Metabolite profiling, histological and oxidative stress responses in the grey mullet, Mugil cephalus exposed to the environmentally relevant concentrations of the heavy metal, Pb (NO3)2.

In this study, a metabolomics approach was applied to investigate the metabolic responses of grey mullet, Mugil cephalus to toxicity induced by heavy metal, Pb (NO3)2. In addition, the study was followed by assessing the peroxidation index and histology of liver as supplementary data. Pb (NO3)2 exposure affected the plasma metabolome, especially four group metabolites including amino acids, methylated metabolites, energetic metabolites and citric acid intermediates. Pb (NO3)2 in medium and high concentrations (15 and 25 µg/l) increased the levels of plasma amino acids compared to control (P < 0.01). In contrast, Pb (NO3)2 decreased the plasma levels of methylated metabolites (P < 0.01). The ketogenic metabolites and glycerol levels significantly elevated in fish exposed to 25 µg/l Pb (NO3)2 (P < 0.01). The plasma glucose levels increased in treatment, 5 µg/l Pb (NO3)2 and after a decline in treatment 15 µg/l Pb (NO3)2 elevated again in treatment 25 µg/l Pb (NO3)2 (P < 0.01).The plasma levels of lactate significantly increased in fish exposed to 5 and 15 µg/l Pb (NO3)2 and then declined to initial levels in treatment, 25 µg/l Pb (NO3)2 (P < 0.01). The plasma levels of TCA cycle intermediates significantly elevated in treatments 15 and 25 µg/l Pb (NO3)2 (P < 0.01). As a biomarker of oxidative stress, the plasma levels of malondialdehyde (MDA) showed significant increases in Pb (NO3)2 exposed fish (P < 0.01). During exposure period, wide ranges of liver tissue damages were also observed in Pb (NO3)2 exposed fish. In conclusion, exposure to Pb (NO3)2 affected the metabolome content of blood in grey mullet, mainly through inducing the biochemical pathways related to the metabolism of the amino acids, energetic metabolites and methylated metabolites. Our results may help to understand the effects of heavy metals on fish hematology from a molecular point of view.

Selenium nanoparticle and selenomethionine as feed additives: effects on growth performance, hepatic enzymes' activity, mucosal immune parameters, liver histology, and appetite-related gene transcript in goldfish (Carassius auratus).

The aim of this study was to assess the effects of different dietary selenium sources, selenium nanoparticle (nSe), and selenomethionine (SeMet) as feed additives on growth performance, hepatic enzymes' activity, biochemical, mucosal immune parameters, liver histology, and appetite-related gene transcript in goldfish (Carassius auratus). At first, goldfish juveniles (n=480; mean 4.54 g) were fed dietary selenium nanoparticle at 0, 0.3, 0.6, and 0.9 mg nSe/kg diet and SeMet at 0, 0.3, 0.6, and 0.9 mg Se/kg for 9 weeks. Growth performance was evaluated using standard procedures. Blood, skin mucus, and tissue samples (liver and intestine) were collected for biochemical, mucosal immune response, histology, and ghrelin and insulin-like growth factor-I (IGF-I) gene expression. The results showed that fish fed diets fortified with 0.6 mg nSe/kg and 0.6 mg Se/kg had a significant higher weight gain, specific growth rates (SGR), and lower feed conversion ratios (FCR) than fish fed basal diets (p<0.05). Furthermore, dietary nSe and SeMet enhanced blood biochemical profiles especially alkaline phosphatase (ALP) (p < 0.05) and mucosal immunity than the control group in goldfish. Moreover, the liver histological investigation showed that fish fed 0.9 mg of SeMet and nSe kg-1 diets had higher liver lesion scores such as karyolysis, lipidosis, and hyperemia while fish fed 0, 0.3, and 0.6 mg of SeMet and nSe kg-1 diets had small liver changes at 9 weeks. The study further established that inclusion of nSe and SeMet in the diet of goldfish greatly promoted ghrelin and IGF-1genes expressions (p <0.05). Overall, dietary nSe performs better than SeMet and basal diets. The results evoked that nSe and SeMet stimulate the growth, biochemical, and mucosal immunity in goldfish at 0.6 mg/kg.