How Japanese eels escape from the stomach of a predatory fish.

Predation shapes diversity in the defensive tactics of prey. One specialized defensive tactic is to escape the digestive system of the predator after capture1,2,3,4,5,6,7,8. While most of these defensive tactics involve passive ejection alive from predators' mouths and vents1,2,3,4,5, active escape from the digestive tracts of predators has recently been observed in certain invertebrate species6,7 and fish8. However, no study has yet uncovered the behavioral patterns and escape routes of the prey within a predator's digestive tract. Here, we report the sequential escape processes of the Japanese eel Anguilla japonica from capture to escape via the gills of predatory fish Odontobutis obscura using an X-ray video system. All captured eels had at least one portion of their bodies swallowed into the stomach of the predator. Surprisingly, after being swallowed, most individuals attempted to escape by going back up the digestive tract towards the esophagus and gill, and some of them succeeded in escaping via the predator's gill. Some eels, whose entire bodies were completely inside the stomach, exhibited circling behavior along the stomach, seemingly searching for possible escape routes. An electro-anesthetization experiment revealed that eels utilize various escape routes through gill clefts, rather than just one.

Environmental DNA Reveals Geographic Distributions of Two eel Species, Anguilla japonica and A. marmorata, in Western Kyushu, Japan.

Some anguillid eels migrate thousands of kilometers from their spawning grounds, dispersing across vast geographic areas to fresh and brackish water habitats, where they settle and grow. Japanese eels (Anguilla japonica) and giant mottled eels (A. marmorata) are both found in Japan, although their distributions differ, and their exact distributions are poorly known. We assumed that topographic distribution patterns of Japanese and giant mottled eels must differ among and within rivers along the northwest coast of Kyushu, Japan. Environmental DNA (eDNA) analysis was conducted at 87 sites in 23 rivers. Japanese eel eDNA was detected in 19 rivers (82.6%) and that of giant mottled eels was detected in eight (34.8%). We detected giant mottled eel eDNA in five rivers where they were previously unknown. eDNA for Japanese eels was detected at six of nine sites in the north (66.7%), 13 of 23 sites in Omura (56.5%), and 37 of 55 sites in the south (67.3%). In contrast, giant mottled eel eDNA was detected at one of nine sites in the north (11.1%), no sites in Omura, and 15 of 55 sites in the south (27.3%). There was no correlation between eDNA concentrations of the two species at 10 sites in the five rivers where eDNA of both species was detected. These findings suggest differences in the distribution of the two eel species and the northern distributional limit of giant mottled eels in the area facing the East China Sea.

Transcriptional regulation of the Japanese flounder Cu,Zn-SOD (Jfsod1) gene in RAW264.7 cells during oxidative stress caused by causative bacteria of edwardsiellosis.

Edwardsiellosis is one of the most important bacterial diseases in fish, sometimes causing extensive economic losses in the aquaculture industry. Our previous studies demonstrated that the Cu,Zn-SOD (sod1) activity has significantly increased in Japanese flounder, Paralichthys olivaceus, hepatopancreas infected by causative bacteria of edwardsiellosis Edwardsiella tarda NUF251. In this study, NUF251 stimulated intracellular superoxide radical production in mouse macrophage RAW264.7 cells, which was reduced by N-acetylcysteine. This result suggests that NUF251 infection causes oxidative stress. To evaluate the regulatory mechanism of Jfsod1 at transcriptional levels under oxidative stress induced by NUF251 infection, we cloned and determined the nucleotide sequence (1124 bp) of the 5'-flanking region of the Jfsod1 gene. The sequence analysis demonstrated that the binding sites for the transcription factors C/EBPα and NF-IL6 involved in the transcriptional regulation of the mammalian sod1 gene existed. We constructed a luciferase reporter system with the 5'-flanking region (-1124/-1) of the Jfsod1 gene, and a highly increased transcriptional activity of the region was observed in NUF251-infected RAW264.7 cells. Further studies using several mutants indicated that deletion of the recognition region of NF-IL6 (-272/-132) resulted in a significant decrease in the transcriptional activity of the Jfsod1 gene in NUF251-infected RAW264.7 cells. In particular, the binding site (-202/-194) for NF-IL6 might play a major role in upregulating the transcriptional activity of the 5'-flanking region of the Jfsod1 gene in response to oxidative stress induced by NUF251 infection. These results could be provided a new insight to understand the pathogenic mechanism of causative bacteria of edwardsiellosis.

