Abstract

An 8-week feeding trial was carried out with juvenile yellow catfish to study the effects of dietary available phosphorus (P) on growth performance, body composition, and hepatic antioxidant property. Six pellet diets were formulated to contain graded available P levels at 0.33, 0.56, 0.81, 1.15, 1.31, and 1.57% of dry matter, respectively. Triplicate tanks with each tank containing 60 juveniles (3.09 ± 0.03 g) were fed one of the six experimental diets for 8 weeks. Specific growth rate, feeding rate, and protein efficiency ratio were significantly higher at 0.81% dietary available P. Efficiency of P utilization distinctly decreased with increasing P level. Body lipid content significantly decreased while body ash and feces P content significantly increased with increasing P level. Quadratic regression analysis indicated that vertebrae P content was maximized at 1.21% dietary available P. Fish fed 1.57% dietary available P had highest activity of hepatic superoxide dismutase and catalase and malonaldehyde content. In conclusion, decreasing dietary available P increased P utilization efficiency and body lipid content while decreased vertebrae P content. Juvenile yellow catfish were subjected to oxidative damage under the condition of high dietary P content (1.57%), and the damage could not be eradicated by their own antioxidant defense system.

Highlights

  • Phosphorus (P) is an important constituent of nucleic acids and cell membranes and is directly involved in all energyproducing cellular reactions [1, 2]

  • The present study showed that lower dietary P level led to higher P utilization; similar results were observed in rainbow trout [24] and black sea bream [25]

  • We found hepatic superoxide dismutase (SOD), CAT, and MDA contents except GPx activities were significantly affected by dietary available P level

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Summary

Introduction

Phosphorus (P) is an important constituent of nucleic acids and cell membranes and is directly involved in all energyproducing cellular reactions [1, 2]. P deficiency or P excess could probably affect the production of ATP, the synthesis of nucleic acids, and the complement of cell membranes, cause anorexia, transient lethargy, reduced growth, and dark coloration [4]. Phosphorus deficiency enhanced lipid peroxidation and induced oxidative stress in plants [5], such as, bean [6], barley [7], and oilseed rape [8]. Overproduction of ROS results in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA [12]. The balance between the activities and the intracellular levels of these antioxidants is broken, and the imbalance will result in the accumulation of malonaldehyde (MDA) and lead to oxidative damage to cell [13]

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