon. 2013 Jan;61:129-38. doi: 10.1016/j.toxicon.2012.11.008. Epub 2012 Nov 21.
In the present study we conducted proteomic and pharmacological characterizations of the venom extracted from the Brazilian tarantula Acanthoscurria paulensis, and evaluated the cardiotoxicity of its two main fractions. The molecular masses of the venom components were identified by mass spectrometry (MALDI-TOF-MS) after chromatographic separation (HPLC). The lethal dose (LD(50)) was determined in mice. Nociceptive behavior was evaluated by intradermal injection in mice and the edematogenic activity by the rat hind-paw assay. Cardiotoxic activity was evaluated on in situ frog heart and on isolated frog ventricle strip. From 60 chromatographic fractions, 97 distinct components were identified, with molecular masses between 601.4 and 21,932.3 Da. A trimodal molecular mass distribution was observed: 30% of the components within 500-1999 Da, 38% within 3500-5999 Da and 21% within 6500-7999 Da. The LD(50) in mice was 25.4 ± 2.4 μg/g and the effects observed were hypoactivity, anuria, constipation, dyspnea and prostration until death, which occurred at higher doses. Despite presenting a dose-dependent edematogenic activity in the rat hind-paw assay, the venom had no nociceptive activity in mice. Additionally, the venom induced a rapid blockage of electrical activity and subsequent diastolic arrest on in situ frog heart preparation, which was inhibited by pretreatment with atropine. In the electrically driven frog ventricle strip, the whole venom and its low molecular mass fraction, but not the proteic one, induced a negative inotropic effect that was also inhibited by atropine. These results suggest that despite low toxicity, A. paulensis venom can induce severe physiological disturbances in mice.
在本研究中，我们对巴西狼蛛 Acanthoscurria paulensis 提取的毒液进行了蛋白质组学和药理学表征，并评估了其两个主要部分的心脏毒性。通过色谱分离（HPLC）后，通过质谱（MALDI-TOF-MS）鉴定了毒液成分的分子质量。在小鼠中测定致死剂量（LD50）。通过在小鼠皮内注射评估痛觉行为，通过大鼠后爪试验评估水肿活性。在原位青蛙心脏和分离的青蛙心室条上评估心脏毒性活性。从 60 个色谱馏分中，鉴定出 97 种不同的成分，其分子质量在 601.4 至 21,932.3 Da 之间。观察到三模态分子质量分布：30%的成分在 500-1999 Da 之间，38%在 3500-5999 Da 之间，21%在 6500-7999 Da 之间。在小鼠中的 LD50 为 25.4±2.4 μg/g，观察到的效应是活动减少、无尿、便秘、呼吸困难和衰竭，直到死亡，高剂量时发生。尽管在大鼠后爪试验中呈现出剂量依赖性的水肿活性，但毒液在小鼠中没有痛觉活性。此外，毒液在原位青蛙心脏制备物上迅速引起电活动阻断和随后的舒张期阻滞，这种阻滞可被阿托品预处理抑制。在电驱动的青蛙心室条上，整个毒液及其低分子质量部分，但不是蛋白质部分，引起负性肌力作用，这种作用也可被阿托品抑制。这些结果表明，尽管毒性低，但 A. paulensis 毒液可在小鼠中引起严重的生理紊乱。
