UMR996 - Inflammation, Chemokines and Immunopathology, INSERM, Univ Paris-Sud, Université Paris-Saclay, 92296 Châtenay-Malabry, France.
Pierre Fabre Dermo-Cosmétique Research & Development, Toxicology Division, Safety Department, Toulouse, France.
Toxicol Sci. 2018 Jan 1;161(1):139-148. doi: 10.1093/toxsci/kfx207.
Allergic contact dermatitis is regarded as the most frequent expression of immunotoxicity in humans. Many odorant terpenes commonly used in fragrance compositions are considered as weak skin sensitizers, whereas some of their autoxidation products, allylic hydroperoxides, are classified as strong sensitizers according to the local lymph node assay. However, the mechanism of their effects on the immune system remains unclear. Since dendritic cells play a key role in allergic contact dermatitis, we studied their activation by the frequently used linalool (LINA) and limonene (LIMO), and their respective sensitizing allylic hydroperoxides (LINA-OOH, LIMO-OOH). The THP-1 cell-line was used as a surrogate for dendritic cells, the model currently employed in the validated h-CLAT in vitro test. Our data showed that allylic hydroperoxides behave differently. Both LINA-OOH and LIMO-OOH oxidized cell surface thiols 30 min after stimulation. However, the oxidative stress induced by LINA-OOH was stronger, with a higher decreased GSH/GSSG ratio and a stronger reactive species production. Moreover, LINA-OOH induced a stronger Nrf2 accumulation in correlation with nqo1 and ho-1 gene expression, 2 Nrf2 target genes. Regarding signaling pathways involved in these effects, P38 mitogen-activated protein kinase and P-ERK were activated in response to LINA-OOH but not with LIMO-OOH. CD54 and CD86 were induced 24-h postexposure. In contrast, LINA and LIMO did not modify THP-1 phenotype. This work underlies that autoxidation forming allylic hydroperoxide (ROOH) does not lead to equal chemical reactivity since LINA-OOH appears to be a stronger activator than LIMO-OOH, in regard to oxidative stress and Nrf2 pathway activation.
变应性接触性皮炎被认为是人类免疫毒性最常见的表现形式。许多常用于香料成分的萜类化合物被认为是较弱的皮肤致敏剂,而它们的一些自动氧化产物烯丙基氢过氧化物则根据局部淋巴结测定法被归类为强致敏剂。然而,它们对免疫系统的作用机制尚不清楚。由于树突状细胞在变应性接触性皮炎中起着关键作用,我们研究了它们被常用的芳樟醇(LINA)和柠檬烯(LIMO)及其各自的敏化烯丙基氢过氧化物(LINA-OOH、LIMO-OOH)激活的情况。THP-1 细胞系被用作树突状细胞的替代品,这是目前在验证的体外 h-CLAT 试验中使用的模型。我们的数据表明,烯丙基氢过氧化物的行为不同。LINA-OOH 和 LIMO-OOH 在刺激后 30 分钟内氧化细胞表面巯基。然而,LINA-OOH 诱导的氧化应激更强,GSH/GSSG 比值降低,活性物质产生更强。此外,LINA-OOH 诱导更强的 Nrf2 积累,与 nqo1 和 ho-1 基因表达相关,这是 2 个 Nrf2 靶基因。关于涉及这些作用的信号通路,P38 有丝分裂原激活蛋白激酶和 P-ERK 在响应 LINA-OOH 时被激活,但在 LIMO-OOH 时没有被激活。CD54 和 CD86 在暴露后 24 小时被诱导。相比之下,LINA 和 LIMO 不会改变 THP-1 表型。这项工作表明,自氧化形成烯丙基氢过氧化物(ROOH)并不会导致相同的化学反应性,因为 LINA-OOH 似乎比 LIMO-OOH 更强地激活,这与氧化应激和 Nrf2 途径的激活有关。