Bensassi Fatma, El Golli-Bennour Emna, Abid-Essefi Salwa, Bouaziz Chayma, Hajlaoui Mohamed Rabeh, Bacha Hassen
Laboratory of Research on Biologically Compatible Compounds, Faculty of Dentistry, Rue Avicenne, 5019 Monastir, Tunisia.
Toxicology. 2009 Oct 1;264(1-2):104-9. doi: 10.1016/j.tox.2009.07.020. Epub 2009 Aug 5.
The mycotoxin, deoxynivalenol (DON), is generally detected in cereal grains and grain-based food products worldwide. Therefore, DON has numerous toxicological effects on animals and humans. The present investigation was conducted to determine the molecular aspects of DON toxicity on human colon carcinoma cells (HT 29). To this aim, we have monitored the effects of DON on (i) cell viability, (ii) Heat shock protein expressions as a parameter of protective and adaptive response, (iii) oxidative damage and (iv) cell death signalling pathway. Our results clearly showed that DON treatment inhibits cell proliferation, did not induce Hsp 70 protein expression and reactive oxygen species generation. We have also demonstrated that this toxin induced a DNA fragmentation followed by p53 and caspase-3 activations. Finally, our findings suggested that oxidative damage is not the major contributor to DON toxicity. This mycotoxin induces direct DNA lesions and could be considered by this fact as a genotoxic agent inducing cell death via an apoptotic process.
霉菌毒素脱氧雪腐镰刀菌烯醇（DON）在全球范围内的谷物及谷物类食品中普遍被检测到。因此，DON对动物和人类具有多种毒理学效应。本研究旨在确定DON对人结肠癌细胞（HT 29）毒性作用的分子机制。为此，我们监测了DON对以下方面的影响：（i）细胞活力；（ii）作为保护和适应性反应参数的热休克蛋白表达；（iii）氧化损伤；（iv）细胞死亡信号通路。我们的结果清楚地表明，DON处理会抑制细胞增殖，不会诱导Hsp 70蛋白表达和活性氧生成。我们还证明，这种毒素会诱导DNA片段化，随后激活p53和caspase-3。最后，我们的研究结果表明，氧化损伤并非DON毒性的主要因素。这种霉菌毒素会诱导直接的DNA损伤，基于这一事实，它可被视为一种通过凋亡过程诱导细胞死亡的遗传毒性剂。