The reciprocal regulation between mitochondrial-associated membranes and Notch signaling in skeletal muscle atrophy.

Skeletal muscle atrophy and the inhibition of muscle regeneration are known to occur as a natural consequence of aging, yet the underlying mechanisms that lead to these processes in atrophic myofibers remain largely unclear. Our research has revealed that the maintenance of proper mitochondrial-associated endoplasmic reticulum membranes (MAM) is vital for preventing skeletal muscle atrophy in microgravity environments. We discovered that the deletion of the mitochondrial fusion protein Mitofusin2 (MFN2), which serves as a tether for MAM, in human induced pluripotent stem (iPS) cells or the reduction of MAM in differentiated myotubes caused by microgravity interfered with myogenic differentiation process and an increased susceptibility to muscle atrophy, as well as the activation of the Notch signaling pathway. The atrophic phenotype of differentiated myotubes in microgravity and the regenerative capacity of Mfn2-deficient muscle stem cells in dystrophic mice were both ameliorated by treatment with the gamma-secretase inhibitor DAPT. Our findings demonstrate how the orchestration of mitochondrial morphology in differentiated myotubes and regenerating muscle stem cells plays a crucial role in regulating Notch signaling through the interaction of MAM.

Astaxanthin Exerts Immunomodulatory Effect by Regulating SDH-HIF-1α Axis and Reprogramming Mitochondrial Metabolism in LPS-Stimulated RAW264.7 Cells.

Astaxanthin (AX) is a carotenoid that exerts potent antioxidant activity and acts in cell membranes and mitochondria, which consist of the bilayer molecules. Targeting mitochondria to ameliorate inflammatory diseases by regulating mitochondrial metabolism has become possible and topical. Although AX has been shown to have anti-inflammatory effects in various cells, the mechanisms are quite different. In particular, the role of AX on mitochondrial metabolism in macrophages is still unknown. In this study, we investigated the effect of AX on mitochondria-mediated inflammation and its mechanisms in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. AX attenuated the mitochondrial O2- production and maintained the mitochondrial membrane potential, implying that AX preserved mitochondrial homeostasis to avoid LPS stimulation-induced mitochondrial dysfunction. Additionally, AX prevented the decrease in mitochondrial complexes I, II, and III, which were caused by LPS stimulation. Especially, AX inhibited the reduction in mitochondrial succinate dehydrogenase (SDH; complex II) activity and upregulated the protein and mRNA level of SDH complex, subunit B. Furthermore, AX blocked the IL-1ß expression by regulating the SDH-HIF-1α axis and suppressed the energy shift from an OXPHOS phenotype to a glycolysis phenotype. These findings revealed important effects of AX on mitochondrial enzymes as well as on mitochondrial energy metabolism in the immune response. In addition, these raised the possibility that AX plays an important role in other diseases caused by SDH mutation and metabolic disorders.

Morin improves dexamethasone-induced muscle atrophy by modulating atrophy-related genes and oxidative stress in female mice.

This study investigated the effect of morin, a flavonoid, on dexamethasone-induced muscle atrophy in C57BL/6J female mice. Dexamethasone (10 mg/kg body weight) for 10 days significantly reduced body weight, gastrocnemius and tibialis anterior muscle mass, and muscle protein in mice. Dexamethasone significantly upregulated muscle atrophy-associated ubiquitin ligases, including atrogin-1 and MuRF-1, and the upstream transcription factors FoxO3a and Klf15. Additionally, dexamethasone significantly induced the expression of oxidative stress-sensitive ubiquitin ligase Cbl-b and the accumulation of the oxidative stress markers malondialdehyde and advanced protein oxidation products in both the plasma and skeletal muscle samples. Intriguingly, morin treatment (20 mg/kg body weight) for 17 days effectively attenuated the loss of muscle mass and muscle protein and suppressed the expression of ubiquitin ligases while reducing the expression of upstream transcriptional factors. Therefore, morin might act as a potential therapeutic agent to attenuate muscle atrophy by modulating atrophy-inducing genes and preventing oxidative stress.

