The effects of acute and chronic exposure to semicarbazide were carried out on the sea cucumber Apostichopus japonicus. A half-maximal lethal concentration of 3.72 g/L of semicarbazide hydrochloride (95% confidence interval 3.43–4.02 g/L) was deduced. At 20, 4, and 2% of the half-maximal lethal concentrations, a 28-days exposure induced morphological alterations, oxidative stress, and acetylcholinesterase (AChE) activity in the respiratory tree, intestinal tract, and longitudinal muscle of A. japonicus. Exposure to 20% of the half-maximal lethal concentration resulted in lesions in the respiratory tree and disintegration in the intestinal tract. Exposure to lower concentration induced a gradual accumulation of lesions in the respiratory tree, intestinal tract, and longitudinal muscle. Levels of markers of oxidative stress and neurotransmission, including superoxide dismutase (SOD), catalase, and AChE, were increased during the initial days of exposure and then decreased. The activity of SOD, catalase, and AChE were highest in A. japonicus exposed to 4%, followed by 20 and 2% of the half-maximal lethal concentration at the same time. At the later stages of the 28-days exposure, marker levels were decreased and close to levels in the control groups. Non-targeted metabolomics indicated that significantly different metabolites were screened out, 28 in the positive ion mode and 38 in the negative ion mode, impairments in neurological function, osmotic pressure regulation, energy metabolism, and protein digestion and absorption following exposure of A. japonicus to semicarbazide. KEGG pathway enrichment showed that the exposure affected pathways related to ABC transporters, central carbon metabolism in cancer, protein digestion and absorption, aminoacyl-tRNA biosynthesis, and biosynthesis of unsaturated fatty acids.
Differential Expression of miRNAs in the Respiratory Tree of the Sea Cucumber Apostichopus japonicus Under Hypoxia Stress
