Silver eel were sampled in 1981 and 1983 in River Brede, Denmark, with outlet to the North Sea. Yellow eel in River Køge-Lellinge, Denmark, with outlet to the Baltic Sea were sampled 1965-1968. Silver eel were aged by burning the otoliths. Silver male ages varied from 4 to 25 years, lengths 30.8 to 45.3 cm, and female silver eel varied from 7 to 25 years, lengths 42.3 to 77.3 cm. von Bertalanffy trajectories of length-at-age of male and female yellow eel were calculated in both rivers. Younger yellow eel had significantly higher annual growth rate compared to older age groups, and females grew significantly faster than males. Two models for natural mortality M were used to estimate number of glass eel needed to produce number of silver eel for each sex and silver age group. Annual silver eel production from River Brede Å was 49.2 kg ha-1, demanding 2,894 glass eel ha-1 and in River Køge-Lellinge, the silver eel production was 48.5 kg ha-1, demanding 5,570 glass eel ha-1. It was calculated that one (0.29 g) thousand glass eel contribute to 8.8 kg silver eel in River Køge-Lellinge, and 17.0 kg silver eel in River Brede. To fulfill the Danish EMP in rivers requires annual stocking of 33 tons or 9.4 million reared on-grown eel (3.5 g) to compensate for 183 tons lost silver eel.

One of the challenges with Japanese eel (Anguilla japonica) seedling production is the slow growth of leptocephali. This issue arises from a fundamental problem with the current methods for raising leptocephali. In essence, the balance between the amount of energy obtained from feeding and kinetic energy significantly differs from that in the natural environment. This slow growth results in a reduced size of metamorphosable leptocephalus and ultimately leads to smaller artificial glass eels. We hypothesize that this reduction in the size of artificial glass eels may be attributed to time-related stress during rearing. Therefore, we propose the "time-over theory" based on a series of phenomena.

Parasitic infections are often not the direct cause of death of fish but the presence of wounds in the fish's body due to parasitic attacks is a trigger factor for secondary infection. Secondary infections can be caused by fungi, bacteria or viruses, which ultimately cause the death of fish. This study aimed to determine the characteristics of parasites and fungi that infected eel (Anguilla sp.) in the waters of Poso, Buol, Toli-toli and Donggala, Central Sulawesi as an important part of the diagnosis of fish disease in the framework of teraupetic strategies. Eel were taken as many as 30 individuals / location for observation of parasites and fungi. Parasitological examination was carried out for external and internal parasites on the mucous layer of the body, gills, intestines and stomach, while fungal isolations were carried out on muscles, skin and tissues that have abnormalities. After identification, the prevalence and intensity were carried out. The results showed that the highest prevalence of parasites were Camallanus sp (70%), Proteacephalus sp (50%) and Gyrodactylus sp (40%), and the nematode Camallanus sp the tapeworm Proteocephalus sp had the highest intensity of 57.5 and 30.8 respectively. Fungal prevalence were found highest in Saprolegnia sp (36%), and Fusarium sp (32%).

The European eel, Anguilla anguilla, was the most important fishery resource in European estuaries for centuries. More recently, most local stocks throughout the species' range have collapsed for a variety of reasons. This article focuses on historical records and the recent collapse in the Neretva estuary (Croatia), the most important eel fishery ground on the eastern Adriatic coast. Historical records were analyzed through an examination of various available databases, including scientific articles, technical literature, and gray literature. Additional descriptions were obtained using local ecological knowledge methodology and interviews with various stakeholders. The comparative analysis shows that the historical eel catch (the 1930s) under pristine habitat conditions should be estimated at 100 tons, officially recognized and additionally estimated. The decline in catches began in the 1960s and was associated with the massive reclamation of important eel lagoons for agriculture and port areas when officially recognized catches at state stations averaged 45 tons per year. The main reasons for this dramatic decline in eel fisheries and biological status in the Neretva estuary are a significant reduction of, an increase in recreational fishery, the establishment of invasive predatory fish species, and strong development of local demand in tourism. The results of this study indicate that the local eel population will rapidly become extinct in the future unless various measures are developed and applied to protect it, restrict fishing and market control, restore habitat, and control invasive and competing species.

