Laboratório de Bioquímica Farmacológica, Centro de Biotecnologia, Universidade Federal do Rio Grande do Sul (UFRGS), Av. Bento Gonçalves, 9500, Cep 91501-970, Porto Alegre, RS, Brazil.
Toxicon. 2013 Nov;74:179-92. doi: 10.1016/j.toxicon.2013.08.061. Epub 2013 Aug 29.
The clinical manifestations of Lonomia obliqua caterpillar envenomation are systemic hemorrhage and acute kidney injury. In an effort to better understand the physiopathological mechanisms of envenomation, a rat model was established to study systemic tissue damage during L. obliqua envenomation. An array of acute venom effects was characterized, including biochemical, hematological, histopathological, myotoxic and genotoxic alterations. Rapid increases in serum alanine and aspartate transaminases, γ-glutamyl transferase, lactate dehydrogenase, hemoglobin, bilirubin, creatinine, urea and uric acid were observed, indicating that intravascular hemolysis and liver and kidney damage had occurred. Treatment with a specific antivenom (antilonomic serum) for up to 2 h post-venom injection neutralized the biochemical alterations. However, treatment after 6 h post-venom injection failed to normalize all biochemical parameters, despite its efficacy in reversing coagulation dysfunction. The hematological findings were consistent with hemolytic anemia and neutrophilic leukocytosis. The histopathological alterations were mainly related to hemorrhage and inflammation in the subcutaneous tissue, lung, heart and kidneys. Signs of congestion and hemosiderosis were evident in the spleen, and hemoglobin and/or myoglobin casts were also detected in the renal tubules. Increased levels of creatine kinase and creatine kinase-MB were correlated with the myocardial necrosis observed in vivo and confirmed the myotoxicity detected in vitro in isolated extensor digitorum longus muscles. Significant DNA damage was observed in the kidneys, heart, lung, liver and lymphocytes. The majority of the DNA lesions in the kidney were due to oxidative damage. The results presented here will aid in understanding the pathology underlying Lonomia's envenomation.
褐钩鳞青斑蛾毛虫螫伤的临床表现为全身性出血和急性肾损伤。为了更好地了解螫伤的病理生理机制,建立了大鼠模型来研究褐钩鳞青斑蛾毛虫螫伤时的全身性组织损伤。研究了一系列急性毒液效应,包括生化、血液学、组织病理学、肌毒性和遗传毒性改变。观察到血清丙氨酸和天冬氨酸转氨酶、γ-谷氨酰转移酶、乳酸脱氢酶、血红蛋白、胆红素、肌酐、尿素和尿酸迅速升高,表明发生了血管内溶血和肝肾功能损伤。在毒液注射后 2 小时内用特定的抗毒液(抗褐钩鳞青斑蛾血清)治疗可中和生化改变。然而,在毒液注射后 6 小时后进行治疗,尽管能逆转凝血功能障碍,但未能使所有生化参数正常化。血液学发现与溶血性贫血和中性粒细胞白细胞增多一致。组织病理学改变主要与皮下组织、肺、心脏和肾脏的出血和炎症有关。脾脏可见充血和含铁血黄素沉着,肾小管中也检测到血红蛋白和/或肌红蛋白管型。肌酸激酶和肌酸激酶-MB 水平升高与体内观察到的心肌坏死相关,并证实了在离体伸趾长肌中检测到的肌毒性。肾脏、心脏、肺、肝脏和淋巴细胞均观察到明显的 DNA 损伤。肾脏中的大多数 DNA 损伤是由于氧化损伤所致。本文的结果将有助于了解褐钩鳞青斑蛾螫伤的病理基础。