Our previous study showed that percutaneous sulfur mustard (SM) exposure induced pulmonary toxicity, which was attenuated by DRDE-07 (S-2[2-aminoethylamino] ethyl phenyl sulphide) pretreatment. The present study aimed to evaluate the protective efficacy of DRDE-07 and its analogues viz., DRDE-30 (S-2(2-aminoethyl amino)ethyl propyl sulphide) and DRDE-35 (S-2(2-aminoethyl amino)ethyl butyl sulphide) against SM. Thirty minutes before percutaneous SM (0.8 LD₅₀) exposure, female Swiss mice were orally gavaged with DRDE-07 and its analogues(0.2 LD₅₀). Animals were sacrificed on day 3 and 7, BAL fluid (BALF) and lung tissue were collected for biochemical, histopathological studies. As results, DRDE-07 and its analogues were beneficial in reducing the number of BALF inflammatory cells, protein level, lactate dehydrogenase (LDH) activity, myeloperoxidase (MPO) and β-glucuronidase activity, while content of BALF and lung reduced glutathione level (GSH) were significantly protected. The pretreatment of DRDE-07 and its analogues inhibited the recruitment of inflammatory cells into the lung. The beneficial effects of DRDE-07 and its analogues were attributed to their antioxidant and anti-inflammatory activity. Among the analogues, DRDE-30 exhibited significant beneficial effects as compared to the other two compounds. These analogues may be considered as prototype candidate molecules as there is no effective antidote for SM toxicity.

我们以前的研究表明，经皮硫芥（SM）暴露会引起肺部毒性，而DRDE-07（S-2 [2-氨基乙基氨基]乙基苯基硫醚）预处理可减轻这种毒性。本研究旨在评估DRDE-07及其类似物的保护功效。，针对SM的DRDE-30（S-2（2-氨基乙基氨基）乙基丙基硫）和DRDE-35（S-2（2-氨基乙基氨基）乙基丁基硫）。在经皮SM（0.8 LD ₅₀）暴露前30分钟，对雌性瑞士小鼠口服DRDE-07及其类似物（0.2 LD ₅₀）。在第3天和第7天处死动物，收集BAL液（BALF）和肺组织用于生化，组织病理学研究。结果，DRDE-07及其类似物有利于减少BALF炎性细胞的数量，蛋白质水平，乳酸脱氢酶（LDH）活性，髓过氧化物酶（MPO）和β-葡萄糖醛酸苷酶活性，而BALF和肺的含量降低了谷胱甘肽水平（ GSH）受到显着保护。DRDE-07及其类似物的预处理抑制了炎症细胞向肺的募集。DRDE-07及其类似物的有益作用归因于其抗氧化和抗炎活性。在类似物中，与其他两种化合物相比，DRDE-30表现出显着的有益作用。