Davies R J, Butcher B T, O'Neil C E, Salvaggio J E
J Allergy Clin Immunol. 1977 Oct;60(4):223-9. doi: 10.1016/0091-6749(77)90134-8.
Toluene diisocyanate (TDI) significantly inhibits the rise in intracellular cyclic 3',5'-adenosine monophosphate (cAMP) that follows in vitro incubation of human lymphocytes with 6.7 x 10(-3) M isoproterenol and 1 x 10(-6) M prostagladin E1 (p less than 0.05). TDI has no significant effect on th production of lymphocyte cAMP following incubation with histamine (1 x 10(-3) M). The inhibitory action of TDI is greatest at a concentration of 3.3 x 10(-4) M and diminishes as the TDI concentration is increased or decreased. TDI also caused four- to fivefold stimulation of lymphocyte cAMP, an effect that is maximal at 1 x 10(-3) M, a concentration which has no significant inhibitory effect on stimulation of cAMP by isoproterenol or prostagladin E1. Conversely, 3.3 x 10(-4) M TDI, which inhibits cAMP production by isoproterenol and prostaglandin, has little stimulatory effect itself on cAMP production. This evidence suggests that TDI might induce obstructive airways disease through pharmacologic mechanisms and that TDI may be acting as a partial agonist.
甲苯二异氰酸酯（TDI）能显著抑制人淋巴细胞在体外与6.7×10⁻³M异丙肾上腺素和1×10⁻⁶M前列腺素E1孵育后细胞内环磷酸腺苷（cAMP）水平的升高（p＜0.05）。TDI与组胺（1×10⁻³M）孵育后对淋巴细胞cAMP的产生无显著影响。TDI的抑制作用在浓度为3.3×10⁻⁴M时最大，随着TDI浓度的增加或降低而减弱。TDI还能使淋巴细胞cAMP增加4至5倍，这种作用在1×10⁻³M时最大，该浓度对异丙肾上腺素或前列腺素E1刺激cAMP无显著抑制作用。相反，抑制异丙肾上腺素和前列腺素产生cAMP的3.3×10⁻⁴M TDI本身对cAMP的产生几乎没有刺激作用。这一证据表明，TDI可能通过药理机制诱发阻塞性气道疾病，并且TDI可能作为一种部分激动剂发挥作用。