Luteinizing hormone receptor (LHR) is a member of the seven-transmembrane (TM) receptor family. Several mutations in LHR have been identified in many mammalian species, leading to either constitutive activation or inactivation of the receptor. Mutations in highly conserved regions of the TM domain have been reported. In this study, we analyzed signal transduction by three constitutively active mutants (designated M410T, L469R, and D590Y) and two inactivating mutants (D383N and Y546F) of eelLHR known as naturally occurring in human LHR . To directly assess the functional effects of these mutations, site-directed mutant receptors were transiently expressed in CHO-K1 cells and cAMP accumulation stimulated by recombinant eelLH (rec-eelLH) was measured by homogeneous time-resolved fluorescence (HTRF) assays. The cAMP response in cells expressing eelLHR wild-type (eLHR-WT) increased in a dose-dependent manner with rec-eelLH ligand stimulation. Cells expressing the activating eelLHR mutants, M410T, L469R, and D590Y, exhibited a 4.0-, 19.1-, and 7.8-fold increase in basal cAMP response, respectively. However, their maximal responses were approximately 73, 53, and 92%, respectively, of the maximal response of LHR-WT. The L469R mutant exhibited a particularly marked increase in cAMP production in the absence of agonist. The maximal responses of the inactivating mutants, D383N and Y546F, were 32 and 24% of LHR-WT, respectively. However, the inactivating mutations did not completely impair signal transduction. Thus, we report here the first characterization of activating and inactivating mutations in eelLHR and we show that these mutations have similar effects as those reported for mammalian LHRs. Moreover, eelLHR with activating mutations showed constitutive cAMP responses. These results provide important data on the signal transduction of constitutively active and inactive LHR mutants. Further studies should aim to identify the mechanism responsible for the significant increase in basal cAMP response in the constitutively activated eelLHR mutants.

We produced a recombinant eel luteinizing hormone (rec-eel LH) analog with high potency in Chinese hamster ovary DG44 (CHO DG44) cells. The eel LH mutant (LH-M), which had a linker comprising the equine chorionic gonadotropin (eCG) β-subunit carboxyl-terminal peptide (CTP) region (amino acids 115 to149), was inserted between the β-subunit and α-subunit of wild-type tethered eel LH (LH-wt). Monoclonal cells transfected with the eel LH-wt and eel LH-M plasmids were isolated from five and nine clones of CHO DG44 cells, respectively. The secreted quantities abruptly increased on day 3, with peak levels of 5,000–7,500 ng/mL on day 9. The molecular weight of eel LH-wt was 32–36 kDa while that of eel LH-M increased to approximately 38–44 kDa, indicating the detection of two bands. Treatment with peptide N-glycanase F decreased the molecular weight by approximately 8 kDa. The oligosaccharides at the eCG β-subunit O-linked glycosylation sites were appropriately modified post-translation. The EC50 value and maximal responsiveness of eel LH-M increased by approximately 2.90- and 1.29-fold, respectively, indicating that the mutant exhibited more potent biological activity than eel LH-wt. Phosphorylated extracellular regulated kinase (pERK1/2) activation resulted in a sharp peak 5 min after agonist treatment, with a rapid decrease thereafter. These results indicate that the new rec-eel LH analog which contains the eCG β-subunit CTP linker comprising O-linked glycosylation sites, had more potent activity than the wild-type in vitro. Taken together, this new eel LH analog can be produced in large quantities using a stable CHO DG44 cell system.