Balenine, Imidazole Dipeptide Promotes Skeletal Muscle Regeneration by Regulating Phagocytosis Properties of Immune Cells.

Balenine is one of the endogenous imidazole dipeptides derived from marine products. It is composed of beta-alanine and 3-methyl-L-histidine, which exist mainly in the muscles of marine organisms. The physiological functions of dietary balenine are not well-known. In this study, we investigated whether the supplementation of dietary balenine was associated with muscle function in a cardiotoxin-indued muscle degeneration/regeneration model. Through morphological observation, we found that the supplementation of balenine-enriched extract promoted the regeneration stage. In addition, the expression of regeneration-related myogenic marker genes, such as paired box protein 7, MyoD1, myogenin, and Myh3, in a group of mice fed a balenine-enriched extract diet was higher than that in a group fed a normal diet. Moreover, the supplementation of balenine-enriched extract promoted the expression of anti-inflammatory cytokines as well as pro-inflammatory cytokines at the degeneration stage. Interestingly, phagocytic activity in the balenine group was significantly higher than that in the control group in vitro. These results suggest that balenine may promote the progress of muscle regeneration by increasing the phagocytic activity of macrophages.

MuRF1 deficiency prevents age-related fat weight gain, possibly through accumulation of PDK4 in skeletal muscle mitochondria in older mice.

Recent studies show that muscle mass and metabolic function are interlinked. Muscle RING finger 1 (MuRF1) is a critical muscle-specific ubiquitin ligase associated with muscle atrophy. Yet, the molecular target of MuRF1 in atrophy and aging remains unclear. We examined the role of MuRF1 in aging, using MuRF1-deficient (MuRF1-/- ) mice in vivo, and MuRF1-overexpressing cell in vitro. MuRF1 deficiency partially prevents age-induced skeletal muscle loss in mice. Interestingly, body weight and fat mass of more than 7-month-old MuRF1-/- mice were lower than in MuRF1+/+ mice. Serum and muscle metabolic parameters and results of indirect calorimetry suggest significantly higher energy expenditure and enhanced lipid metabolism in 3-month-old MuRF1-/- mice than in MuRF1+/+ mice, resulting in suppressed adipose tissue gain during aging. Pyruvate dehydrogenase kinase 4 (PDK4) is crucial for a switch from glucose to lipid metabolism, and the interaction between MuRF1 and PDK4 was examined. PDK4 protein levels were elevated in mitochondria from the skeletal muscle in MuRF1-/- mice. In vitro, MuRF1 interacted with PDK4 but did not induce degradation through ubiquitination. Instead, SUMO posttranscriptional modification (SUMOylation) of PDK4 was detected in MuRF1-overexpressing cells, in contrast to cells without the RING domain of MuRF1. MuRF1 deficiency enhances lipid metabolism possibly by upregulating PDK4 localization into mitochondrial through prevention of SUMOylation. Inhibition of MuRF1-mediated PDK4 SUMOylation is a potential therapeutic target for age-related dysfunction of lipid metabolism and muscle atrophy.

Morin attenuates dexamethasone-mediated oxidative stress and atrophy in mouse C2C12 skeletal myotubes.

Glucocorticoids are the drugs most commonly used to manage inflammatory diseases. However, they are prone to inducing muscle atrophy by increasing muscle proteolysis and decreasing protein synthesis. Various studies have demonstrated that antioxidants can mitigate glucocorticoid-induced skeletal muscle atrophy. Here, we investigated the effect of a potent antioxidative natural flavonoid, morin, on the muscle atrophy and oxidative stress induced by dexamethasone (Dex) using mouse C2C12 skeletal myotubes. Dex (10 µM) enhanced the production of reactive oxygen species (ROS) in C2C12 myotubes via glucocorticoid receptor. Moreover, Dex administration reduced the diameter and expression levels of the myosin heavy chain protein in C2C12 myotubes, together with the upregulation of muscle atrophy-associated ubiquitin ligases, such as muscle atrophy F-box protein 1/atrogin-1, muscle ring finger protein-1, and casitas B-lineage lymphoma proto-oncogene-b. Dex also significantly decreased phosphorylated Foxo3a and increased total Foxo3a expression. Interestingly, Dex-induced ROS accumulation and Foxo3a expression were inhibited by morin (10 µM) pretreatment. Morin also prevented the Dex-induced reduction of myotube thickness, together with muscle protein degradation and suppression of the upregulation of atrophy-associated ubiquitin ligases. In conclusion, our results suggest that morin effectively prevents glucocorticoid-induced muscle atrophy by reducing oxidative stress.

