A 2 x 3 factorial experiment was conducted to investigate the effects of silymarin-nanohydrogle (0, 500 free; 500 nano) and a mycotoxin (0; 2.2 mg/kg), silymarin contaminated diet on productive performance and certain serum biochemical parameters using 72 Japanese quail chicks in days 7-35 of age. Six experimental treatments consisting inclusion of 0 or 2.2 mg/kg aflatoxins in a basal diet fed to the birds receiving 0 or 500 mg/L silymarin in two free- or nanohydrogle forms via drinking water. Daily weight gain (DWG) and European production index (EPI) reduced by 6.7% and 13.6% while feed intake (FI) and FCR increased by 3.76% and 12% in the birds fed on the diet containing 2.2 mg/kg aflatoxin, respectively (p < .05). Administration of silymarin-nanohydrogle through drinking water improved FI and DWG by 3.7% and 8.1%, respectively (p < .05). Mean serum alkaline phosphatase (ALP) activity elevated by 26.1% and serum concentration of total protein (TP), glucose (GLU) and high density lipoproteins (HDL) declined by 14.4%, 6.1% and 27.1% in the birds fed on the aflatoxin-contaminated diet, respectively (p < .05). Mean serum concentration of BUN (86.4%) and GLU (12.0%) increased and Ca (10.3%) decreased in birds receiving 500 mg/kg silymarin-nanohydrogle (p < .05). The birds receiving silymarin-nanohydrogle in drinking water showed lesser liver and spleen percentage (p < .05). It was concluded that inclusion of 500 mg/kg silymarin-nanohydrogle in drinking water could significantly compensate the impaired growth performance and alter hepatic function in Japanese quails fed on a diet contaminating 2.2 mg aflatoxins.

In order to study the effects and mechanism of florfenicol (FFC) on the kidney function of broilers, 180 1-day-old broilers were randomly divided into 6 groups, 30 in each group. Except for the control group, different doses of FFC were added to drinking water in the other 5 groups (0.15 g/L, 0.3 g/L, 0.6 g/L, 1.2 g/L and 1.8 g/L). After continuous administration for 5 days, renal histopathological changes, serum renal function indicators, renal peroxidation products and antioxidant factors, and apoptotic factors were detected in broilers aged 21 and 42 days. The results showed that compared with the control group, the kidney tissue structure was disordered, the glomerulus was atrophic, the cystic cavity was enlarged, and the epithelial cells of renal tubules were seriously vacuolated in broilers of treatment groups. And with the growth of broilers, the kidney injury of broilers in the low-dose FFC group was relieved. FFC significantly increased the contents of uric acid (UA), blood urea nitrogen (BUN), creatinine (CRE) in serum and malondialdehyde (MDA) in kidney of broilers, but significantly reduced the levels of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) in kidney. FFC significantly inhibited the mRNA relative transcriptional levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase-1 (NQO-1), and increased the mRNA and protein expression levels of p53, Caspase-3 and Caspase-6 in kidney tissue of broilers. It is concluded that FFC has certain nephrotoxicity to broilers, and its effect on kidney is dose-dependent and reversible. FFC causes intense lipid peroxidation in broiler kidney by inhibiting the expression of related factors in the downstream signal pathway of Nrf2. FFC can also up-regulate the expression of pro-apoptotic factors and accelerate the abnormal apoptosis of renal cells, thus seriously affecting the renal function of broilers.