Cai-Xia Liu

Differential effects of acute and chronic zinc (Zn) exposure on hepatic lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco

The present study is conducted to determine the potential mechanisms of Zn on hepatic lipid deposition and metabolism for yellow catfish Pelteobagrus fulvidraco with 8-week chronic exposure to low Zn levels (Zn levels: 0.05, 0.35 and 0.86mg/l Zn, respectively) and 96-h acute exposure to a high Zn level (Zn level: 4.71mg/l Zn, respectively). For that purpose, hepatic lipid deposition and Zn accumulation, hepatic carnitine palmitoyltransferase I (CPT I) and lipoprotein lipase (LPL) activities, and the hepatic mRNA expression of ten genes involved in lipid metabolism are determined. Chronic (8 weeks) exposure to low Zn levels apparently increases hepatic lipid content, hepatosomatic index (HSI) (P<0.05) and LPL activity, and reduces hepatic CPT I activity. In contrast, the acute (96h) exposure to high Zn level reduces hepatic lipid content, HSI and LPL activity, and increases CPT I activity. The change of mRNA levels of genes related to lipid metabolism is Zn concentration-dependent. Pearson correlations among mRNA expression levels, lipid content, CPT I and LPL activities in liver are also observed in yellow catfish with the 8-week chronic Zn exposure. For the first time, our study demonstrates the effect of waterborne Zn exposure on lipid metabolism at the molecular levels in fish, which may contribute to understanding the mechanism of Zn-induced hepatic toxicity in fish.

Effect of waterborne zinc exposure on metal accumulation, enzymatic activities and histology of Synechogobius hasta

The present study was conducted to determine the metal accumulation, antioxidant enzymatic response, hepatic intermediary metabolism and histological changes in Synechogobius hasta exposed to 0.35 (control), 9.7 and 19.2mg/L Zn, respectively, on the 0, 4th, 8th and 12th day. Waterborne Zn exposure significantly reduced hepatosomatic index, hepatic lipid contents and fatty liver occurrence rate, increased Zn, Fe and Mn contents and reduced the contents of Cu and Ca in liver, and increased muscle Zn content. Waterborne Zn exposure also significantly influenced enzymatic activities involved in antioxidant responses (superoxide dismutase, catalase, glutathione-S-transferase, malondialdehyde) in liver and spleen, and changed hepatic intermediary enzymatic activities (succinate dehydrogenase, malic dehydrogenase, lactate dehydrogenase, lipoprotein lipase, hepatic lipase), impaired the histological structure of the gill and spleen, and reduced vacuolated hepatocytes. Thus, our study demonstrated for the first time that waterborne Zn exposure could reduce fatty liver syndrome in S. hasta.

Protective effects of calcium on copper toxicity in Pelteobagrus fulvidraco: Copper accumulation, enzymatic activities, histology

The present study was conducted to determine interactive effects of waterborne co-exposure of copper (Cu) and calcium (Ca) on Cu accumulation, enzymatic activities and histology in yellow catfish Pelteobagrus fulvidraco and test the prediction that Ca could protect against Cu--induced toxicity in the fish species. Yellow catfish were exposed to 0, 1.0, 2.0 mg Cu/l, in combination with 0 and 50 mg Ca/l. Waterborne Cu and Ca co-exposure influenced the majority of tested enzymatic activities (succinate dehydrogenase, malic dehydrogenase, lactate dehydrogenase, lipoprotein lipase and hepatic lipase), and changed Cu contents in several organs (gill, liver, kidney, gastrointestine and muscle). For histological observations, at the same Ca level, waterborne Cu exposure induced injuries in gills and liver. However, Ca addition seemed to mitigate the severity of Cu--induced injuries. Thus, our study demonstrated that Ca had the capacity to reduce Cu toxicity in P. fulvidraco.

Differential effects of the chronic and acute zinc exposure on carnitine composition, kinetics of carnitine palmitoyltransferases I (CPT I) and mRNA levels of CPT I isoforms in yellow catfish Pelteobagrus fulvidraco.

