The University of New Mexico College of Pharmacy, Department of Pharmaceutical Sciences, Albuquerque, NM, USA.
Toxicol Appl Pharmacol. 2010 Jun 15;245(3):344-51. doi: 10.1016/j.taap.2010.03.020. Epub 2010 Mar 28.
Polycyclic aromatic hydrocarbons (PAHs) and arsenic are both environmental agents that are known to have significant immunotoxicity. Previous studies have shown that PAH exposure of spleen cells in vitro produces significant immune suppression of humoral immunity, especially when P450 activation products are examined. Exposure to arsenic, particularly sodium arsenite, has also been found to be suppressive to antibody responses in vitro and in vivo. The purpose of the present studies was to examine the immunotoxicity of PAHs and arsenite following coexposures with the theory being that the agents may exert synergistic actions, which might be based on their different mechanisms of action. Spleen cells were isolated from male C57BL/6J wild-type mice and treated with PAHs and/or arsenic (arsenite or arsenate). Immunotoxicity assays were used to assess the T-dependent antibody response (TDAR) to sheep red blood cells (SRBCs), measured by a direct plaque-forming cell (PFC) assay. Cell viability was measured by trypan blue staining. Spleen cell viability was not altered following 4 days of PAH and/or arsenic treatment. However, the TDAR demonstrated suppression by both PAHs and arsenic in a concentration-dependent manner. p53 was also induced by NaAsO(2) (As(3)(+)) and PAHs alone or in combination. The PAHs and their metabolites investigated included benzo[a]pyrene (BaP), BaP-7,8-diol, BaP-7,8-diol-9,10-epoxide (BPDE), 7,12-dimethylbenz[a]anthracene (DMBA), DMBA-3,4-diol, dibenzo[a,l]pyrene (DB[a,l]P). PAH metabolites were found to be more potent than parent compounds in producing immunosuppression and inducing p53 expression. Interestingly, DB[a,l]P, a potent carcinogenic PAH not previously characterized for immunotoxicity, was also found to be strongly immunosuppressive. Arsenite (NaAsO(2), As(3)(+)) was found to produce immunosuppression at concentrations as low as 0.5 microM and was immunosuppressive at a 10-fold lower concentration than sodium arsenate (Na(2)HAsO(4), As(5)(+)). Coexposure of spleen cell cultures to PAHs and As(3)(+), both at individual low-effect concentrations, was found to produce profound suppression of the TDAR demonstrating synergy between these two chemical classes of agents.
多环芳烃 (PAHs) 和砷都是已知具有显著免疫毒性的环境因素。先前的研究表明,体外暴露于脾细胞中的多环芳烃会显著抑制体液免疫,尤其是当检查 P450 激活产物时。体外和体内研究还发现,砷暴露,特别是亚砷酸钠,对抗体反应具有抑制作用。本研究的目的是研究 PAHs 和亚砷酸盐共同暴露后的免疫毒性,理论上这些因素可能会产生协同作用,这可能基于它们不同的作用机制。从雄性 C57BL/6J 野生型小鼠中分离脾细胞,并使用 PAHs 和/或砷(亚砷酸盐或砷酸盐)处理。使用直接溶血空斑形成细胞 (PFC) 测定法评估 T 依赖性抗体反应 (TDAR) 来评估免疫毒性测定,以绵羊红细胞 (SRBC) 作为测定指标。通过台盼蓝染色测量细胞活力。在 4 天的 PAH 和/或砷处理后,脾细胞活力没有改变。然而,TDAR 显示出 PAHs 和砷以浓度依赖的方式抑制。p53 也被 NaAsO(2) (As(3)(+)) 和 PAHs 单独或联合诱导。研究中包括的 PAHs 及其代谢物包括苯并[a]芘 (BaP)、BaP-7,8-二醇、BaP-7,8-二醇-9,10-环氧化物 (BPDE)、7,12-二甲基苯并[a]蒽 (DMBA)、DMBA-3,4-二醇、二苯并[a,l]芘 (DB[a,l]P)。与母体化合物相比,PAH 代谢物在产生免疫抑制和诱导 p53 表达方面更为有效。有趣的是,DB[a,l]P,一种以前未被表征为免疫毒性的强致癌 PAH,也被发现具有很强的免疫抑制作用。亚砷酸盐 (NaAsO(2),As(3)(+)) 已被发现可在低至 0.5μM 的浓度下产生免疫抑制作用,其免疫抑制作用比砷酸钠 (Na(2)HAsO(4),As(5)(+)) 低 10 倍。在个体低效应浓度下共同暴露于脾细胞培养物中的 PAHs 和 As(3)(+) 被发现可显著抑制 TDAR,表明这两种化学类别的试剂之间存在协同作用。