We studied the effects of the tartrazine-metabolite sulfanilic acid on the physiology of pancreatic AR42J cells. Sulfanilic acid (1 μM-1 mM) induced a slow and progressive increase in intracellular free-calcium concentration that reached a plateau. The effect of sulfanilic acid was not concentration-dependent. Stimulation of cells with thapsigargin (1 μM) after treatment with sulfanilic acid (1 mM) induced a smaller Ca²⁺ response compared with that obtained with thapsigargin alone. Sulfanilic acid induced a concentration-dependent production of reactive oxygen species; however, this effect was not Ca²⁺-dependent. Depolarization of mitochondrial membrane potential was observed at the concentration of 1 mM sulfanilic acid. In the presence of the compound a decrease in the GSH/GSSG ratio was observed. A decrease in the expression of superoxide dismutase 2 was noted. Finally, stimulation of cells with CCK-8 led to a concentration-dependent increase of trypsin secretion that was impaired by pretreatment of cells with sulfanilic acid. Preincubation of cells with the antioxidant melatonin (100 μM) reduced the effect of sulfanilic acid on trypsin secretion. We conclude that sulfanilic acid might induce oxidative stress, which could alter Ca²⁺ signaling and enzyme secretion in pancreatic AR42J cells. This creates a situation potentially leading to damage of the exocrine pancreas.

我们研究了酒石黄素代谢物磺胺酸对胰腺AR42J细胞生理的影响。磺胺酸（1μM-1mM）诱导细胞内游离钙浓度缓慢而逐步升高，并达到稳定水平。磺胺酸的作用不是浓度依赖性的。与仅用thapsigargin相比，用磺胺酸（1 mM）处理后用thapsigargin（1μM）刺激细胞引起较小的Ca ²⁺响应。磺胺酸引起浓度依赖性的活性氧生成；但是，这种作用不是Ca ²⁺-依赖。在1 mM磺胺​​酸的浓度下观察到线粒体膜电位的去极化。在化合物存在下，观察到GSH / GSSG比降低。注意到超氧化物歧化酶2的表达降低。最后，用CCK-8刺激细胞会导致胰蛋白酶分泌的浓度依赖性增加，而磺胺酸预处理会削弱胰蛋白酶的分泌。用抗氧化剂褪黑激素（100μM）对细胞进行预培养会降低磺胺酸对胰蛋白酶分泌的影响。我们得出的结论是，磺胺酸可能诱导氧化应激，这可能会改变胰腺AR42J细胞中的Ca ²⁺信号传导和酶分泌。这造成了潜在地导致外分泌胰腺受损的情况。