CAJ | 학술논문

本试验旨在研究T-2毒素对BALB/c小鼠生长性能、血常规指标、血清生化指标和肝脏抗氧化能力的影响。选用平均体重约为20 g的BALB/c小鼠80只,随机分成4个组,每个组20个重复,每个重复1只小鼠。4个组分别为对照组和3个不同T-2毒素剂量组,即0.4、1.0和2.5 mg/kg BW组,连续灌服28 d。结果表明,2.5 mg/kg BW组小鼠死亡率达25%,平均日增重和平均日采食量极显著降低(P<0.01),心脏、肝脏、脾脏、肺脏、肾脏和大脑的脏器系数显著或极显著增加( P<0.05或P<0.01),睾丸、精囊腺、子宫和卵巢等生殖系统脏器系数显著或极显著降低(P<0.05或P<0.01)。与对照组相比,0.4和1.0 mg/kg BW组肝脏脏器系数极显著增加( P<0.01),白细胞( WBC)、淋巴细胞( LY)、单核细胞( MO)、中性粒细胞( GR)数量均显著或极显著增高(P<0.05或P<0.01)。与对照组相比,2.5 mg/kg BW组MO、GR、血小板(PLT)数量极显著增高( P<0.01),但红细胞数量( RBC)和血红蛋白( HGB)含量显著或极显著降低( P<0.05或P<0.01)。血清生化指标显示,随T-2毒素剂量的增加,葡萄糖( GLU)、尿素( urea)、肌酐(CRE)含量和碱性磷酸酶(ALP)、丙氨酸氨基转移酶(ALT)活性呈增加趋势,但甘油三酯( TG)和白蛋白( ALB)含量呈降低趋势,与对照组相比均差异显著或极显著( P<0.05或 P<0.01)。随T-2毒素剂量的增加,小鼠肝脏组织中丙二醛( MDA)含量呈增加趋势,超氧化物歧化酶( SOD)、过氧化氢酶( CAT)、谷胱甘肽过氧化物酶( GSH-Px)活性呈降低趋势。由此可知, T-2毒素剂量在低于1.0 mg/kg BW时对BALB/c小鼠具有免疫刺激作用,高剂量的T-2毒素抑制动物生长性能、引起肝脏和肾脏组织损伤、对肝脏的抗氧化能力也具有显著的抑制作用,呈剂量效应关系。
본시험지재연구T-2독소대BALB/c소서생장성능、혈상규지표、혈청생화지표화간장항양화능력적영향。선용평균체중약위20 g적BALB/c소서80지,수궤분성4개조,매개조20개중복,매개중복1지소서。4개조분별위대조조화3개불동T-2독소제량조,즉0.4、1.0화2.5 mg/kg BW조,련속관복28 d。결과표명,2.5 mg/kg BW조소서사망솔체25%,평균일증중화평균일채식량겁현저강저(P<0.01),심장、간장、비장、폐장、신장화대뇌적장기계수현저혹겁현저증가( P<0.05혹P<0.01),고환、정낭선、자궁화란소등생식계통장기계수현저혹겁현저강저(P<0.05혹P<0.01)。여대조조상비,0.4화1.0 mg/kg BW조간장장기계수겁현저증가( P<0.01),백세포( WBC)、림파세포( LY)、단핵세포( MO)、중성립세포( GR)수량균현저혹겁현저증고(P<0.05혹P<0.01)。여대조조상비,2.5 mg/kg BW조MO、GR、혈소판(PLT)수량겁현저증고( P<0.01),단홍세포수량( RBC)화혈홍단백( HGB)함량현저혹겁현저강저( P<0.05혹P<0.01)。혈청생화지표현시,수T-2독소제량적증가,포도당( GLU)、뇨소( urea)、기항(CRE)함량화감성린산매(ALP)、병안산안기전이매(ALT)활성정증가추세,단감유삼지( TG)화백단백( ALB)함량정강저추세,여대조조상비균차이현저혹겁현저( P<0.05혹 P<0.01)。수T-2독소제량적증가,소서간장조직중병이철( MDA)함량정증가추세,초양화물기화매( SOD)、과양화경매( CAT)、곡광감태과양화물매( GSH-Px)활성정강저추세。유차가지, T-2독소제량재저우1.0 mg/kg BW시대BALB/c소서구유면역자격작용,고제량적T-2독소억제동물생장성능、인기간장화신장조직손상、대간장적항양화능력야구유현저적억제작용,정제량효응관계。
This study was conducted to investigate the effects of T-2 toxin on growth performance, blood rou-tine examination, serum biochemical indexes and antioxidant ability of liver in mice. A total of 80 BALB/c mice weighted about 20 g were randomly allotted to 4 groups with 20 replicates per group and 1 mouse per rep-licate. The mice were fed one of the 4 kinds of diets [0 (control), 0.4, 1.0, 2.5 mg/kg BW T-2 toxin ex-posed daily via intragastric administration] for 28 days. The results showed as follows: in 2. 5 mg/kg BW group, the morality of mice was close to 25%, and average daily gain and average daily feed intake were sig-nificantly decreased (P<0.01). However, the organ coefficients of heart, liver, spleen, lung, kidney and brain in 2.5 mg/kg BW group were increased markedly (P<0.05 or P<0.01), but those of testis, seminal vesicle, uterus and ovaries were reduced significantly(P<0.05 or P<0.01). Compared with control group, or-gan coefficient of liver and the counts of white blood cell(WBC), lymphocyte(LY), monocytes(MO), neutrophil granulocyte (GR) were significantly increased in 0.4 and 1.0 mg/kg BW groups (P<0.05 or P<0.01), respectively. Additionally, compared with control group, the counts of MO, GR and platelet(PLT) in 2.5 mg/kg BW group were significantly increased (P<0.01), however, red blood count (RBC) and he-moglobin(HGB) content were significantly reduced(P<0.05 or P<0.01), respectively. Furthermore, in ser-um biochemical indexes, the contents of glucose(GLU), urea and creatinine(CRE), and the activities of al-kaline phosphatase(ALP) and alanine aminotransferase(ALT) had improved trends with the increase of T-2 toxin dose, but the contents of triglyceride(TG) and albumin(ALB) had reduced trends, and those were sig-nificantly different with those of control group(P<0.05 or P<0.01). In addition, with the increase of T-2 tox-in dose, the content of malondialdehyde(MDA) in liver tissue was also advanced, then the activities of super-oxide dismutase(SOD), catalase(CAT) and glutathione peroxidase(GSH-Px) had decreased trends. It is concluded that the supplementation of T-2 toxin under 1.0 mg/kg BW can induce the immunostimulation. Nev-ertheless, the excessive dose can cause the inhibition of growth performance, induce organ damage of liver and kidney, and reduce the antioxidant ability of liver significantly with dose-effect relationship.