Study On Calcium Signaling And Endoplasmic Reticulum Damage Of Coelomocytes During UV-induced Autolysis In Sea Cucumber

Sea cucumber is an important marine invertebrate, and shows high nutritional values. However, sea cucumber possesses strong ability of autolysis, which leads to huge economic losses. In this paper, we investigate coelomocytes calcium signaling and endoplasmic reticulum injury in cucumber autolysis process. Sea cucumber does not have the immune system, the immune stress responses of individuals rely mainly on immune function coelomocytes to complete, so the research coelomocytes immunological characteristics in cucumber cells autolysis process is important. Calciumions as an inner major cell messenger involved and regulate many physiological activities of cells and tissues, including metabolism, muscle contraction, secretion and cell division, so this experiment study calcium changes in sea cucumber autolysis process, with a view to sea cucumber autolysis mechanism to do some basic research.In this paper, using TEM to observe the microstructure changes in coelomocytes including damage of the endoplasmic reticulum and apoptosis characteristic structure, using flow cytometry detecting the change of apoptosis rate statistically in sea cucumber autolysis process detected; Finally, using flow cytometry and LCSM through Fluo-3/AM detecting changes in the concentration of calcium in sea cucumber autolysis process and detecting calcium transport-related endoplasmic reticulum calcium pump Ca²⁺-ATP enzyme activity changes.Calcium overload is a important initiation factor caused by apoptosis, Studies have shown that calcium concentration in coelomocytes increased as sea cucumber autolysis process occurs, fresh coelomocytes apoptosis rate of less than 5% and the rate of apoptosis 4h autolysis cucumbers up to 20%; Endoplasmic reticulum serious injury substantially dissolved after 4h; Apoptotic pathway probably mainly by the damage caused by the endoplasmic reticulum, the endoplasmic reticulum pathway induced apoptosis.