Astaxanthin Prevents Atrophy in Slow Muscle Fibers by Inhibiting Mitochondrial Reactive Oxygen Species via a Mitochondria-Mediated Apoptosis Pathway.

Astaxanthin (AX) is a carotenoid that exerts potent antioxidant activity and acts in the lipid bilayer. This study aimed to investigate the effects of AX on muscle-atrophy-mediated disturbance of mitochondria, which have a lipid bilayer. Tail suspension was used to establish a muscle-atrophied mouse model. AX diet fed to tail-suspension mice prevented loss of muscle weight, inhibited the decrease of myofiber size, and restrained the increase of hydrogen peroxide (H2O2) production in the soleus muscle. Additionally, AX improved downregulation of mitochondrial respiratory chain complexes I and III in the soleus muscle after tail suspension. Meanwhile, AX promoted mitochondrial biogenesis by upregulating the expressions of adenosine 5'-monophosphate-activated protein kinase (AMPK) α-1, peroxisome proliferator-activated receptor (PPAR)-γ, and creatine kinase in mitochondrial (Ckmt) 2 in the soleus muscle of tail-suspension mice. To confirm the AX phenotype in the soleus muscle, we examined its effects on mitochondria using Sol8 myotubes derived from the soleus muscle. We found that AX was preferentially detected in the mitochondrial fraction; it significantly suppressed mitochondrial reactive oxygen species (ROS) production in Sol8 myotubes. Moreover, AX inhibited the activation of caspase 3 via inhibiting the release of cytochrome c into the cytosol in antimycin A-treated Sol8 myotubes. These results suggested that AX protected the functional stability of mitochondria, alleviated mitochondrial oxidative stress and mitochondria-mediated apoptosis, and thus, prevented muscle atrophy.

Suppressive effects of sulfated polysaccharide ascophyllan isolated from Ascophyllum nodosum on the production of NO and ROS in LPS-stimulated RAW264.7 cells.

In this study, we found that a sulfated polysaccharide isolated from the brown alga Ascophyllum nodosum, ascophyllan, showed suppressive effects on stimulated RAW264.7 cells. Ascophyllan significantly inhibited expression of inducible nitric oxide synthase mRNA and excessive production of nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells in a dose-dependent manner without affecting the viability of RAW264.7 cells. Ascophyllan also reduced the elevated level of intracellular reactive oxygen species (ROS) in LPS-stimulated RAW264.7 cells. Furthermore, preincubation with ascophyllan resulted in concentration-dependent decrease in ROS production in phorbol 12-myristate-13-acetate-stimulated RAW264.7 cells. Our results suggest that ascophyllan can exhibit anti-inflammatory effects on stimulated macrophages mainly through the attenuation of NO and ROS productions.

Influence of the interposition of pink muscle fibers in the dorsal ordinary muscle on the postmortem hardness of meat in various fishes.

We previously showed that the tenderization of ordinary muscle during ice storage is affected by the interposition of pink muscle fibers in the ordinary muscle. However, little is known about whether or not the interposition of pink muscle fibers affects the hardness of raw fish meat. To clarify the influence of the interposition of pink muscle fibers in the dorsal ordinary muscle on hardness of meat, the breaking strengths and the fiber types of the dorsal ordinary muscle of eight fish species (a total of 37 specimens) were discriminated. The breaking strengths among fish species were within a range of 6.5-19.1 N/cm2 . Pink muscle fibers were found in the dorsal ordinary muscle of six out of the eight fish species ranging from 0.0 to 56.0% in quantity ratio, and 0.0 to 19.3% in area ratio, respectively. The quantity ratio and area ratio of pink muscle fibers in the dorsal ordinary muscles of all eight fish species samples positively correlated with the breaking strength. Relative to the quantity ratio (p < .05), the area ratio (p < .02) of pink muscle fibers was more representative of postmortem texture hardness. In conclusion, the high interposition ratio of pink muscle fibers in ordinary muscle could potentially improve the postmortem hardness, the texture, and even the flesh quality of raw fish meat.

