Chen K L, Chiout P W
Department of Animal Science, National Chia-Yi University, Taiwan.
Poult Sci. 2001 Mar;80(3):295-301. doi: 10.1093/ps/80.3.295.
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.
本研究的目的是确定诱导骡鸭脂肪肝的砷的剂量和化合物形式，并研究其对组织残留的影响。在试验1中，随机选择104只8周龄的鸭子进行六种日粮处理之一，在试验2中则进行七种日粮处理之一。试验1中分别给予不同水平的洛克沙胂：0、10、20、30、40或50毫克/天。在试验2中，实验处理为相同水平（11.36毫克/天）但砷源不同，包括不含砷的对照组、洛克沙胂（3-硝基-4-羟基苯胂酸）、对氨基苯胂酸、苯胂酸、邻硝基苯胂酸、三氧化二砷或五氧化二砷。两个试验均持续3周，1周进行处理，随后2周停药。试验1的结果表明，每天40毫克洛克沙胂的剂量会增加肝脏重量并导致脂肪肝，而每天给予50毫克则具有致死性。在试验2中，给予砷（11.36毫克/天）1周后，洛克沙胂、三氧化二砷和五氧化二砷组的采食量显著降低（P<0.05），而该处理仅使洛克沙胂组的活体重增加显著降低（P<0.05）。单独给予洛克沙胂会增加（P<0.05）血清胆固醇（CHOL）、白蛋白（ALB）和总蛋白（TP），而在各处理中只有三氧化二砷显著降低血清三酰甘油（TG）浓度（P<0.05）。在洛克沙胂、对氨基苯胂酸和苯胂酸组中，血清高密度脂蛋白（HDL）下降幅度更大（P<0.05），对氨基苯胂酸处理显著增加极低密度脂蛋白（VLDL）（P<0.05）。停药2周后，与对照组相比，洛克沙胂、三氧化二砷和五氧化二砷处理组的肝脏重量和相对肝脏重量更重（P<0.05）。与对照组相比，三氧化二砷或五氧化二砷处理组的CHOL、TG、TP和ALB水平显著更高（P<0.05）。洛克沙胂和对氨基苯胂酸处理显著降低血浆HDL并增加VLDL（P<0.05）。洛克沙胂、三氧化二砷和五氧化二砷组的肌酸激酶（CK）水平显著高于对照组（P<0.05）。在砷源中，洛克沙胂、三氧化二砷和五氧化二砷会导致骡鸭脂肪肝。
