Study On The Toxic Effects Of DCOIT On Nile Tilapia (Oreochromis Niloticus) And Pacific White Shrimp(Litopenaeus Vannamei)

DCOIT(4,5-dichloro-2-n-octyl-4-isothiazolin-3-one)is the main component of Sea-Nine211,a new antifouling agent to replace tributyltin(TBT)because of its fast degradation and high antifouling activity.Despite its high degradation capacity,DCOIT still accumulates in the environment,with a concentration of 3.3?g/L (environment concentration)detected in seawater from the Spanish marinas.Previous studies have shown that environment concentration of DCOIT can affect non-target organisms(rodents,mollusks,bony fishes,etc.)and damage the nervous conduction,endocrine and reproductive systems of animals.However,there are still some limitations in related studies.Firstly,there is a lack of in-depth research on the effect of DCOIT on the energy metabolism of aquatic animals.Secondly,only DCOIT is available to evaluate the acute toxicity of Marine decapod,but the study on the toxicity mechanism is lacking.Thirdly,considering the increasingly extensive application of DCOIT and its unstable degradation capacity,it is necessary to explore the toxic effects and mechanism of high concentration DCOIT on aquatic animals.Therefore,this study explores the different concentrations of DCOIT toxicity and metabolic effects on bony fishes Nile tilapia(Oreochromis niloticus)and large decapoda Pacific white shrimp(Litopenaeus vannamei),from growth,physiological,histological,molecular and transcriptional levels.This work advances theunderstanding of the toxic mechanism of DCOIT,which is necessary for its evaluation.This study also bring new thinking on the toxicity mechanism of antifouling agent.The results and conclusions of this study are as follows:1.Study on the toxic effects of antifouling agent DCOIT on Nile tilapiaTo explore the toxic and metabolic effects of different concentrations of DCOIT on Nile tilapia(Oreochromis niloticus),as well as the role of endoplasmic reticulum stress(ER stress)in mediating its toxicity and metabolic changes,this experiment was carried out on the male Nile tilapia DCOIT acute(4 d)and chronic(28 d)exposure experiment(0,3,15,and 30?g/L DCOIT),and explored the toxicity from behavioral,respiratory rate,nerve signal transduction,energy metabolism,ER stress and liver histology.In addition,Nile tilapia hepatocytes were exposed to 0,3,15,30,300?g/L DCOIT for 24 hours to determine ER stress levels.The results showed that after 4 days of acute DCOIT exposure,the hyper-locomotor activities of tilapia in the 15?g/L and 30?g/L DCOIT exposure group was significantly reduced(P<0.05),and the respiration rate of tilapia in the 15?g/L and 30?g/L DCOIT exposure group was significantly increased(P<0.05).ER stress induced by acute exposure to 3?g/L DCOIT leads to accumulation of triglycerides(TG)in the liver of tilapia.After 28 days of chronic exposure,chronic ER stress leads to pathological changes in the liver of tilapia.At the cellular level,300?g/L DCOIT can induce ER stress in hepatocytes.In addition,after 4 days of acute exposure,DCOIT will cause the change of AChE in tilapia brain,thus leading motor behavior disruption.In this study,it was pointed out that after tilapia was exposed to DCOIT,there was a significant change in energy metabolism and impaired nerve transmission,and there was a direct link between DCOIT-induced endoplasmic reticulum function and lipid metabolism.This study demonstrates that DCOIT significantly changed the energy metabolism and impaired the nerve transmission,and that changes in lipid metabolism are directly related to endoplasmic reticulum function after exposure to an antifouling agent.2.Study on the toxic effects of antifouling agent DCOIT on Pacific white shrimpTo explore the toxic effect of different concentrations of DCOIT on Pacific white shrimp(Litopenaeus vannamei),this study took juvenile shrimp as the research object and conducted a 28 days exposure experiment of DCOIT(0,3,15,30?g/L),to explore the toxicity of DCOIT on shrimp at the level of growth,physiology,tissue and transcriptome.This study showed that exposure to 30?g/L DCOIT significantly reduced the survival and weight gain of L.vannamei(P<0.05),and enhanced the activity of Na~+/K~+-ATPase(P<0.05).Melanin deposition was found in the gills of L.vannamei exposed to DCOIT at 15 and 30?g/L.In addition,the levels of lactic acid(LD),triglyceride(TG)and pyruvate in the hepatopancreas of L.vannamei exposed to30?g/L DCOIT were significantly higher than those in the control group(P<0.05),and the hepatopancreas exposed to 15 and 30?g/L DCOIT showed structural damage.Hepatopancreatic transcriptome results showed that compared with 3?g/L DCOIT exposure,15?g/L DCOIT exposure showed more differential expressed genes(DEGs),involving two biological processes:starch and sucrose metabolism,and choline metabolism in cancer.This study indicates that L.vannamei is sensitive to the antifouling agent DCOIT and DCOIT can induce toxic reaction by affecting gene expression at the concentration of 15?g/L and interfere shrimp metabolism,growth and survival at 30?g/L.3.Comparison of toxic effects of antifouling agent DCOIT on fish and shrimpCombined with the results of this study and the reported relevant literature,the study compared the toxic effects of DCOIT on fish and shrimp.Firstly,in terms of growth and survival,L.vannamei was more sensitive to DCOIT,while tilapia showed better resistance and adaptability.Secondly,after exposure to DCOIT,lipid metabolism disorders occurred to varying degrees in the liver of fish and the hepatopancreas of L.vannamei.The possible cause of lipid metabolism disorders in fish was that DCOIT induced ER stress and excessive vitellogenin(VTG),while that in shrimp still needs to be further explored.Thirdly,tilapia and L.vannamei have different biological pathways to resist DCOIT chronic exposure,with protein processing in endoplasmic reticulum in tilapia,while starch and sucrose metabolism pathway in L.vannamei.Fourthly,DCOIT causes blackgill symptoms in L.vannamei and is even visible to the naked eye,which is not found in fish.Fifthly,DCOIT can also affect the nerve conduction system of bony fish,thus affecting the behavior of fish.DCOIT interferes with fish endocrine by activating estrogen in bony fish.DCOIT can also be toxic to the reproductive system of fish.However,little research has been done on the toxic effects of DCOIT on the nervous,endocrine and reproductive systems of shrimp.In conclusion,due to the difference in physiological structure between bony fish and shrimp,DCOIT has different toxic effects on them.However,studies on the toxicity of DCOIT on shrimp are very limited,and more information on the toxicity of shrimp is needed to comprehensively compare the toxic effects of DCOIT on fish and shrimp.