Dietary Sodium Nitrite Causes Similar Modifications to Splenic Inflammatory Gene Expression as a High-Fat Diet.

Sodium nitrite (NaNO2) is a widely used food additive. The present study compared the outcomes from intakes of dietary NaNO2 and a high-fat diet (HFD), and assessed their combined effects on inflammatory gene expression in the immune tissues of the mouse. In experiment I, mice were fed a standard low-fat diet (LFD) without or with NaNO2 (0.02 and 0.08%, w/w) for 11 wk. In experiment II, mice were fed an LFD without or with NaNO2 (0.02%) or HFD without or with NaNO2 (0.02%) for 11 wk. Inflammatory gene expression in the immune tissues was then measured. NaNO2 consumption and HFD feeding each resulted in increased splenic mRNAs for cell markers of neutrophils (Ngp, NE, Ly6g, Mpo) and eosinophils (Epo, Ear6), and an S100 family member (S100A8). In contrast, NaNO2 consumption and HFD feeding each resulted in decreased splenic mRNAs for cell markers of macrophages (Emr1, Itgax, CD68, CD206, Dectin-1, TLRs 4, 6, and 7), T- (CD3, CD4), NK- (CD56) and B-cells (CD20, CD40), pro- and anti-inflammatory cytokines (TNF-α, IL-6, IL-1ß, IFN-γ, IL-18, IL-10, TGF-ß), interleukin receptor antagonists (IL1ra, IL6ra) and cell adhesion molecules (ICAM-1, VCAM-1). However, dietary NaNO2 combined with HFD feeding caused no further decrease in these transcript levels compared with dietary NaNO2 alone. These NaNO2- or HFD-induced modifications were less profound in the liver and abdominal adipose tissues than in the spleen. These findings indicate that dietary NaNO2 has similar modulatory effects to HFD feeding on splenic inflammatory genes.

Ultra-high-purity iron is a novel and very compatible biomaterial.

Metals and alloys are used widely in bone prosthetic materials, stents and dental tissue reconstructions. The most common materials are stainless steels and cobalt-chromium-nickel and titanium alloys. These alloys can be easily deformed but are hard to break. However, their affinity for cells and tissues is very low. In addition, they can sometimes provoke unexpected metal allergies. Iron is an abundant trace element essential for humans. However, excess amounts in particular of Fe2+ ions are toxic. We previously succeeded in obtaining 99.9996% ultra-high-purity iron (ABIKO iron). The chemical properties of ABIKO iron are completely different from that of conventional pure iron. For example, the reaction rate in hydrochloric acid is very slow and there is barely any corrosion. Here, we found that, in the absence of any type of coating, mammalian cells could easily attach to, and normally proliferate and differentiate on, ABIKO iron. On the other hand, cell densities and proliferation rate of the surfaces of plates made from Co-Cr-Mo or Ti-6Al-4V were significantly reduced. In addition, several stress and iron response genes, HSP70, SOD1, ATM and IRP2 did not change in the cells on ABIKO iron, while these genes were induced with exogenous application of FeSO4. Cells also secreted and fastened some organics on ABIKO iron. In vitro collagen binding assay showed that ABIKO iron binds higher amount of collagens. These findings highlight ABIKO iron as a novel biocompatible prosthetic material.

Therapeutic effects of an orally administered edible seaweed-derived polysaccharide preparation, ascophyllan HS, on a Streptococcus pneumoniae infection mouse model.

