Chitooligosaccharide supplementation in low-fish meal diets for Pacific white shrimp (Litopenaeus vannamei): Effects on growth, innate immunity, gut histology, and immune-related genes expression.

This study evaluated the effects of supplementing chitooligosaccharide (COS) in low fish meal (FM) diets on growth, immune response, intestine and hepatopancrease histology, and expression of inflammatory and immune-related genes in Pacific white shrimp (Litopenaeus vannamei). A basal diet was formulated using FM and soybean meal (SM) as primary protein sources and considered as a high FM (HFM) diet, then a low FM (LFM) diet was prepared by substituting 50% of FM with SM and supplemented with 0, 0.3, 0.6, 0.9, 1.2 or 1.5 g COS kg-1 diet (LFM, COS3, COS6, COS9, COS12 and COS15 diets). Each diet was fed to quadruplicate groups of shrimp (0.9 g) to apparent satiation three times daily for eight weeks. At the end of the experiment no significant changes in growth and survival rate were observed among treatments (P > 0.05). FM replacement led to significant (P < 0.05) reduction of serum lysozyme activity and significant improvements were obtained by adding 0.3 or 0.6 g kg-1 COS to the LFM diet. A significant decrease in nitric oxide synthase activity was found in LFM group and no beneficial effects could be achieved by COS application. LFM group showed higher hepatopancrease superoxide dismutase and glutathione peroxidase activities than HFM group and further enhancements were obtained by COS application. Hepatopancrease total antioxidant capacity and alkaline phosphatase activity decreased in LFM group and COS supplementation improved their values. Expression of lysozyme, crustin, Pen3 and proPo genes were significantly up-regulated in hepatopancrease of groups received 0.3-0.9 g COS kg-1 diet. FM substitution enhanced the expression of HSP70 and inflammatory genes such as AIF and TNF in hepatopancrease and intestine, and COS administration at a moderate level down-regulated their expression level. Remarkable enhancement in intestinal fold height was obtained by inclusion of 0.3 or 0.6 g COS kg-1 diet compared to the group received LFM diet. Shrimps fed HFM and COS containing diets exhibited higher number of E-cells within their hepatopancrease tubules than the LFM group. The findings in this study clearly demonstrated that COS could enhance non-specific immune response and antioxidant activity, and ameliorate the negative impacts of high SM diets on gut and hepatopancrease health in pacific white shrimp. The optimum inclusion level of COS seems to be 0.3-0.6 g kg-1 of diet.

R492X mutation in PTEN-induced putative kinase 1 induced cellular mitochondrial dysfunction and oxidative stress.

The identification of rare monogenic forms of Parkinson's disease (PD) has provided tremendous insights into the molecular pathogenesis of the disorder. Mitochondrial dysfunction and oxidative stress are thought to play a prominent role in the pathogenesis of PD, but how the monogenic mutation gene causes the disease onset or progression is largely unknown. In this study we investigated the effects of wild-type and R492X mutation in the PTEN-induced putative kinase 1 (PINK1). Cell cultures show that R492X PINK1 mutation induces the generation of cellular reactive oxidative species (ROS), degrades cell membrane potential, causes cytochrome C (Cyt.C) release from mitochondrial to cytoplasm, attenuates mitochondrial complex I activity, and lastly, causes changes in mitochondrial numbers and morphology; especially when cells are treated with 1-Methyl-4-phenylpyridinium ion (MPP(+)). Our results suggest that the R492X mutation can cause mitochondrial dysfunction and oxidative stress and can associate with MPP(+) to induce mitochondrial dysfunction and oxidative stress.