Abstract：
The intertidal organism Tegillarca granosa can survive under frequent hypoxia/reoxygenation (H/R) exposure. Sulfides as accompanying products in benthic hypoxic environments, may play an important regulatory role, but the mechanisms are not well understood. This article investigated the physiological and molecular changes of T. granosa after adding different concentrations of sulfides (0.1, 0.5, 1 mM) at 72 h into a 120-h exposure to hypoxia, as well as the recovery state of 24 h of reoxygenation. The results indicated that H/R stress induces ROS production and mild mitochondrial depolarization in clams, and sulfide can participate in its regulation. Among them, a low concentration of sulfide up-regulated glutathione content and alternative oxidase activity, maintained the stability of antioxidant enzymes, and up-regulated the expression of the survival genes XIAP/BCL-xl which mediate cell survival via the NFκB signaling pathway. High concentrations of sulfide had a significant inhibitory effect on the p38/MPAK pathway and inhibited intrinsic apoptosis caused by ROS accumulation during reoxygenation. Taken together, our study suggested that different concentrations of sulfides are involved in regulating the endogenous apoptosis of clams during H/R.
摘要：
潮间带生物Tegilarcagranosa可以在频繁的缺氧/复氧（H/R）暴露下存活。硫化物作为底栖缺氧环境中的伴随产品，可以发挥重要的调节作用，但是机制还没有得到很好的理解。本文研究了T.granosa在低氧暴露120h后，在72h添加不同浓度的硫化物（0.1，0.5，1mM）后的生理和分子变化。以及24h复氧的恢复状态。结果表明，H/R胁迫可诱导蛤仔体内ROS的产生和线粒体轻度去极化，硫化物可以参与其调节。其中,低浓度的硫化物上调谷胱甘肽含量和替代氧化酶活性，保持抗氧化酶的稳定性，并上调存活基因XIAP/BCL-xl的表达，这些基因通过NFκB信号通路介导细胞存活。高浓度的硫化物对p38/MPAK通路有明显的抑制作用，并抑制复氧过程中ROS积累引起的内源性细胞凋亡。一起来看,我们的研究表明，在H/R过程中，不同浓度的硫化物参与调节蛤仔内源性凋亡。