The present study is conducted to determine the effect of acute and chronic zinc (Zn) exposure on carnitine concentration, carnitine palmitoyltransferases I (CPT I) kinetics, and expression levels of CPT I isoforms in liver, muscle and heart of yellow catfish Pelteobagrus fulvidraco. To this end, yellow catfish are subjected to chronic waterborne Zn exposure (0.05 mg Zn L(-1), 0.35 mg Zn L(-1) and 0.86 mg Zn L(-1), respectively) for 8 weeks and acute Zn exposure (0.05 mg Zn L(-1) and 4.71 mg L(-1)Zn, respectively) for 96 h, respectively. Reduced Michaelis-Menten constants (Km) and maximal reaction rates (Vmax) values in liver and muscle are observed in fish exposed to chronic Zn concentration. In contrast, Vmax and Km values in heart increase with increasing Zn concentration. Chronic Zn exposure also significantly influences the contents of free carnitine (FC), total carnitine (TC) and acylcarnitine (AC) in liver and heart, but not in muscle. The acute Zn exposure significantly increases FC, AC, TC contents in liver and muscle, but reduces their contents in heart. The chronic and acute Zn exposure influences the mRNA levels of four CPT I isoforms (CPT Iα1b, CPT Iβ, CPT Iα2a and CPT Iα1a) in liver, muscle and heart. Furthermore, correlations are observed in the mRNA levels between CPT I isoforms and Km, and between isoforms expression and activity of CPT I. Thus, chronic and acute Zn exposure shows differential effects on carnitine content, CPT I kinetics and mRNA levels of four CPT I isoforms in yellow catfish, which provides new mechanism for Zn exposure on lipid metabolism and also novel insights into Zn toxicity in fish.

Effects of waterborne copper exposure on carnitine composition, kinetics of carnitine palmitoyltransferases I (CPT I) and mRNA levels of CPT I isoforms in yellow catfish Pelteobagrus fulvidraco

The present study was conducted to determine the effect of waterborne copper (Cu) exposure on carnitine concentration, carnitine palmitoyltransferases I (CPT I) kinetics, and expression levels of four CPT I isoforms in the liver, muscle and heart of yellow catfish Pelteobagrus fulvidraco. Yellow catfish were exposed to four waterborne copper (Cu) concentrations (2 (control), 24 (low), 71 (medium), 198 (high) μg Cu/l, respectively) for 6weeks. Waterborne Cu exposure increased maximal reaction rates (Vmax) in the liver and muscle, but not in the heart. Michaelis-Menten constants (Km) tended to increase in the liver, but decreased in the heart after Cu exposure. The contents of total carnitine (TC) and acylcarnitine (AC) in the liver, and free carnitine (FC) in the muscle increased with increasing waterborne Cu concentrations, while FC content in the muscle declined with the increase of Cu levels. Waterborne Cu exposure also significantly influenced carnitine composition and profiles in heart. The mRNA expression of CPT Iα1a, CPT Iα1b and CPT Iα2a in the liver, and CPT Iα1a, CPT Iα1b and CPT Iβ in the muscle as well as CPT Iα1a in the heart were up-regulated by Cu exposure. Additionally, correlations were observed in the expression levels of CPT I isoforms and Km for carnitine, and between CPT I isoform expression and CPT I activity. To our knowledge, for the first time, the present study provided evidence that waterborne Cu exposure could influence carnitine composition, CPT I kinetics and mRNA levels of four CPT I isoforms in yellow catfish, which served to increase our understanding of the mechanisms underlying lipid catabolism during Cu exposure.

Differential effects of dietary Cu deficiency and excess on carnitine status, kinetics and expression of CPT I in liver and muscle of yellow catfish Pelteobagrus fulvidraco.

The present study was conducted to determine the effect of dietary Cu deficiency and excess on carnitine status, kinetics and expression of CPT I in the liver and muscle of juvenile yellow catfish Pelteobagrus fulvidraco. To this end, yellow catfish were fed 0.76 (Cu deficiency), 4.18 (adequate Cu) and 92.45 (Cu excess) mg Cu kg(-1) diet, respectively, for 8 weeks. In the liver, Cu deficiency did not significantly affect the contents of FC, TC and AC, and the ratios of AC/FC and FC/TC. However, Cu excess reduced FC, TC and AC contents, and the ratio of AC/FC, but increased FC/TC ratio. In the muscle, dietary Cu levels showed no significant effects on the contents of FC, TC and AC as well as the ratio of FC/TC, but Cu excess significantly increased the ratio of AC/FC. Compared to the adequate Cu group, dietary Cu deficiency did not significantly affect the Vmax and Km values, and the ratio of Vmax/Km in the liver and muscle. However, Cu excess decreased Vmax and Vmax/Km ratio in the liver, and increased Vmax in the muscle. The mRNA expression of CPT Iα1a, CPT Iα1b, CPT Iα2a and CPT Iβ in the liver and muscle was influenced by dietary Cu levels. To our knowledge, the present study provided, for the first time, evidence that dietary Cu deficiency and excess differentially influenced carnitine status, kinetics and expression profiles of CPT I of yellow catfish, which would extend our understanding on Cu nutrition in fish.