Mass mortality is often observed in cultured oysters during the period following spawning in the summer season. To examine the underlying causes leading to this phenomenon, thermotolerance of the Pacific oyster Crassostrea gigas was assessed using pre- and postspawning oysters that were sequentially treated with sublethal (37°C) and lethal heat shocks (44°C). The effects were examined on a range of immune and metabolic parameters in addition to mortality rate. A preventative 37°C significantly reduced oyster mortality after exposure to a second heat shock of 44°C, but in postspawning oysters mortality remained at 80%, compared with < 10% in prespawning oysters. Levels of the 72 kDa and 69 kDa heat shock proteins were low in the gill tissue from postspawning oysters stimulated by heat shock, indicating spawning reduced heat shock protein synthesis. The postspawning oysters had depleted glycogen stores in the mantle tissue and reduced adenylate energy charge after heat shock, indicative of lower energy for metabolic activity. A cumulative effect of spawning and heat shock was observed on the immunocompetence of oysters, demonstrated by reduced hemocyte phagocytosis and hemolymph antimicrobial activity. These results support the hypothesis that the energy expended during reproduction compromises the thermotolerance and immune status of oysters, leaving them easily subject to mortality if heat stress occurs in postspawning stage. This study improves our understanding of oyster summer mortality and has implications for the long-term persistence of mollusks under the influence of global warming.
A 9‐week feeding experiment was conducted to evaluate the effects of dietary vitamin E supplementation on growth, lipid peroxidation and fatty acid composition of black sea bream fed oxidized oil. The FL and OL diets contained fresh fish oil and oxidized oil, respectively, without additional vitamin E supplementation. Another four α‐tocopherol levels (150, 250, 450 and 800 mg kg−1 diet) were used within the OL diet, giving a total of six experimental diets. Fish were hand‐fed to apparent satiation twice daily. At end of the trial, the weight gain and survival rate of fish were significantly reduced by diets with oxidized oil, whereas hepatosomatic index was remarkably high in fish fed oxidized oil diet. However, vitamin E supplementation to diet significantly improved growth performance and increased vitamin E content in the liver. Although, liver thiobarbituric acid reactive substances and docosahexaenoic acid were significantly increased by dietary oxidized oil, their levels were reduced by dietary vitamin E supplementation. Our results indicate that the fish were performing the best at intermediate concentrations of α‐tocopherol and a dose of >150 mg α‐tocopherol kg−1 diet could reduce lipid peroxidation and improve fish growth performance when oxidized oils exist in diet.
Three isonitrogenous diets containing 60 g kg–1, 90 g kg–1 or 120 g kg–1 lipid were formulated and fed to the Litopenaeus vannamei (2.00 ± 0.08 g) under two salinities (25 or 3 psu) in triplicate for 8 weeks. Shrimp fed 90 g kg–1 lipid had higher weight gain and specific growth rate than shrimp fed the other two diets regardless of salinity, and the hepatosomatic index increased with increasing dietary lipid at both salinities. The shrimp at 3 psu had significantly lower survival and ash content, higher condition factor, weight gain and specific growth rate than the shrimp at 25 psu. Increasing dietary lipid level induced the accumulation of serum MDA regardless of salinity, and at 3 psu, it reduced the serum GOT and GPT activities and the mRNA expression of TNF‐α in intestine and gill of L. vannamei. The hepatopancreatic triacylglycerol lipase (TGL) and CPT‐1 mRNA expression showed the highest value in shrimp fed 90 g kg–1 lipid diet at 3 psu. This study indicates that 120 g kg–1 dietary lipid may negatively affect the growth and induce oxidative damage in shrimp, but can improve immune defence at low salinity; 60 g kg–1 dietary lipid cannot afford the growth and either has no positive impact on the immunology for L. vannamei at 3 psu.