The immune response of teleosts (bonefish) is altered by diazinon (DZN), an organophosphate pesticide. It has been suggested that such alteration is due to the extraneuronal cholinergic system in fish leukocytes that renders these cells a target of pesticides.

Diazoxon (DZO), the oxon metabolite of DZN, has been attributed immunotoxic effects. Still, to date there are no reports on the effects of DZO upon parameters involved in the signaling cascade of immune response cells. Therefore, this work evaluated the effect of DZO on key parameters of cell signaling (intracellular Ca²⁺ flux, ERK 1/2 phosphorylation), cell proliferation, and antiproliferative processes (apoptosis, senescence, mitochondrial membrane potential) in spleen mononuclear cells of Nile tilapia fish. The results obtained show that DZO does not affect cell proliferation but causes a lack of response to stimulation with PMA and ionomycin to release intracellular calcium. In addition, it inhibits ERK 1/2 phosphorylation and causes loss of mitochondrial membrane potential, apoptosis, and senescence. These results suggest that the lack of cell response to release intracytoplasmic Ca²⁺ inhibits ERK which disrupts the mitochondrial membrane potential, leading to cell apoptosis and senescence. These findings prove that DZO significantly affects key parameters involved in the survival of immune response cells.

硬骨鱼（骨鱼）的免疫反应被有机磷农药二嗪农（DZN）改变。已经表明，这种改变是由于鱼白细胞中的神经外胆碱能系统引起的，这些系统使这些细胞成为农药的靶标。

重氮酮（DZO）是DZN的氧代谢产物，被认为具有免疫毒性作用。但是，迄今为止，尚无关于DZO对免疫应答细胞的信号级联反应所涉及参数的影响的报道。因此，这项工作评估了DZO对细胞信号传导关键参数（细胞内Ca ²⁺尼罗罗非鱼鱼脾单核细胞中的通量，ERK 1/2磷酸化），细胞增殖和抗增殖过程（凋亡，衰老，线粒体膜电位）。获得的结果表明，DZO不会影响细胞增殖，但会引起对PMA和离子霉素刺激释放细胞内钙的反应的缺乏。此外，它抑制ERK 1/2磷酸化并导致线粒体膜电位丧失，细胞凋亡和衰老。这些结果表明缺乏对释放胞质内Ca ²⁺的细胞反应会抑制ERK，从而破坏线粒体膜电位，从而导致细胞凋亡和衰老。这些发现证明，DZO显着影响免疫应答细胞存活所涉及的关键参数。