Abstract: We investigated the toxic effects of ammonia-N on juvenile lined seahorse (Hippocampus erectus). The half lethal concentration of ammonia-N to lined seahorses for 96 hours (96 h LC₅₀) was evaluated under normal oxygen level (4.32-5.12 mg·L^-1) and high oxygen level (8.22-9.46 mg·L^-1), respectively. We examined the histopathological changes of gill and liver of juvenile lined seahorses under ammonia-N stress (control, 6, 9, 12 mg·L^-1). The results showed that the 96h LC₅₀ of ammonia-N and non-ionic ammonia to juvenile lined seahorses at normal oxygen level was 10.22 and 0.16 mg·L^-1, with a safe concentration of 1.02 and 0.016 mg·L^-1, respectively. When treated with high dissolved oxygen, the 96h LC₅₀ of ammonia-N and nonionic ammonia to juvenile lined seahorses increased to 12.68 and 0.2 mg·L^-1, with a safety upper limit of 1.27 and 0.02 mg·L^-1, respectively. The juvenile lined seahorses exposed to ammonia displayed histopathologic abnormalities in gill and liver, which were dependent on dose and duration. AmmoniaN stress caused gill lesions, including telangiectasis, vascular congestion and fracture, necrosis of epithelial cell and hyperplasia of chloride cells. Nucleomegaly, hepatocytes swelling, sinusoids dilatation and blurred cell contour were observed in liver. The enhancement of ammonia-N stress increased liver lesions, causing hydropic degeneration, dissolution and vacuolation of hepatocytes, resulting in loose organization of hepatic tissue. In summary, ammonia nitrogen stress above threshold to juvenile lined seahorse would damage the structure of gill and liver tissue. Appropriately increasing the concentration of dissolved oxygen could effectively alleviate the toxicity of ammonia N on juvenile lined seahorse.

Key words: yield., pepper, rhizosphere soil environment, grafting, root-borne disease