Ascophyllan HS is a commercially available preparation of the edible brown alga Ascophyllum nodosum containing ascophyllan, a sulfated polysaccharide with diverse beneficial biological activities. In this study, the effects of ascophyllan HS were evaluated in a severe intranasal Streptococcus pneumoniae infection mouse model. The control untreated mice started to die on day 7 and 80% had died by day 14 post-infection. Continuous oral administration of ascophyllan HS before and after bacterial infection resulted in a remarkable increase in survival rate, with 90% of the low (167 mg/kg body weight/day) and 100% of the high (500 mg/kg body weight/day) dose ascophyllan HS-treated mice surviving at day 14 post-infection. Histopathological observation of the lungs of the infected mice revealed the induction of typical pneumonia features in the alveolar spaces of the untreated control mice, such as extensive infiltration of inflammatory cells, edema, and fibrin deposition. In contrast, notable levels of lung injuries or alterations were not observed in the ascophyllan HS-treated mice, and only a minor lesion was observed in one mouse. Furthermore, bacterial burdens in the lungs were significantly reduced in the ascophyllan HS-treated mice as compared to the control mice at day 4 post-infection. Significantly higher levels of IL-12 were detected in the serum of ascophyllan HS-treated mice than that of control mice measured at the end of the infection experiment (day 14). These results suggest that orally administered ascophyllan HS exerts a therapeutic effect on S. pneumoniae infection by activating the host defense systems. This is the first report of the therapeutic effect of an orally administered seaweed polysaccharide preparation on S. pneumoniae infection. Our findings suggest that ascophyllan HS has the potential to be developed as nutraceuticals and pharmaceuticals applicable for humans as well as a safe and promising therapeutic agent against S. pneumoniae infection.

Application of Bio-Impedance Analysis to Estimate the Condition of Yellowtail (Seriola quinqueradiata) Muscle at Different Storage Temperatures.

Changes in impedance at 2 kHz, adenosine triphosphate (ATP) content, and muscle contraction were evaluated in yellowtail during 0 (ice), 5, 10, 15, and 20°C storage. Histological changes during ice storage were also measured. At any temperature, although impedance increased with both rigor mortis and ATP consumption during early storage, it began to decrease rapidly when ATP was almost depleted. Moreover, temporarily increasing impedance had a strong relationship with ATP content; decreasing impedance had a significant correlation with storage temperature after ATP depletion. Furthermore, impedance increased with narrowing of intercellular spaces when sarcolemma was intact and decreased with expansion of intercellular spaces when sarcolemma was leaky. Meanwhile, changes of sarcolemma and intercellular spaces were accompanied by ATP change. Thus, ATP is one significant physiological factor for impedance change, and temperature greatly influenced impedance after depletion of ATP. Results suggest that impedance analysis can be used as a convenient and nondestructive method to diagnose condition of tissue at different storage temperatures. Bioelectromagnetics. 2019;40:488-497. © 2019 Bioelectromagnetics Society.

Relationship between the characteristics of rigor-mortis-related actomyosin and muscle fiber types in the ordinary muscle of various fishes.

BACKGROUND: Rigor mortis occurs when muscle extension vanishes through the irresistible coupling of actin and myosin by the consumption of adenosine triphosphate as energy. To clarify the cause of the differences in the progression of rigor mortis, seven fish species were used as samples. The superprecipitation reaction and Mg2+ -ATPase activity of actomyosin in dorsal ordinary muscle were measured, and the slope of the regression line between these two variables was calculated for each fish specimen. The fiber types of the dorsal ordinary muscle in each sample fish were discriminated by the stability of actomyosin ATPase at acid and alkaline preincubations. RESULT: Positive correlations were found between Mg2+ -ATPase activity and the superprecipitation reaction of actomyosin in all 27 fish specimens. The slopes of the regression lines were different not only between fish species but also in fish specimens within the same species. The area ratios of pink muscle fibers and the IIa and/or IIb subtypes of white muscle fibers in the dorsal ordinary muscle were also different between fish species, as well as in specimens within the same fish species. A positive correlation was found between the area ratios of pink muscle fibers in dorsal ordinary muscle and the slopes of the regression line. CONCLUSION: It was suggested that the differences in characteristics of rigor-mortis-related actomyosin of fish might have been caused by the differences in the interposition ratio of muscle fiber types, especially of the pink muscle fiber type, in the dorsal ordinary muscle. © 2019 Society of Chemical Industry.

Effect of blood deposition phenomenon on flesh quality of yellowtail (Seriola quinqueradiata) during storage.

