TY - JOUR
T1 - Pathway of deoxynivalenol-induced apoptosis in human colon carcinoma cells
AU - Bensassi, Fatma
AU - Golli, Emna
AU - Abid-Essefi, Salwa
AU - Bouaziz, Chayma
AU - Hajlaoui, Mohamed Rabeh
AU - Bacha, Hassen
PY - 2009/10/1
Y1 - 2009/10/1
N2 - 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.
AB - 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.
KW - Apoptosis
KW - DNA damage
KW - DON
KW - Hsp 70
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=69649097529&partnerID=8YFLogxK
U2 - 10.1016/j.tox.2009.07.020
DO - 10.1016/j.tox.2009.07.020
M3 - Article
C2 - 19664677
AN - SCOPUS:69649097529
SN - 0300-483X
VL - 264
SP - 104
EP - 109
JO - Toxicology
JF - Toxicology
IS - 1-2
ER -