Toxicity Of Mycotoxins To BHK Cell And Its Action Mechanisms

This paper reviews discuss the effect of OchratoxinA,AflatoxinB1 and Zralenone,Deoxynivalenol,Fumonisin and T-2 toxin on the viability and its action mechanisms were studied using BHK-cells as empirical model. The theoretic evidence will provide for later study and clinical research.Cell viability was test by MTT assay, cell DNA damage by Single cell gel electrophoresis, SCGE assay, cell apoptosis by DNA Ladder method, SOD activity by xanthine oxidase assay and MDA value in cell cultured solution by TBA assay. The results showed that, a dose-and time-dependent inhibitory effect of OTA on cell viability were observed on BHK cells. Cell viability was significantly decreased after 12 hours exposure to 2.5,5,10,20 and 40μg.mL-1 OTA(P<0.05).24 hours after treated with 40μg.mL-1OTA, nearly 90% of the cell viability were lose. DNA damage was increased as comPared with that observed in untreated control. Average tail length and the tail rate in each treated group were significantly enhanced compared with that in the control (P＜0.01), excePt 2.5μg.mL-1 OTA treated group.40μg.mL-1 OTA led to a 80-fold increase of the tail rate vs. control. The activity of SOD decreased significantly (P<0.05), on the contrary MDA concentration increased greatly (P＜0.05) in each toxin group. The activity of SOD of the high dose group (40μg.mL-1 OTA) have only one fourth,though MDA concentration increased 5 times that of the control at 24 hours after exPosure. DNA Ladder was detected in the experiment treated with 40μg.mL-1 OTA for 24 h.BHK cells were incubated in the presence of AFB1 after 24 hours. Cell viability was significantly decreased exposure to 2.5,5,10,20 and 40μg.mL-1 AFB1 (P<0.05),40μg.mL-1AFB1, nearly 70% of the cells were died. DNA damage was increased as compared with that observed in untreated control. Average tail length and the tail rate in each treated group were significantly enhanced comPared with that in the control (P＜0.01), excePt 2.5μg.mL-1 AFB1 treated group.40μg.mL-1 AFB, led to a 70-fold increase of the tail rate vs.control. The activity of SOD decreased significantly (P<0.05), and MDA concentration increased greatly (P<0.01) in each toxin group on the contrary. MDA concentration of the high dose group(40μg.mL-1 AFB1) increased 7 times that of the control at both 12 hours and 24 hours after exPosure. DNA Ladder was not detected in the experiment. These results indicated that the increasing concentration of lipid peroxiation in the cells after exposure to AFB1 and decreasing activity of SOD led the liPid Peroxiation to accumulate in the cells. At the same time, with increasing AFB1 concentration and exPosure time, DNA damage was more and more severe.Zralenone,Deoxynivalenol,Fumonisin and T-2 toxin significantly decreased viability of BHK-cells (P＜0.05). Nearly 95% of the cells treated with 40μg.mL-1ZEA were died after 24 hours. The extent of DNA damage in the four mycotoxins treated cells was significant increased, The tail rate of 40μg.mL-1 Fu group was up to more than 80-fold of that in control group. DNA Ladder was detected in the experiment with 40μg.mL-1 OTA for 24 h. The activity of SOD decreased significantly (P<0.05), on the contrary MDA concentration increased greatly (P<0.05) in each toxin group. The activity of SOD of the high dose group (40μg.mL-1 DON) have only one fifth.Though MDA concentration increased 10 times with 1μg.mL-1 T-2 that of the control at 24 hours after exposure.These results demonstrate that the increasing concentration of lipid peroxiation and decreasing activity of SOD induced by the six mycotoxins effect a change in cell viability. Moreover, the six mycotoxins led to DNA damage, finally it induced cell aPoPtosis.