کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4529054 | 1625942 | 2015 | 8 صفحه PDF | دانلود رایگان |
• Cd2+ induces Cdc42 and MAPKs pathway related gene of Litopenaeus vannamei up-regulation.
• Reduction of THC, increase of ROS production and apoptotic cell rate were observed when the shrimps exposure to Cd2+.
• DsRNA-suppression of LvCdc42 and MAPKs during Cd2+ stress reduces the ROS production and apoptosis.
• We conclude that LvCdc42 and MAPKs play key roles in Cd2+ stress responses of shrimps.
Cadmium, one of the most toxic heavy metals in aquatic environments, has severe effects on marine invertebrates and fishes. The MAPK signaling pathway plays a vital role in stress responses of animals. The mitogen-activated protein kinase (MAPK) signaling pathway plays a vital role in animals’ stress responses, including mediation of apoptosis induced by the Rho GTPase Cdc42. However, there is limited knowledge about its function in shrimps, although disorders exacerbated by environmental stresses (including heavy metal pollution) have caused serious mortality in commercially cultured shrimps. Thus, we probed roles of Cdc42 in Litopenaeus vannamei shrimps (LvCdc42) during cadmium exposure by inhibiting its expression using dsRNA-mediated RNA interference. The treatment successfully reduced expression levels of MAPKs (including p38, JNK, and ERK). Cadmium exposure induced significant increases in expression levels of LvCdc42 and MAPKs, accompanied by reductions in total hemocyte counts (THC) and increases in apoptotic hemocyte ratios and ROS production. However, all of these responses were much weaker in LvCdc42-suppressed shrimps, in which mortality rates were higher than in controls. Our results suggest that the MAPK pathway plays a vital role in shrimps’ responses to Cd2+. They also indicate that LvCdc42 in shrimps participates in its regulation, and thus plays key roles in ROS production, regulation of apoptosis and associated stress responses.
Journal: Aquatic Toxicology - Volume 163, June 2015, Pages 89–96