Effects of Aquatic Plants on Nutrient Concentration in Water and Growth Performance of Fantail Goldfish in an Aquaculture System

The effects of two aquatic plants, duckweed (Lemna sp.) and azolla (Azolla sp.), on the growth performance of fantail goldfish (Carassius auratus) and dissolved nutrient concentrations were studied. The experiments were carried out in triplicate sets over a period of seven weeks. Eight specimens of fantail goldfish (length = 5.16 ± 0.06 cm; body weight = 2.30 ± 0.06 g) were released into each of the aquariums containing 40 L of water. Submerged sponge filters were used as the substrate (bed) for the nitrifying bacteria to facilitate nitrification. The fish were provided feed at the rate of 2% of their body weight twice daily. In situ and ex situ water parameters (temperature, dissolved oxygen, pH, total suspended solids, ammonia, nitrite, nitrate, and phosphate), body weight and length of the Fantail goldfish, and wet weight of aquatic plants were measured weekly. The results showed no significant differences (p > 0.05) in any of the three aquariums in water temperature, pH, and dissolved oxygen. Survival of the fish was 100%. The highest food conversion ratio and specific growth rate were observed in the aquarium stocked with duckweed, followed by the aquarium with azolla and the control set (p < 0.05). The concentrations of nutrients (ammonia and nitrate) were recorded lowest (p < 0.05) in the aquarium with azolla, followed by duckweed and the control. The results suggested that aquatic plants were effective in absorbing nutrients and can serve as biofilters to create better conditions for the growth of the fantail goldfish.

Nesfatin-1 stimulates the hypothalamus-pituitary-interrenal axis hormones in goldfish

Stress in vertebrates is mediated by the hypothalamus-pituitary-adrenal (in mammals)/interrenal (in fish) (HPA/I) axis, which produces the corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and corticosteroids, respectively. Nesfatin-1, a novel anorexigenic peptide encoded in the precursor nucleobindin-2 (NUCB2), is increasingly acknowledged as a peptide that influences the stress axis in mammals. The primary aim of this study was to characterize the putative effects of nesfatin-1 on the fish HPI axis, using goldfish ( Carassius auratus) as an animal model. Our results demonstrated that nucb2/nesfatin-1 transcript abundance was detected in the HPI tissues of goldfish, with most abundant expression in the pituitary. NUCB2/nesfatin-1-like immunoreactivity was found in the goldfish hypothalamus, pituitary, and interrenal cells of the head kidney. GPCR12, a putative receptor for nesfatin-1, was also detected in the pituitary and interrenal cells. NUCB2/nesfatin-1-like immunoreactivity was observed in ACTH-expressing pituitary corticotrophs. Acute netting and restraint stress upregulated nucb2/nesfatin-1 mRNA levels in the forebrain, hypothalamus, and pituitary, as well as crf and crf-r1 expression in the forebrain and hypothalamus. Intraperitoneal and intracerebroventricular administration of nesfatin-1 increased cortisol release and hypothalamic crf mRNA levels, respectively. Finally, we found that nesfatin-1 significantly stimulated ACTH secretion from dispersed pituitary cells in vitro. Collectively, our data provide the first evidence showing that nesfatin-1 is a stress responsive peptide, which modulates the stress axis hormones in fish.

Seasonally Related Disruption of Metabolism by Environmental Contaminants in Male Goldfish (Carassius auratus)

Endocrine disrupting chemicals mimic or disrupt action of the natural hormones, adversely impacting hormonal function as well as cardiovascular, reproductive, and metabolic health. Goldfish are seasonal breeders with an annual reproductive cycle regulated by neuroendocrine signaling which involves allocation of metabolic energy to sustain growth and reproduction. We hypothesize that seasonal changes in physiology alter overall vulnerability of goldfish to metabolic perturbation induced by environmental contaminants. In this study, we assess effects of endogenous hormones, individual contaminants and their mixture on metabolism of goldfish at different reproductive stages. Exposure effects were assessed using 1H-NMR metabolomics profiling of male goldfish midbrain, gonad and liver harvested during early recrudescence (October), mid-recrudescence (February) and late recrudescence (June). Compounds assessed include bisphenol A, nonylphenol, bis(2-ethylhexyl) phthalate, fucosterol and a tertiary mixture (DEHP + NP + FS). Metabolome-level responses induced by contaminant exposure across tissues and seasons were benchmarked against responses induced by 17β-estradiol, testosterone and thyroid hormone (T3). We observe a clear seasonal dependence to metabolome-level alteration induced by hormone or contaminant exposures, with February (mid-recrudescence) the stage at which male goldfish are most vulnerable to metabolic perturbation. Responses induced by contaminant exposures differed from those induced by the natural hormones in a season-specific manner. Exposure to the tertiary mixture induced a functional gain at the level of biochemical pathways modeling over responses induced by individual components in select tissues and seasons. We demonstrate the importance of seasonally driven changes in physiology altering overall vulnerability of goldfish to metabolic perturbation induced by environmental contaminants, the relevance of which likely extends to other seasonally-breeding species.

Transcriptome Analysis Provides Insights into Hepatic Responses to Trichloroisocyanuric Acid Exposure in Goldfish (Carassius auratus)

In this study, goldfish (Carassius auratus) were exposed to 0 (control group) and 0.81 mg/L TCCA for four consecutive days. The liver transcriptome, the molecular indices of oxidative stress, and gills histopathology were investigated. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that energy metabolism-related pathways such as glycolysis/gluconeogenesis were significantly enriched, suggesting their perturbation in the liver of goldfish. Additionally, TCCA exposure also caused pathological damage in gills, which compromised physiological function and decreased oxygen intake capacity of gills, thus leading to the enhancement of anaerobic metabolism. This finding was confirmed by the significant upregulation of lactate dehydrogenase in the liver of goldfish. Moreover, many phase I and phase II metabolic enzymes might be activated to alleviate TCCA-induced toxicity in goldfish, and glutathione S-transferases (GSTs) and cytochrome P450s (CYPs) play a crucial role in the metabolism of TCCA in the liver of goldfish. Furthermore, the antioxidant enzyme analysis showed that TCCA exposure induced oxidative damage in the liver and partially impaired the antioxidant defense system of goldfish, evidenced by decreased superoxide dismutase (SOD) and catalase (CAT), and increased malondialdehyde (MDA) level. In summary, this study will improve our understanding of the molecular mechanisms of the TCCA-induced toxicity in goldfish.