Abstract
Copper (Cu) is a common heavy metal pollutant in aquatic environments that originates from natural as well as anthropogenic sources. The present study investigated whether Cu causes oxidative damage and induces changes in the expression of genes that encode tight junction (TJ) proteins, cytokines and antioxidant-related genes in the intestine of the grass carp (Ctenopharyngodon idella). We demonstrated that Cu decreases the survival rate of fish and increases oxidative damage as measured by increases in malondialdehyde and protein carbonyl contents. Cu exposure significantly decreased the expression of genes that encode the tight junction proteins, namely, claudin (CLDN)-c, -3 and -15 as well as occludin and zonula occludens-1, in the intestine of fish. In addition, Cu exposure increases the mRNA levels of the pro-inflammatory cytokines, specifically, IL-8, TNF-α and its related signalling factor (nuclear factor kappa B, NF-κB), which was partly correlated to the decreased mRNA levels of NF-κB inhibitor protein (IκB). These changes were associated with Cu-induced oxidative stress detected by corresponding decreases in glutathione (GSH) content, as well as decreases in the copper, zinc-superoxide dismutase (SOD1) and glutathione peroxidase (GPx) activities and mRNA levels, which were associated with the down-regulated antioxidant signalling factor NF-E2-related factor-2 (Nrf2) mRNA levels, and the Kelch-like-ECH-associated protein1 (Keap1) mRNA levels in the intestine of fish. Histidine supplementation in diets (3.7 up to 12.2 g/kg) blocked Cu-induced changes. These results indicated that Cu-induced decreases in intestinal TJ proteins and cytokine mRNA levels might be partially mediated by oxidative stress and are prevented by histidine supplementation in fish diet.
Highlights
Heavy metals occur naturally in aquatic environments, and excess heavy metals are harmful to fish [1]
percent weight gain (PWG), specific growth rate (SGR), feed efficiency (FE), protein efficiency ratio (PER) and FI were the lowest in fish that had been fed with the histidine-unsupplemented basal diet, and the values increased with increasing dietary histidine levels up to 7.9 mg/kg diet (PWG, SGR, FE and PER) and 5.9 mg/kg diet (FI); the levels decreased with additional increases in histidine concentrations
The dietary histidine requirement of young grass carp (279.1– 685.4 g) as estimated using a quadratic regression analysis based on the PWG (Fig 2) was 7.63 g/kg, which corresponded to 24.76 g/kg dietary protein
Summary
Heavy metals occur naturally in aquatic environments, and excess heavy metals are harmful to fish [1]. Our previous studies demonstrated that either waterborne Cu or dietary Cu exposure could cause lipid peroxidation and protein oxidation in the intestine of carps [7,8]. Al-Bairuty et al reported that waterborne Cu-exposure resulted in swollen goblet cells and villus tip erosion in the rainbow trout (Oncorhynchus mykiss) intestine [9]. These studies focused on heavy metal-induced intestinal histopathological changes in fish. To the best of our knowledge, few studies have investigated the mechanisms of heavy metal-induced intestinal damage in fish
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