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The present study was conducted to determine hepatic lipid metabolism and metal-element composition in Synechogobius hasta exposed to waterborne chronic copper (Cu) concentrations of control, 57, and 118 μg Cu/l, respectively, for 30 days. Growth decreased, but hepatosomatic index, viscerosomatic index, and hepatic lipid content increased with increasing waterborne Cu levels. Staining with oil red O showed extensive steatosis in liver of Cu-exposed fish. Cu exposure increased hepatic 6-phosphogluconate dehydrogenase, glucose-6-phosphate dehydrogenase, and malic enzyme activities, whereas fatty acid synthetase, isocitrate dehydrogenase, and carnitine palmitoyltransferases I activities remained unaffected. Cu, zinc, iron, and manganese contents were also changed in several tissues (gill, liver, spleen, gastrointestinal tract, and muscle) in a tissue-, dose-, and time-dependent manner. This was the first study to examine the effects of waterborne Cu exposure on several enzymatic activities mediating hepatic lipogenesis and lipolysis in fish as well as to show that waterborne Cu exposure could enhance the metabolism of lipid synthesis and consequently induce the increase of hepatic lipid deposition in S. hasta.

It is known that the biological half-life of silver in the central nervous system is longer than in other organs. However, the potential toxicity of silver nanoparticles (NPs) on brain tissue and the underlying mechanism(s) of action are not well understood. In this study, neurotoxicity of silver NPs was examined in rat after intragastric administration. After a two-week exposure to low-dose (1 mg/kg, body weight) or high-dose (10 mg/kg) silver NPs, the pathological and ultrastructural changes in brain tissue were evaluated with H&E staining and transmission electron microscopy. The mRNA expression levels of key tight junction proteins of the blood-brain barrier (BBB) were analyzed by real-time RT-PCR, and several inflammatory factors were assessed in blood using ELISA assay. We observed neuron shrinkage, cytoplasmic or foot swelling of astrocytes, and extra-vascular lymphocytes in silver NP exposure groups. The cadherin 1 (2(-ΔΔCt): 1.45-fold/control) and Claudin-1 (2(-ΔΔCt): 2.77-fold/control) were slightly increase in mRNA expression levels, and IL-4 significantly increased after silver NP exposure. It was suggest that silver NP can induce neuronal degeneration and astrocyte swelling, even with a low-dose (1 mg/kg) oral exposure. One potential mechanism for the effects of silver NPs to the nervous cells is involved in inflammatory effects.