Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Denver, Aurora, Colorado, United States of America.
Department of Pathology, School of Medicine, University of Colorado Denver, Aurora, Colorado, United States of America.
PLoS One. 2014 Jan 8;9(1):e85402. doi: 10.1371/journal.pone.0085402. eCollection 2014.
To identify effective therapies against sulfur mustard (SM)-induced skin injuries, various animals have been used to assess the cutaneous pathology and related histopathological changes of SM injuries. However, these efforts to establish relevant skin injury endpoints for efficacy studies have been limited mainly due to the restricted assess of SM. Therefore, we employed the SM analog nitrogen mustard (NM), a primary vesicating and bifunctional alkylating agent, to establish relevant endpoints for efficient efficacy studies. Our published studies show that NM (3.2 mg) exposure for 12-120 h in both the hairless SKH-1 and haired C57BL/6 mice caused clinical sequelae of toxicity similar to SM exposure in humans. The NM-induced cutaneous pathology-related structural changes were further analyzed in this study and quantified morphometrically (as percent length or area of epidermis or dermis) of skin sections in mice showing these lesions. H&E stained skin sections of both hairless and haired mice showed that NM (12-120 h) exposure caused epidermal histopathological effects such as increased epidermal thickness, epidermal-dermal separation, necrotic/dead epidermis, epidermal denuding, scab formation, parakeratosis (24-120 h), hyperkeratosis (12-120 h), and acanthosis with hyperplasia (72-120 h). Similar NM exposure in both mice caused dermal changes including necrosis, edema, increase in inflammatory cells, and red blood cell extravasation. These NM-induced cutaneous histopathological features are comparable to the reported lesions from SM exposure in humans and animal models. This study advocates the usefulness of these histopathological parameters observed due to NM exposure in screening and optimization of rescue therapies against NM and SM skin injuries.
为了寻找有效的治疗方法来对抗硫芥(SM)引起的皮肤损伤,人们使用了各种动物来评估 SM 损伤的皮肤病理学和相关组织病理学变化。然而,由于 SM 的限制,这些建立相关皮肤损伤终点的努力主要受到了限制。因此,我们采用 SM 类似物氮芥(NM),一种原发性发泡剂和双功能烷化剂,来建立有效的疗效研究相关终点。我们发表的研究表明,NM(3.2mg)暴露于无毛 SKH-1 和有毛 C57BL/6 小鼠 12-120 小时会导致类似于人类暴露于 SM 后的毒性临床后遗症。本研究进一步分析了 NM 诱导的皮肤病理学相关结构变化,并对显示这些病变的小鼠皮肤切片进行了形态计量学(以表皮或真皮的长度或面积百分比)定量。H&E 染色的无毛和有毛小鼠皮肤切片显示,NM(12-120 小时)暴露会导致表皮组织病理学效应,如表皮厚度增加、表皮-真皮分离、坏死/死亡表皮、表皮剥落、结痂形成、角化过度(24-120 小时)、角化过度(12-120 小时)和棘层肥厚伴增生(72-120 小时)。在这两种小鼠中,类似的 NM 暴露还会导致真皮变化,包括坏死、水肿、炎症细胞增多和红细胞外渗。这些 NM 诱导的皮肤组织病理学特征与报告的 SM 暴露在人类和动物模型中的损伤相似。这项研究主张,由于 NM 暴露而观察到的这些组织病理学参数在筛选和优化 NM 和 SM 皮肤损伤的救援疗法方面是有用的。