This study aimed to produce single-chain recombinant eel follicle-stimulating hormone (rec-eel FSH) analogs with high activity in Chinese hamster ovary DG44 (CHO DG44) cells. We recently reported that an O-linked glycosylated carboxyl-terminal peptide (CTP) of the equine chorionic gonadotropin (eCG) β-subunit plays contributes on high activity and time-dependent secretion in mammalian cells. We constructed a mutant (FSH-M) in which a linker including the eCG β-subunit CTP region (amino acids 115 to149) was inserted between the β-subunit and α-subunit of wild-type single chain eel FSH (FSH-wt). Plasmids containing eel FSH-wt and eel FSH-M were transfected into CHO DG44 cells. Single cells expressing each protein were isolated from 10 and 7 clones, respectively. Secretion increased gradually during the cultivation period and peaked at 4,000–5,000 ng/mL on day 9. The molecular weight of eel FSH-wt was 34–40 kDa, while that of eel FSH-M increased substantially, with two bands at 39–46 kDa. Treatment with PNGase F to remove the N glycosylation sites decreased the molecular weight remarkably to approximately 8 kDa. The EC50 value and maximal responsiveness of eel FSH-M were approximately 1.23- and 1.06-fold higher than those of eel FSH-wt, indicating that the mutant showed slightly higher biological activity. Phosphorylated extracellular regulated kinase (pERK1/2) activation exhibited a sharp peak at 5 min, followed by a rapid decline. These findings indicate that the new rec-eel FSH molecule with the eCG β-subunit CTP linker showed potent activity and could be produced in massive quantities using the stable CHO DG44 cell system.

The different vegetable oils used in canned fish as filling medium have a preserving effect and contribute to the palatability of the product. In this study, the colour of European eels and the filling medium (sunflower oil, olive oil or spicy olive oil) was measured at different steps of the canning process. The sensorial characteristics of canned eels packed in the different oils were also evaluated. Colour scores (CieLab values) were higher in canned eels packed in sunflower and spicy olive oil than in canned eels packed in olive oil. The changes in colour parameters depended on the type of oil, the stage of the process and the storage time. Colour changes in canned eels packed in olive oil were highest during the sterilization process. Spicy olive oil was the filling medium in which the colour change was greatest, probably due to the migration of some of the spice components into the oil. Organoleptic properties were directly related to the type of oil used as the filling medium. The canned eels packed in sunflower oil were those awarded the highest scores in consumer tests, although the preferences varied depending on the age and gender of the consumers.

We analyzed signal transduction of three constitutively activating mutants (M410T, L469R, and D590Y) and two inactivating mutants (D417N and Y558F) of the eel luteinizing hormone receptor (eel LHR), known to occur in human LHR. The objective of this study was to assess the functional effects of these mutations in signal transduction and cell surface loss of receptor. Mutant receptors were transiently expressed in Chinese hamster ovary (CHO-K1) cells. Eel LH-stimulated accumulation of cyclic adenosine monophosphate (cAMP) was measured by homogeneous time-resolved fluorescence (HTRF) assays. The loss of receptors from the cells surface was measured using an enzyme-linked immunosorbent assay (ELISA) in human embryonic kidney (HEK) 293 cells. The cAMP response in cells expressing the wild type eel LHR was increased in a dose-dependent manner using eel LH ligand stimulation. Compared with the wild type, cells expressing the activating mutants (M410T, L469R, and D590Y), exhibited a 4.0-, 19.1-, and 7.8-fold increase in basal cAMP response without agonist stimulation, respectively. Their maximal responses to agonist stimulation were approximately 65%, 52%, and 98%, respectively, of those of the wild type. The inactivating mutants (D417N and Y558F) did not completely impair signal transduction, and their maximal responses were only 33% and25 % of those of wild type. These data clearly showed that the eel LHR-L469R and D590Y, activating mutants enhanced the rate of the loss of cell surface receptors following treatment with eel LH. Thus, the loss of cell surface receptors in cells expressing mutant eel LHRs was consistent with the eel LH agonist-induced production of cAMP. Our results suggested that the activation of the eel LHR requires appropriate loss of LHR-ligand complexes from the cell surface.