CAJ | 학술논문

为了考察饲料中高浓度黄曲霉毒素B1( AFB1)对凡纳滨对虾Litopenaeus vannamei幼虾肝胰腺的影响，在水温为(28.06±0.09)℃的条件下，给体质量为(0.30±0.02) g的凡纳滨对虾幼虾投喂每千克饲料中含黄曲霉毒素B1( AFB1)为1600μg的饲料，对照组饲喂正常配合饲料，每组设3个平行，饲喂8周后取样，测定AFB1及其代谢产物黄曲霉毒素M1( AFM1)在幼虾肝胰腺、肠道、肌肉中的残留量，以及肝胰腺和血淋巴中的生化指标，并观察肝小管的显微结构。结果表明：幼虾持续8周摄入含高浓度AFB1的饲料时，肝胰腺中AFB1的残留量(2.11μg/kg)高于肠道残留量(0.11μg/kg)，肌肉中未检测到残留量；同样，肝胰腺中AFM1的残留量(0.32μg/kg)高于肠道残留量(0.05μg/kg)，肌肉中未检测到残留量；试验组幼虾肝胰腺中丙二醛(MDA)含量(62.60 nmol/mg)显著高于对照组(21.38 nmol/mg)(P<0.05)，但两组血淋巴中 MDA 含量无显著性差异(P>0.05)；试验组幼虾肝胰腺中超氧化物歧化酶(SOD)活性(26.25 U/mg)显著低于对照组(36.70 U/mg)(P<0.05)，但两组血淋巴中SOD活性无显著性差异(P>0.05)；对照组幼虾肝胰腺中活性氧(ROS)含量显著高于试验组(P<0.05)；试验组幼虾血淋巴中酚氧化酶(PO)活性显著高于对照组(P<0.05)。从切片显微结构观察可见，幼虾肝胰腺细胞受到损伤，损伤规律为近消化道损伤严重，逐渐向肝胰腺边缘扩散，表现为肝胰腺细胞紧缩，出现空泡区，食道周围肝细胞消失，严重的仅残留肝小管，甚至肝小管消失。研究表明，长时间投喂含有高浓度AFB1的饲料，凡纳滨对虾幼虾的肝胰腺受损且某些代谢生化指标受到不同程度的影响，同时在肝胰腺和肠道有黄曲霉毒素残留。
위료고찰사료중고농도황곡매독소B1( AFB1)대범납빈대하Litopenaeus vannamei유하간이선적영향，재수온위(28.06±0.09)℃적조건하，급체질량위(0.30±0.02) g적범납빈대하유하투위매천극사료중함황곡매독소B1( AFB1)위1600μg적사료，대조조사위정상배합사료，매조설3개평행，사위8주후취양，측정AFB1급기대사산물황곡매독소M1( AFM1)재유하간이선、장도、기육중적잔류량，이급간이선화혈림파중적생화지표，병관찰간소관적현미결구。결과표명：유하지속8주섭입함고농도AFB1적사료시，간이선중AFB1적잔류량(2.11μg/kg)고우장도잔류량(0.11μg/kg)，기육중미검측도잔류량；동양，간이선중AFM1적잔류량(0.32μg/kg)고우장도잔류량(0.05μg/kg)，기육중미검측도잔류량；시험조유하간이선중병이철(MDA)함량(62.60 nmol/mg)현저고우대조조(21.38 nmol/mg)(P<0.05)，단량조혈림파중 MDA 함량무현저성차이(P>0.05)；시험조유하간이선중초양화물기화매(SOD)활성(26.25 U/mg)현저저우대조조(36.70 U/mg)(P<0.05)，단량조혈림파중SOD활성무현저성차이(P>0.05)；대조조유하간이선중활성양(ROS)함량현저고우시험조(P<0.05)；시험조유하혈림파중분양화매(PO)활성현저고우대조조(P<0.05)。종절편현미결구관찰가견，유하간이선세포수도손상，손상규률위근소화도손상엄중，축점향간이선변연확산，표현위간이선세포긴축，출현공포구，식도주위간세포소실，엄중적부잔류간소관，심지간소관소실。연구표명，장시간투위함유고농도AFB1적사료，범납빈대하유하적간이선수손차모사대사생화지표수도불동정도적영향，동시재간이선화장도유황곡매독소잔류。
Juvenile Pacific white leg shrimp Litopenaeus vannamei with body weight of ( 0 . 30 ± 0 . 02 ) g were fed normal diet and the diet containing high-concentration (1600 μg/kg) of aflatoxin B1(AFB1) at (28. 06±0. 09)℃for 8 weeks with triplication to evaluate the effects of the dietary AFB1 on hepatopancreas. The residues of AFB1 and its metabolite AFM1 in hepatopancreas, intestine, and muscle and biochemical indices in hepatopancreas and hae-molymph were measured in the shrimp, and hepatopancreatic microstructure were observed in the juvenile shrimp fed the diet containing high level of aflatoxin B1 at the end of feeding trial. The results showed that there was higher residues of aflatoxin B1 in hepatopancreas (2. 11 μg/kg) than in intestine (0. 11 μg/kg) in the juvenile shrimp fed the diet containing high-concentration of aflatoxin B1 for a long term, no residues detected in muscle. Higher residual amount of AFM1 was found in the hepatopancreas (0. 32 μg/kg) than in the intestine (0. 05 μg/kg), no residues detected in muscle in the juvenile shrimp fed the diet containing high level of aflatoxin B1 at the end of feeding trial. There was significantly higher malonaldhyde (MDA) level (62. 60 nmol/mL) in hepatopancreas than that in control group ( 21 . 38 nmol/mL ) ( P<0 . 05 ) , without significant difference in serum MDA level ( P>0. 05). There was significantly lower activity of superoxide dismutase (SOD) (26. 25 U/mg) in treatment group than that in the control group (36. 70 U/mg) (P<0. 05), without significant difference in serum (P>0. 05). The content of reactive oxygen species ( ROS) in the hepatopancreas was shown to be significantly higher in treatment group than in the control group (P<0. 05). The phenol oxidase (PO) activity in serum was significantly higher in the experimental group than in the control group(P<0. 05). Under a microscope, the damaged hepatopancreas cells were found to be serious close to the digestive tract injury, and gradually spread to the edge of heptopancreas whose cells became tighter, hepatic cells around esophagus were disappeared, even only in the residual hepatic tu-bules. In conclusion, the hepatopancreatic and some biochemical indices will be influenced by high levels of AFB1 for a long time, and residues of AFB1 and AFM1 in hepatopancreas and gut.