Abstract
This study was designed to investigate the possibility of copper (Cu) to induce oxidative stress and biochemical perturbations in Nile tilapia liver, spleen, gills, kidney, intestine and muscle and the role of Vitamin C (Vit. C) and/or β-glucan in alleviating its toxic effects.Nile tilapia fish were randomly allotted into five groups of twenty-five each, group one served as control without any treatment, group two exposed to Cu (100µg/liter water), group three to five exposed to Cu plus Vit. C (500 mg/Kg diet), β-glucan (100mg/Kg diet) or combination of Vit. C and β-glucan respectively. Fish exposed to copper significantly (P≤0.05) reduced final weight, total gain, weight gain%, RGR and significantly deteriorate FCR and PER compared to control, while, Vitamin C and/or β-glucan supplementation markedly improved the mentioned parameters. Copper exposure reduce blood serum total protein, triglycerides and total cholesterol concentrations, while significantly increased serum uric acid, urea and concentrations compared with control. Moreover, copper exposure increased serum GOT, GPT, CAT and SOD enzymes activitiesand significantly reduced phagocytic index and activity compared to control. Vitamin C and/or β-glucan supplementation with copper exposure maintained the previous parameters near the normal and modulated antioxidant enzymes. Also, Vit. C or β-glucan reduce Cu residue in Nile tilapia muscle. Cu exposure leading to various pathological changes in liver (necrosis and mild vacuolation), kidney (tubular vacuolation), spleen (lymphoid depletion), gills (lamella fusion), intestine (enteritis) and muscles (Zenker’s necrosis), while dietary Vit.C and/or β-glucan supplementation reduce the pathological lesions induced by copper exposure.The present study could concluded thatdietary supplementation of 500 mg/Kg coated vitamin C plus 100 mg/Kg β-glucan reduced the harmful effects of Cu on Nile tilapia.

Key words: Nile tilapia – Copper toxicity – Vitamin C – β-glucan–Growth performance – Histopathological changes.