Oral treatment of mule ducks with arsenicals for inducing fatty liver.

The aim of this study was to determine the dosage and the compounds of arsenic that induce fatty liver in mule ducks and also to investigate their effects on tissue residues. One hundred four ducks, 8 wk old, were randomly selected for one of six dietary treatments in Trial 1 or one of seven dietary treatments in Trial 2. Different levels of roxarsone were administrated: 0, 10, 20, 30, 40, or 50 mg/d, respectively, in Trial 1. In Trial 2, the experimental treatments were of the same level (11.36 mg/d) with different sources of arsenic that included the control without As, roxarsone (3-nitro-4-hydroxyphenylarsonic acid), arsanilic acid, phenylarsonic acid, O-nitro-phenylarsonic acid, As2O3, or As2O5. Both trials lasted 3 wk, with 1 wk on the treatment followed by 2 wk of withdrawal. Results in Trial 1 showed that a dose of 40 mg roxarsone/d increased liver weight and caused fatty liver, whereas administration of 50 mg/d was lethal. In Trial 2, administration of arsenic (11.36 mg/d) for 1 wk significantly depressed feed intake in the roxarsone, As2O3, and As2O5 groups (P < 0.05), whereas the treatment significantly decreased only live weight gain in the roxarsone group (P < 0.05). Administration of roxarsone alone increased (P < 0.05) serum cholesterol (CHOL), albumin (ALB), and total protein (TP), whereas only As2O3 among treatments significantly decreased serum triacylglycerol (TG) concentration (P < 0.05). In the roxarsone, arsanilic acid, and phenylarsonic acid groups, serum high density lipoprotein (HDL) decreased to a greater extent (P < 0.05), and arsanilic acid treatment significantly increased the very low density lipoprotein (VLDL) (P < 0.05). After 2 wk of withdrawal, liver weights and relative liver weights were heavier in the treatment groups of roxarsone, As2O3, and As2O5 as compared to the control (P < 0.05). Levels of CHOL, TG, TP, and ALB were significantly higher in the groups treated with As2O3 or As2O5 as compared to the control (P < 0.05). The roxarsone and arsanilic acid treatments significantly decreased HDL and increased VLDL in plasma (P < 0.05). The creatine kinase (CK) level in the roxarsone, As2O3, and As2O5 groups was significantly higher compared to the control group (P < 0.05). Among the As sources, roxarsone, As2O3, and As2O5 caused fatty liver in mule ducks.