硒对T-2毒素引起培养软骨细胞超微结构与功能改变的拮抗作用

The Antagonistic Effect of Se on the T-2 Toxin-induced Changes of Ultrastructure and Function of Cultured Chicken Embryo Chondrocyte

当培养液中存在0.01ppmT-2毒素时,可引起离体培养鸡胚软骨细胞胞外基质胶原微原纤维和质膜P面膜内蛋白颗粒明显减少,线粒体内膜细胞色素c氧化酶活力和H^+-ATP酶活力及其对OIigomycin敏感性明显下降。在0.01ppmT-2毒素存在下,加入1ppm Na_2SeO_3到培养液中,则胶原微原纤维和质膜膜内蛋白颗粒的减少不再呈现,细胞色素c氧化酶活力和H^+-ATP酶活力及其对Oligomycin敏感性的下降幅度明显减小。这些结果表明硒能够显著的拮抗T-2毒素引起的软骨细胞超微结构和功能的改变。从亚细胞水平和分子水平为阐明缺硒是大骨节病发病的重要条件和硒在预防大骨节病中的作用机理提供了依据。

The T-2 toxin was extracted from strain of Fusarium tricinetum, which is similar in structure with the Fusarinm mycotoxin found in grains in Kashin-Beck disease(KBD) area. When 0.01 ppm T-2 toxin was added to cultured media, it resulted in a significant decrease of the collagen microfibrils in extracellular matrix and LMPs(intramembrane particles) on P-face of plasma membrane of chicken embryo chondrocytes. T-2 toxin obviously reduced the mitochondrial activities of cytochrome c oxidase and H^+-ATPase. And the sensitivity to oligomycin of H^+-ATPase was also decreased. Adding of lppm Na_2SeO_3 in the presence of 0.011ppm T-2 toxin, the decrease of collagen microfibrils and IMPs on P-face of plasma membrane could not be seen. And the activities of cytochrome c oxidase、H^+-ATPase and the sensitivity to oligomycin of H^+-ATPase were less decreased. These results showed that Se can obviously antagonize the T-2 toxin-induced changes of ultrastructrue and function of chondrocytes and that Se deficiency was an important condition for the pathogenesis of KBD. the mechanism for the preventive effect of Se on KBD could be elucidated in subcellular and molecular level.