We examined the influence of blood deposition on flesh quality of ordinary muscle in yellowtail. This study compared the flesh quality changes in upper and under-sides of yellowtails killed by two different methods: spinal-cord destruction (SCD) with blood removal and suffocation in air without blood removal (SA). The under-sides of the SA group showed the highest values for a*, cathepsin B and B + L activities, the lowest value in breaking strength and the greatest degradation of myosin heavy chain (MHC) among the four groups. However, the values of the SCD-upper group indicated the best flesh quality. In addition, the white blood cells presented the highest cathepsin B and B + L activities among the blood components. These results indicate that blood has the tendency to deposit downward in accordance with the direction of placement. This phenomenon influences the distribution of white blood cells which contain enzymes that accelerate the deterioration of flesh quality. The texture of fish muscle is an important part of the flesh quality. In captured fishery (purse-seine fishery and dragnet fishery), it is impossible to immediately and completely remove blood. Therefore, suffocation in air is the common method after the fish is caught. The commercial value of fish is decreased and the price varies greatly when these fish enter market circulation. In our study, we examined the influence of blood deposition on the flesh quality of yellowtail during storage. The degradation of structural proteins accelerated in the deposited blood which contain proteases. The movement and deposition of blood caused the difference of quality on both sides, which seriously affected the quality of fish during preservation. Our study has some theoretical guidance for muscle softening and give a better understanding of the adverse effect of blood during preservation.

Morin suppresses cachexia-induced muscle wasting by binding to ribosomal protein S10 in carcinoma cells.

Cachexia, observed in most cancer patients, is a syndrome that includes wasting of bodily energy reserves and is characterized by muscle atrophy and fat loss. We have previously demonstrated that isoflavones, such as genistein and daidzein, prevent muscle wasting in tumor-bearing mice. In this study, we examined the effect of morin, a flavonoid, on cachexia. The wet weight and myofiber size of muscles in Lewis lung carcinoma (LLC) cell-bearing mice fed a normal diet were decreased, compared with those in control mice fed a normal diet. In contrast, intake of morin prevented the reduction of muscle wet weight and myofiber size. Moreover, the tumor weight in mice fed the morin diet was lower than that in mice fed the normal diet. Both cell viability and protein synthetic ability of LLC cells were reduced by treatment with morin, but C2C12 myotubes were not affected. Binding assay using morin-conjugated magnetic beads identified ribosomal protein S10 (RPS10) as a target protein of morin. Consistent with the result of morin treatment, knockdown of RPS10 suppressed LLC cell viability. These results suggest that morin indirectly prevents muscle wasting induced by cancer cachexia by suppressing cancer growth via binding to RPS10.

Dietary supplementation with alkylresorcinols prevents muscle atrophy through a shift of energy supply.

It has been reported that phytoextracts that contain alkylresorcinols (ARs) protect against severe myofibrillar degeneration found in isoproterenol-induced myocardial infarction. In this study, we examined the effect of dietary ARs derived from wheat bran extracts on muscle atrophy in denervated mice. The mice were divided into the following four groups: (1) sham-operated (control) mice fed with normal diet (S-ND), (2) denervated mice fed with normal diet (D-ND), (3) control mice fed with ARs-supplemented diet (S-AR) and (4) denervated mice fed with ARs-supplemented diet (D-AR). The intake of ARs prevented the denervation-induced reduction of the weight of the hind limb muscles and the myofiber size. However, the expression of ubiquitin ligases and autophagy-related genes, which is associated with muscle proteolysis, was slightly higher in D-AR than in D-ND. Moreover, the abundance of the autophagy marker p62 was significantly higher in D-AR than in D-ND. Muscle atrophy has been known to be associated with a disturbed energy metabolism. The expression of pyruvate dehydrogenase kinase 4 (PDK4), which is related to fatty acid metabolism, was decreased in D-ND as compared with that in S-ND. In contrast, dietary supplementation with ARs inhibited the decrease of PDK4 expression caused by denervation. Furthermore, the abnormal expression pattern of genes related to the abundance of lipid droplets-coated proteins that was induced by denervation was improved by ARs. These results raise the possibility that dietary supplementation with ARs modifies the disruption of fatty acid metabolism induced by lipid autophagy, resulting in the prevention of muscle atrophy.